◀ Back to PIK3R1
PIK3CA — PIK3R1
Pathways - manually collected, often from reviews:
-
BioCarta the co-stimulatory signal during t-cell activation:
MHC II/TCR-CD3 complex (CD3G-HLA-DRB1-TRA@-CD3D-TRB@-HLA-DRA-CD3E-CD3Z)
→
PI3K complex (PIK3CA-PIK3R1)
(T cell activation, activates)
-
BioCarta the co-stimulatory signal during t-cell activation:
SHP-2 (PTPN11)
→
PI3K complex (PIK3CA-PIK3R1)
(T cell activation, inhibits)
-
BioCarta the co-stimulatory signal during t-cell activation:
PI3K complex (PIK3CA-PIK3R1)
→
LCK
(T cell activation, activates)
-
BioCarta the co-stimulatory signal during t-cell activation:
PI3K complex (PIK3CA-PIK3R1)
→
ITK
(T cell activation, activates)
-
BioCarta actions of nitric oxide in the heart:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta actions of nitric oxide in the heart:
VEGF/VEGF R complex (VEGF-FLT4_KDR_FLT1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta fc epsilon receptor i signaling in mast cells:
RAS (HRAS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta phospholipids as signalling intermediaries:
S1P/EDG1/G-beta/G-gamma/G-alpha-i complex (EDG1-GNB1-GNGT1-GNAI1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta role of erbb2 in signal transduction and oncology:
RAS (HRAS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta corticosteroids and cardioprotection:
glucocorticoid/glucocorticoid receptor/glucocorticoid/glucocorticoid receptor complex (NR3C1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta inactivation of gsk3 by akt causes accumulation of b-catenin in alveolar macrophages:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta regulation of bad phosphorylation:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta trka receptor signaling pathway:
NGF/TRkA complex (NTRK1-NGFB)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta ras-independent pathway in nk cell-mediated cytotoxicity:
AR ligand/Activating receptors complex (CD28_FCGR3B_FCGR3A_CD2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta regulation of eif-4e and p70s6 kinase:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta regulation of bad phosphorylation:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
-
BioCarta regulation of bad phosphorylation:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
BioCarta regulation of bad phosphorylation:
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta vegf hypoxia and angiogenesis:
VEGF/VEGF R complex (VEGF-FLT4_KDR_FLT1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta il-7 signal transduction:
IL-7/IL-7Ra/IL-2R-gamma/JAK1/JAK3 complex (ITGA2B-Il7r-IL2RG-JAK1-JAK3)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta il-2 receptor beta chain in t cell activation:
CBL
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta role of pi3k subunit p85 in regulation of actin organization and cell migration:
PI3K regulatory subunit polypeptide 1 (PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
BioCarta role of pi3k subunit p85 in regulation of actin organization and cell migration:
PDGF/PDGF R complex (PDGFRA-PDGFA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta inhibition of cellular proliferation by gleevec:
PI3K complex (PIK3CA-PIK3R1)
→
AKT (AKT1)
(modification, activates)
-
BioCarta akt signaling pathway:
GH/GH R complex (GH1-GHR)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta egf signaling pathway:
EGF/EGF-R complex (EGF-EGFR)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta tumor suppressor arf inhibits ribosomal biogenesis:
p14arf (CDKN2A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta role of erk5 in neuronal survival pathway:
neurotrophin/TRkA complex (NTF3_BDNF_NGFB-NTRK1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta corticosteroids and cardioprotection:
G-gamma/G-beta/GTP complex (GNGT1-GNB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta pdgf signaling pathway:
PDGF/PDGF/PDGF R/PDGF R complex (PDGFA-PDGFRA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta human cytomegalovirus and map kinase pathways:
PI3K complex (PIK3CA-PIK3R1)
→
CREB (CREB1)
(modification, activates)
-
BioCarta skeletal muscle hypertrophy is regulated via akt-mtor pathway:
IGF-1/IGF-1R complex (IGF1-IGF1R)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta ctcf: first multivalent nuclear factor:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
BioCarta il-2 receptor beta chain in t cell activation:
CRKL
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta t cell receptor signaling pathway:
PI3K complex (PIK3CA-PIK3R1)
→
Vav (VAV1)
(modification, activates)
-
BioCarta the co-stimulatory signal during t-cell activation:
CD28/CD80 complex (CD80-CD28)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta nerve growth factor pathway (ngf):
NGF/NGF R/NGF/NGF R complex (NGFB-NGFR)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
BioCarta cxcr4 signaling pathway:
g-gamma/g-beta complex (GNGT1-GNB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
NCI Pathway Database VEGFR1 specific signals:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database p75(NTR)-mediated signaling:
NGF (dimer)/p75(NTR) complex (NGF-NGFR)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Roux et al., J Biol Chem 2001*
Evidence: mutant phenotype, other species
-
NCI Pathway Database IL3-mediated signaling events:
IL3/IL3RA/CSF2RB (dodecamer)/YWHAZ/SHC complex (CSF2RB-YWHAZ-SHC1-IL3-IL3RA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Barry et al., J Biol Chem 2009, Gold et al., J Biol Chem 1994, Sato et al., EMBO J 1993
Evidence: mutant phenotype, assay
-
NCI Pathway Database E-cadherin signaling in the nascent adherens junction:
DLG1 (DLG1)
→
PI3K complex (PIK3CA-PIK3R1)
(translocation, activates)
Laprise et al., J Biol Chem 2004*
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
VAV1 (VAV1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Manetz et al., Mol Cell Biol 2001, Barker et al., Mol Biol Cell 1995
Evidence: assay, other species
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
Antigen/IgE/Fc epsilon R1/LYN/SYK complex (IGHE-SYK-LYN-MS4A2-FCER1G-FCER1A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Manetz et al., Mol Cell Biol 2001, Barker et al., Mol Biol Cell 1995
Evidence: assay, other species
-
NCI Pathway Database IL23-mediated signaling events:
STAT3 (STAT3)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Parham et al., J Immunol 2002, Cho et al., J Immunol 2006
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database IL23-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL23/IL23R/JAK2/TYK2 complex (IL23A-IL12B-IL23R-IL12RB1-JAK2-TYK2)
(modification, activates)
Parham et al., J Immunol 2002, Cho et al., J Immunol 2006
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
PI3K Class2 beta polypeptide (PIK3C2B)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Arcaro et al., EMBO J 2002*
Evidence: assay
-
NCI Pathway Database CDC42 signaling events:
CDC42/GTP complex (CDC42)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Tolias et al., J Biol Chem 1995*, Zheng et al., J Biol Chem 1994*, Keely et al., Nature 1997*
Evidence: assay, physical interaction
-
NCI Pathway Database EPHB forward signaling:
Ephrin B2/EPHB4 complex (EFNB2-EPHB4)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Maekawa et al., Arterioscler Thromb Vasc Biol 2003*
Evidence: assay
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
SHC/GRB2/SOS1/GAB1/PI3K complex (SHC1-GRB2-SOS1-GAB1-PIK3CA-PIK3R1)
→
SHC/GRB2/SOS1/GAB1 complex (SHC1-GRB2-SOS1-GAB1)
(modification, collaborate)
Obermeier et al., EMBO J 1993, Cunningham et al., J Biol Chem 1997, Holgado-Madruga et al., Proc Natl Acad Sci U S A 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
SHC/GRB2/SOS1/GAB1/PI3K complex (SHC1-GRB2-SOS1-GAB1-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Obermeier et al., EMBO J 1993, Cunningham et al., J Biol Chem 1997, Holgado-Madruga et al., Proc Natl Acad Sci U S A 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
SHC/GRB2/SOS1/GAB1 complex (SHC1-GRB2-SOS1-GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Obermeier et al., EMBO J 1993, Cunningham et al., J Biol Chem 1997, Holgado-Madruga et al., Proc Natl Acad Sci U S A 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
None
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, collaborate)
Augustine et al., Mol Cell Biol 1991, Gómez et al., J Immunol 1997
Evidence: assay, other species
-
NCI Pathway Database VEGFR1 specific signals:
VEGFR1 homodimer/PLGF homodimer complex (FLT1-PGF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Cai et al., Diabetes 2003*, Igarashi et al., Biochem Biophys Res Commun 1998
Evidence: other species
-
NCI Pathway Database IL4-mediated signaling events:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Blaeser et al., J Exp Med 2003*
Evidence: other species
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
PKC zeta (PRKCZ)
(modification, activates)
Gómez et al., Exp Cell Res 1995, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, other species
-
NCI Pathway Database Nongenotropic Androgen signaling:
T-DHT/AR/PELP1/Src/PI3K complex (AR-PELP1-SRC-PIK3CA-PIK3R1)
→
T-DHT/AR/PELP1/Src complex (AR-PELP1-SRC)
(modification, collaborate)
Castoria et al., J Cell Biol 2003
Evidence: physical interaction, other species
-
NCI Pathway Database Nongenotropic Androgen signaling:
T-DHT/AR/PELP1/Src/PI3K complex (AR-PELP1-SRC-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Castoria et al., J Cell Biol 2003
Evidence: physical interaction, other species
-
NCI Pathway Database Nongenotropic Androgen signaling:
T-DHT/AR/PELP1/Src complex (AR-PELP1-SRC)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Castoria et al., J Cell Biol 2003
Evidence: physical interaction, other species
-
NCI Pathway Database VEGFR3 signaling in lymphatic endothelium:
VEGFR3/VEGFC-D complex (FLT4-FIGF_VEGFC)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Mäkinen et al., EMBO J 2001, Salameh et al., Blood 2005
Evidence: assay
-
NCI Pathway Database VEGFR3 signaling in lymphatic endothelium:
SHC/GRB2/SOS1 complex (SOS1-GRB2-SHC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Mäkinen et al., EMBO J 2001, Salameh et al., Blood 2005
Evidence: assay
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
IRS2 (IRS2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET9/GFRalpha1/GDNF/SHC/GAB1/Grb2 complex (RET-GFRA1-GDNF-SHC1-GRB2-GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
Gab1 (GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
PTEN (PTEN)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
PI3K complex (PIK3CA-PIK3R1)
→
PI3K Class2 beta polypeptide (PIK3C2B)
(modification, activates)
-
NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1/IL2R gamma/JAK3/FES/IRS2 complex (IL4-IL4R-JAK1-IL2RG-JAK3-FES-IRS2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Jiang et al., J Immunol 2001, Wurster et al., Mol Cell Biol 2002, Sun et al., Nature 1995, Izuhara et al., Blood 1996
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
RAC1/GTP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
Cozzolino et al., Mol Biol Cell 2003
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Cozzolino et al., Mol Biol Cell 2003
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Cozzolino et al., Mol Biol Cell 2003
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GDP complex (RHOA)
(modification, activates)
Cozzolino et al., Mol Biol Cell 2003
Evidence: mutant phenotype
-
NCI Pathway Database Nongenotropic Androgen signaling:
RAC1-CDC42/GDP complex (RAC1_CDC42)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Papakonstanti et al., Mol Endocrinol 2003*
Evidence: assay
-
NCI Pathway Database Nongenotropic Androgen signaling:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Papakonstanti et al., Mol Endocrinol 2003*
Evidence: assay
-
NCI Pathway Database Nongenotropic Androgen signaling:
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Papakonstanti et al., Mol Endocrinol 2003*
Evidence: assay
-
NCI Pathway Database EPHA2 forward signaling:
Ephrin A1/EPHA2/PI3K complex (EFNA1-EPHA2-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Fang et al., J Biol Chem 2008, Pandey et al., J Biol Chem 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database EPHA2 forward signaling:
Ephrin A1/EPHA2/PI3K complex (EFNA1-EPHA2-PIK3CA-PIK3R1)
→
Ephrin A1/EPHA2 complex (EFNA1-EPHA2)
(modification, collaborate)
Fang et al., J Biol Chem 2008, Pandey et al., J Biol Chem 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database EPHA2 forward signaling:
PI3K complex (PIK3CA-PIK3R1)
→
Ephrin A1/EPHA2 complex (EFNA1-EPHA2)
(modification, collaborate)
Fang et al., J Biol Chem 2008, Pandey et al., J Biol Chem 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by Stem cell factor receptor (c-Kit):
LYN (LYN)
→
PI3K complex (PIK3CA-PIK3R1)
(cell migration, collaborate)
Price et al., Biochem Biophys Res Commun 1999*
Evidence: assay
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1)
→
AKT1 (AKT1)
(modification, activates)
-
NCI Pathway Database SHP2 signaling:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database SHP2 signaling:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database SHP2 signaling:
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GTP complex (RHOA)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database SHP2 signaling:
PI3K complex (PIK3CA-PIK3R1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
TRPV1 (TRPV1)
(modification, activates)
Zhang et al., EMBO J 2005
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
Src (SRC)
(modification, activates)
Zhang et al., EMBO J 2005
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
Tie2/Ang1 complex (ANGPT1-TEK)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Fujikawa et al., Exp Cell Res 1999, Audero et al., J Biol Chem 2004, Kontos et al., Mol Cell Biol 1998
Evidence: assay, physical interaction, other species
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
PI3K complex (PIK3CA-PIK3R1)
→
FAK (PTK2)
(modification, activates)
Kim et al., Circ Res 2000*
Evidence: assay
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
Tie2/Ang1/Shc complex (ANGPT1-TEK-SHC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Fujikawa et al., Exp Cell Res 1999, Audero et al., J Biol Chem 2004, Kontos et al., Mol Cell Biol 1998
Evidence: assay, physical interaction, other species
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS1 complex (INSR-INS-IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Lavan et al., J Biol Chem 1992*, Hadari et al., J Biol Chem 1992*, Okamoto et al., Biochem J 1993*, Giorgetti et al., J Biol Chem 1993*
Evidence: assay
-
NCI Pathway Database IL6-mediated signaling events:
GRB2/SOS1/GAB family/SHP2/PI3K complex (GRB2-SOS1-GAB1_GAB2-PTPN11-PIK3CA-PIK3R1)
→
AKT1 (AKT1)
(modification, activates)
Jee et al., J Invest Dermatol 2002
Evidence: mutant phenotype
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
E2/ER alpha (dimer)/PELP1/Src complex (ESR1-PELP1-SRC)
→
E2/ER alpha (dimer)/PELP1/Src/PI3K complex (ESR1-PELP1-SRC-PIK3CA-PIK3R1)
(modification, collaborate)
Simoncini et al., Nature 2000, Haynes et al., J Biol Chem 2003, Greger et al., Mol Cell Biol 2007, Cheskis et al., Steroids 2008
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
E2/ER alpha (dimer)/PELP1/Src complex (ESR1-PELP1-SRC)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Simoncini et al., Nature 2000, Haynes et al., J Biol Chem 2003, Greger et al., Mol Cell Biol 2007, Cheskis et al., Steroids 2008
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
E2/ER alpha (dimer)/PELP1/Src/PI3K complex (ESR1-PELP1-SRC-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Simoncini et al., Nature 2000, Haynes et al., J Biol Chem 2003, Greger et al., Mol Cell Biol 2007, Cheskis et al., Steroids 2008
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Johnston et al., J Biol Chem 1995
Evidence: physical interaction
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1-PIK3CA-PIK3R1)
(modification, collaborate)
Johnston et al., J Biol Chem 1995
Evidence: physical interaction
-
NCI Pathway Database IL2-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/IRS1-2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-IRS2_IRS1-PIK3CA-PIK3R1)
(modification, collaborate)
Johnston et al., J Biol Chem 1995
Evidence: physical interaction
-
NCI Pathway Database IFN-gamma pathway:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Nguyen et al., J Biol Chem 2001
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF/SHC/GAB1/Grb2 complex (RET-GFRA1-GDNF-SHC1-GRB2-GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
IRS2 (IRS2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Hennige et al., Mol Cell Endocrinol 2000, Hayashi et al., Oncogene 2000, Maeda et al., Biochem Biophys Res Commun 2004
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
alpha6/beta4 Integrin/Met complex (ITGA6)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Trusolino et al., Cell 2001
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
alpha6/beta4 Integrin/Met complex (ITGA6)
→
alpha6/beta4 Integrin/Met /SHC/PI3K complex (ITGA6-SHC1-PIK3CA-PIK3R1)
(modification, collaborate)
Trusolino et al., Cell 2001
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
PI3K complex (PIK3CA-PIK3R1)
→
SHC (SHC1)
(modification, collaborate)
Trusolino et al., Cell 2001
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
PI3K complex (PIK3CA-PIK3R1)
→
alpha6/beta4 Integrin/Met /SHC/PI3K complex (ITGA6-SHC1-PIK3CA-PIK3R1)
(modification, collaborate)
Trusolino et al., Cell 2001
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
SHC (SHC1)
→
alpha6/beta4 Integrin/Met /SHC/PI3K complex (ITGA6-SHC1-PIK3CA-PIK3R1)
(modification, collaborate)
Trusolino et al., Cell 2001
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET9/GFRalpha1/GDNF/Shank3/Grb2 complex (RET-SHANK3-GRB2-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Schuetz et al., J Cell Biol 2004
Evidence: mutant phenotype, assay
-
NCI Pathway Database BCR signaling pathway:
CD19 (CD19)
→
PI3K/BCAP/CD19 complex (CD19-PIK3CA-PIK3R1)
(modification, collaborate)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
CD19 (CD19)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN/SYK complex (LYN-SYK-CD79B-CD79A)
→
PI3K/BCAP/CD19 complex (CD19-PIK3CA-PIK3R1)
(modification, activates)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN/SYK complex (LYN-SYK-CD79B-CD79A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
PI3K/BCAP/CD19 complex (CD19-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
VAV2 (VAV2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Okada et al., Immunity 2000, Weng et al., J Biol Chem 1994
Evidence: assay, physical interaction
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Royal et al., Mol Biol Cell 2000*, Ishibe et al., Mol Cell 2004*, Bosse et al., Mol Cell Biol 2007
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Royal et al., Mol Biol Cell 2000*, Ishibe et al., Mol Cell 2004*, Bosse et al., Mol Cell Biol 2007
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Royal et al., Mol Biol Cell 2000*, Ishibe et al., Mol Cell 2004*, Bosse et al., Mol Cell Biol 2007
Evidence: mutant phenotype
-
NCI Pathway Database Osteopontin-mediated events:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Chellaiah et al., Mol Biol Cell 1996
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Okano et al., Biochem Biophys Res Commun 2003*
-
NCI Pathway Database BCR signaling pathway:
PI3K/BCAP/CD19 complex (CD19-PIK3CA-PIK3R1)
→
AKT1 (AKT1)
(modification, activates)
Inabe et al., Blood 2002*
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF complex (RET-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Fukuda et al., J Biol Chem 2002
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF/IRS1 complex (RET-IRS1-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Melillo et al., Oncogene 2001
Evidence: mutant phenotype, assay
-
NCI Pathway Database FGF signaling pathway:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Ong et al., Proc Natl Acad Sci U S A 2001
Evidence: assay
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
HGF(dimer)/MET(dimer)/GAB1 complex (MET-GAB1-HGF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Yu et al., J Biol Chem 2001, Yu et al., J Biol Chem 2002*, Graziani et al., J Biol Chem 1991*, Schaeper et al., Proc Natl Acad Sci U S A 2007, Ponzetto et al., Cell 1994
Evidence: assay, physical interaction
-
NCI Pathway Database PAR1-mediated thrombin signaling events:
G beta/gamma complex (GNB1-GNG2)
→
G beta/gamma/PI3K complex (GNB1-GNG2-PIK3CA-PIK3R1)
(modification, collaborate)
Ellis et al., J Biol Chem 1999*, Rahman et al., Circ Res 2002*
Evidence: genetic interaction
-
NCI Pathway Database PAR1-mediated thrombin signaling events:
G beta/gamma complex (GNB1-GNG2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Ellis et al., J Biol Chem 1999*, Rahman et al., Circ Res 2002*
Evidence: genetic interaction
-
NCI Pathway Database PAR1-mediated thrombin signaling events:
G beta/gamma/PI3K complex (GNB1-GNG2-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Ellis et al., J Biol Chem 1999*, Rahman et al., Circ Res 2002*
Evidence: genetic interaction
-
NCI Pathway Database Integrins in angiogenesis:
alphav/beta3 Integrin/JAM-A complex (F11R-ITGAV-ITGB3)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Naik et al., J Cell Sci 2006
Evidence: mutant phenotype, assay
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
Rac1b/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Chartier et al., J Cell Sci 2006
Evidence: mutant phenotype, assay
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
NGF (dimer)/TRKA complex (NTRK1-NGF)
→
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
(modification, activates)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
NGF (dimer)/TRKA complex (NTRK1-NGF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
→
4.1N (EPB41L1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
→
PIKE/GTP/4.1N complex (AGAP2-EPB41L1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K complex (PIK3CA-PIK3R1)
→
4.1N (EPB41L1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K complex (PIK3CA-PIK3R1)
→
PIKE/GTP/4.1N complex (AGAP2-EPB41L1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database S1P2 pathway:
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Sugimoto et al., Mol Cell Biol 2003, Arikawa et al., J Biol Chem 2003, Gonda et al., Biochem J 1999
-
NCI Pathway Database S1P2 pathway:
RhoA (RHOA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
Sugimoto et al., Mol Cell Biol 2003, Arikawa et al., J Biol Chem 2003, Gonda et al., Biochem J 1999
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
None
→
E2/ER alpha (dimer)/PELP1/Src/PI3K complex (ESR1-PELP1-SRC-PIK3CA-PIK3R1)
(modification, activates)
Haynes et al., Circ Res 2000, Hisamoto et al., J Biol Chem 2001, Haynes et al., J Biol Chem 2003, Greger et al., Mol Cell Biol 2007
Evidence: assay
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
E2/ER alpha (dimer)/PELP1/Src/PI3K complex (ESR1-PELP1-SRC-PIK3CA-PIK3R1)
→
AKT1 (AKT1)
(modification, activates)
Haynes et al., Circ Res 2000, Hisamoto et al., J Biol Chem 2001, Haynes et al., J Biol Chem 2003, Greger et al., Mol Cell Biol 2007
Evidence: assay
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer)/SHC/GRB2/GAB2 complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-CSF2-CSF2RA)
→
GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer)/SHC/GRB2/GAB2/PI3K complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-CSF2-CSF2RA-PIK3CA-PIK3R1)
(modification, collaborate)
Dijkers et al., Oncogene 1999, Gu et al., Mol Cell Biol 2000, Guthridge et al., EMBO J 2006, Sato et al., EMBO J 1993
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer)/SHC/GRB2/GAB2 complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-CSF2-CSF2RA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Dijkers et al., Oncogene 1999, Gu et al., Mol Cell Biol 2000, Guthridge et al., EMBO J 2006, Sato et al., EMBO J 1993
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dodecamer)/SHC/GRB2/GAB2/PI3K complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-CSF2-CSF2RA-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Dijkers et al., Oncogene 1999, Gu et al., Mol Cell Biol 2000, Guthridge et al., EMBO J 2006, Sato et al., EMBO J 1993
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
None
→
SHC/GRB2/SOS1/GAB1/PI3K complex (SHC1-GRB2-SOS1-GAB1-PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Maeda et al., Biochem Biophys Res Commun 2004, Asai et al., Development 2006*
Evidence: assay, other species
-
NCI Pathway Database S1P2 pathway:
IRS1 (IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Okamoto et al., Mol Cell Biol 2000*
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
RET51/GFRalpha1/GDNF complex (RET-GFRA1-GDNF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Murakami et al., Oncogene 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Signaling events regulated by Ret tyrosine kinase:
PI3K complex (PIK3CA-PIK3R1)
→
Crk/p130 Cas/Paxillin complex (CRK-BCAR1-PXN)
(modification, activates)
Murakami et al., Oncogene 1999
Evidence: assay, physical interaction
-
NCI Pathway Database FGF signaling pathway:
PI3K complex (PIK3CA-PIK3R1)
(transcription, inhibits)
Mochizuki et al., Oncogene 2002*, Flaumenhaft et al., J Cell Biol 1992*, Roghani et al., J Biol Chem 1996*
Evidence: mutant phenotype, assay
-
NCI Pathway Database Nectin adhesion pathway:
PDGF-BB/PDGFRB (dimer) complex (PDGFRB-PDGFB)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Kanzaki et al., J Cell Sci 2008
Evidence: mutant phenotype
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R beta/gamma/JAK1/Fyn/JAK3 complex (IL2RB-JAK1-FYN-IL2-IL2RG-JAK3)
→
IL2/IL2R beta/gamma/JAK1/Fyn/JAK3/PI3K complex (IL2RB-JAK1-FYN-IL2-IL2RG-JAK3-PIK3CA-PIK3R1)
(modification, collaborate)
Augustine et al., Mol Cell Biol 1991
Evidence: assay, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R beta/gamma/JAK1/Fyn/JAK3 complex (IL2RB-JAK1-FYN-IL2-IL2RG-JAK3)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Augustine et al., Mol Cell Biol 1991
Evidence: assay, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R beta/gamma/JAK1/Fyn/JAK3/PI3K complex (IL2RB-JAK1-FYN-IL2-IL2RG-JAK3-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Augustine et al., Mol Cell Biol 1991
Evidence: assay, other species
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Cascone et al., Blood 2003*
Evidence: mutant phenotype, assay
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
None
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
Gu et al., Mol Cell Biol 2000, Lindemann et al., J Biol Chem 2003, Akbar et al., Eur J Immunol 1996, Ahmed et al., Proc Natl Acad Sci U S A 1997, Reif et al., J Biol Chem 1997
Evidence: mutant phenotype, assay, other species
-
NCI Pathway Database Reelin signaling pathway:
RELN/VLDLR/DAB1 complex (RELN-VLDLR-DAB1)
→
RELN/VLDLR/DAB1/PI3K complex (RELN-VLDLR-DAB1-PIK3CA-PIK3R1)
(modification, collaborate)
Bock et al., J Biol Chem 2003
Evidence: assay, other species
-
NCI Pathway Database Reelin signaling pathway:
RELN/VLDLR/DAB1 complex (RELN-VLDLR-DAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Bock et al., J Biol Chem 2003
Evidence: assay, other species
-
NCI Pathway Database Reelin signaling pathway:
RELN/VLDLR/DAB1/PI3K complex (RELN-VLDLR-DAB1-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Bock et al., J Biol Chem 2003
Evidence: assay, other species
-
NCI Pathway Database Reelin signaling pathway:
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Bock et al., J Biol Chem 2003
Evidence: assay, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R beta/gamma/JAK1/LCK/JAK3/PI3K complex (IL2RB-JAK1-LCK-IL2-IL2RG-JAK3-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Tsujino et al., Genes Cells 1999, Merida et al., J Immunol 1991, Taichman et al., J Biol Chem 1993, González-García et al., J Biol Chem 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R beta/gamma/JAK1/LCK/JAK3/PI3K complex (IL2RB-JAK1-LCK-IL2-IL2RG-JAK3-PIK3CA-PIK3R1)
→
IL2/IL2R beta/gamma/JAK1/LCK/JAK3 complex (IL2RB-JAK1-LCK-IL2-IL2RG-JAK3)
(modification, collaborate)
Tsujino et al., Genes Cells 1999, Merida et al., J Immunol 1991, Taichman et al., J Biol Chem 1993, González-García et al., J Biol Chem 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database IL2-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL2/IL2R beta/gamma/JAK1/LCK/JAK3 complex (IL2RB-JAK1-LCK-IL2-IL2RG-JAK3)
(modification, collaborate)
Tsujino et al., Genes Cells 1999, Merida et al., J Immunol 1991, Taichman et al., J Biol Chem 1993, González-García et al., J Biol Chem 1997
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by VEGFR1 and VEGFR2:
Gab1 (GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Caron et al., Cell Signal 2009*
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events mediated by PTP1B:
PTP1B (PTPN1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
Venable et al., J Biol Chem 2000*
Evidence: mutant phenotype, other species
-
NCI Pathway Database Ephrin B reverse signaling:
Ephrin B1/EPHB1-2 complex (EFNB1-EPHB1_EPHB2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Prévost et al., Blood 2004
-
NCI Pathway Database IL4-mediated signaling events:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database E-cadherin signaling in keratinocytes:
E-cadherin/Ca2+/beta catenin-gamma catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1_JUP-CTNNA1-CTNND1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Xie et al., Mol Biol Cell 2005, Xie et al., J Biol Chem 2007
Evidence: assay, physical interaction
-
NCI Pathway Database IGF1 pathway:
IGF-1R heterotetramer/IGF1/IRS1 complex (IGF1R-IGF1-IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Mur et al., Endocrinology 2003
Evidence: assay
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
alpha6/beta4 Integrin/Laminin complex (ITGA6-ITGB4)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Chartier et al., J Cell Sci 2006
Evidence: mutant phenotype, assay
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
PI3K complex (PIK3CA-PIK3R1)
→
E-cadherin (CDH1)
(modification, collaborate)
Chartier et al., J Cell Sci 2006
Evidence: mutant phenotype, assay
-
NCI Pathway Database Insulin Pathway:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dimer)/YWHAZ/SHC/PI3K complex (CSF2RB-JAK2-YWHAZ-SHC1-PIK3CA-PIK3R1-CSF2-CSF2RA)
→
GMCSF/GMR alpha/CSF2RB/JAK2 (dimer)/YWHAZ/SHC complex (CSF2RB-JAK2-YWHAZ-SHC1-CSF2-CSF2RA)
(modification, collaborate)
Guthridge et al., Blood 2004, Guthridge et al., EMBO J 2006, Barry et al., J Biol Chem 2009, Gold et al., J Biol Chem 1994, Sato et al., EMBO J 1993
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dimer)/YWHAZ/SHC/PI3K complex (CSF2RB-JAK2-YWHAZ-SHC1-PIK3CA-PIK3R1-CSF2-CSF2RA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Guthridge et al., Blood 2004, Guthridge et al., EMBO J 2006, Barry et al., J Biol Chem 2009, Gold et al., J Biol Chem 1994, Sato et al., EMBO J 1993
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database GMCSF-mediated signaling events:
GMCSF/GMR alpha/CSF2RB/JAK2 (dimer)/YWHAZ/SHC complex (CSF2RB-JAK2-YWHAZ-SHC1-CSF2-CSF2RA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Guthridge et al., Blood 2004, Guthridge et al., EMBO J 2006, Barry et al., J Biol Chem 2009, Gold et al., J Biol Chem 1994, Sato et al., EMBO J 1993
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database BCR signaling pathway:
B-cell antigen/BCR complex/LYN complex (LYN-CD79B-CD79A)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Marshall et al., J Exp Med 2000, Anderson et al., Curr Biol 2000
Evidence: assay, physical interaction
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
Antigen/IgE/Fc epsilon R1/Fyn complex (FYN-FCER1A-MS4A2-IGHE-FCER1G)
→
GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
Antigen/IgE/Fc epsilon R1/Fyn complex (FYN-FCER1A-MS4A2-IGHE-FCER1G)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
GAB2 (GAB2)
→
GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
GAB2 (GAB2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
SHP2 (PTPN11)
→
GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
SHP2 (PTPN11)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database Fc-epsilon receptor I signaling in mast cells:
GAB2/PI3K/SHP2 complex (GAB2-PTPN11-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997, Gadina et al., J Immunol 1999
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997, Gadina et al., J Immunol 1999
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database IL2-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
RHOA/GTP complex (RHOA)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997, Gadina et al., J Immunol 1999
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database IL2-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2 complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11)
(modification, collaborate)
Gadina et al., J Biol Chem 2000, Gu et al., Mol Cell Biol 2000, Merida et al., J Immunol 1991, Truitt et al., J Biol Chem 1994, Kanazawa et al., Cell Immunol 1994, Gómez et al., J Immunol 1997, Gadina et al., J Immunol 1999
Evidence: mutant phenotype, assay, physical interaction, other species
-
NCI Pathway Database IL2 signaling events mediated by STAT5:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
→
STAT5 (dimer)-active (STAT5B/STAT5A)
(transcription, activates)
Moriggl et al., Immunity 1999, Brennan et al., Immunity 1997
Evidence: mutant phenotype, other species
-
NCI Pathway Database Nongenotropic Androgen signaling:
T-DHT ()
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Papakonstanti et al., Mol Endocrinol 2003*
Evidence: assay
-
NCI Pathway Database Plasma membrane estrogen receptor signaling:
None
→
E2/ER alpha (dimer)/PELP1/Src/PI3K complex (ESR1-PELP1-SRC-PIK3CA-PIK3R1)
(modification, collaborate)
Simoncini et al., Nature 2000, Haynes et al., J Biol Chem 2003
Evidence: mutant phenotype, assay
-
NCI Pathway Database IL5-mediated signaling events:
IL5/IL5RA/CSF2RB (hexamer)/JAK2/JAK2 complex (CSF2RB-IL5-IL5RA-JAK2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Dijkers et al., Oncogene 1999
Evidence: mutant phenotype, assay
-
NCI Pathway Database Signaling events mediated by VEGFR1 and VEGFR2:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Dance et al., J Biol Chem 2006*
-
NCI Pathway Database E-cadherin signaling in the nascent adherens junction:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Pece et al., J Biol Chem 1999*
Evidence: mutant phenotype, assay
-
NCI Pathway Database Osteopontin-mediated events:
Gelsolin/PI-3-4-5-P3/PI3K complex (GSN-PIK3CA-PIK3R1)
→
Gelsolin/PI-3-4-5-P3 complex (GSN)
(modification, collaborate)
Chellaiah et al., Mol Biol Cell 1996
Evidence: physical interaction
-
NCI Pathway Database Osteopontin-mediated events:
Gelsolin/PI-3-4-5-P3/PI3K complex (GSN-PIK3CA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Chellaiah et al., Mol Biol Cell 1996
Evidence: physical interaction
-
NCI Pathway Database Osteopontin-mediated events:
Gelsolin/PI-3-4-5-P3 complex (GSN)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Chellaiah et al., Mol Biol Cell 1996
Evidence: physical interaction
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Palacios et al., EMBO J 2001, Lamorte et al., Anticancer Res 2003*, Tushir et al., EMBO J 2007
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
ARF6/GDP complex (ARF6)
(modification, activates)
Palacios et al., EMBO J 2001, Lamorte et al., Anticancer Res 2003*, Tushir et al., EMBO J 2007
Evidence: mutant phenotype
-
NCI Pathway Database Signaling events mediated by Hepatocyte Growth Factor Receptor (c-Met):
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Palacios et al., EMBO J 2001, Lamorte et al., Anticancer Res 2003*, Tushir et al., EMBO J 2007
Evidence: mutant phenotype
-
NCI Pathway Database IL3-mediated signaling events:
IL3/IL3RA/CSF2RB (dodecamer)/JAK2/JAK2/SHC/GRB2/GAB2 complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-IL3-IL3RA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Gu et al., Mol Cell Biol 2000, Gu et al., Mol Cell 1998
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL3-mediated signaling events:
IL3/IL3RA/CSF2RB (dodecamer)/JAK2/JAK2/SHC/GRB2/GAB2 complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-IL3-IL3RA)
→
IL3/IL3RA/CSF2RB (dodecamer)/JAK2/JAK2/SHC/GRB2/GAB2/PI3K complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-IL3-IL3RA-PIK3CA-PIK3R1)
(modification, collaborate)
Gu et al., Mol Cell Biol 2000, Gu et al., Mol Cell 1998
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
Tie2/Ang2 complex (ANGPT2-TEK)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
-
NCI Pathway Database IL3-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL3/IL3RA/CSF2RB (dodecamer)/JAK2/JAK2/SHC/GRB2/GAB2/PI3K complex (CSF2RB-JAK2-SHC1-GRB2-GAB2-IL3-IL3RA-PIK3CA-PIK3R1)
(modification, collaborate)
Gu et al., Mol Cell Biol 2000, Gu et al., Mol Cell 1998
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 beta fragment/IL1R1/IL1RAP complex (IL1B-IL1R1-IL1RAP)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Sizemore et al., Mol Cell Biol 1999, Reddy et al., J Biol Chem 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
IL1 beta fragment/IL1R1/IL1RAP complex (IL1B-IL1R1-IL1RAP)
→
IL1 beta fragment/IL1R1/IL1RAP/PI3K complex (IL1B-IL1R1-IL1RAP-PIK3CA-PIK3R1)
(modification, collaborate)
Sizemore et al., Mol Cell Biol 1999, Reddy et al., J Biol Chem 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
IL1 beta fragment/IL1R1/IL1RAP/PI3K complex (IL1B-IL1R1-IL1RAP-PIK3CA-PIK3R1)
(modification, collaborate)
Sizemore et al., Mol Cell Biol 1999, Reddy et al., J Biol Chem 1997
Evidence: mutant phenotype, assay, physical interaction
-
NCI Pathway Database IL2-mediated signaling events:
RAF1 (RAF1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
Blanchard et al., Oncogene 2000, Lundin Brockdorff et al., Cytokine 2002, Karnitz et al., Mol Cell Biol 1995
Evidence: mutant phenotype, other species
-
NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1/IL2R gamma/JAK3/IRS1 complex (IL4-IL4R-JAK1-IL2RG-JAK3-IRS1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Johnston et al., J Biol Chem 1995, Sun et al., Nature 1995
Evidence: assay, physical interaction, other species
-
NCI Pathway Database IL1-mediated signaling events:
RelA (RELA)
→
IL1 beta fragment/IL1R1/IL1RAP/PI3K complex (IL1B-IL1R1-IL1RAP-PIK3CA-PIK3R1)
(modification, collaborate)
Sizemore et al., Mol Cell Biol 1999, Reddy et al., J Biol Chem 1997
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL1-mediated signaling events:
NF kappa B1 p50 (NFKB1)
→
IL1 beta fragment/IL1R1/IL1RAP/PI3K complex (IL1B-IL1R1-IL1RAP-PIK3CA-PIK3R1)
(modification, collaborate)
Sizemore et al., Mol Cell Biol 1999, Reddy et al., J Biol Chem 1997
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IFN-gamma pathway:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Nguyen et al., J Biol Chem 2001
Evidence: mutant phenotype
-
NCI Pathway Database E-cadherin signaling in the nascent adherens junction:
Src (SRC)
→
PI3K complex (PIK3CA-PIK3R1)
(translocation, activates)
Pang et al., J Biol Chem 2005*, Fukuyama et al., Oncogene 2006
Evidence: mutant phenotype, physical interaction, other species
-
NCI Pathway Database Signaling events mediated by VEGFR1 and VEGFR2:
Gab1 (GAB1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Carmeliet et al., Cell 1999, Chabot et al., Mol Cell Biol 2009*
Evidence: physical interaction
-
NCI Pathway Database E-cadherin signaling in keratinocytes:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Calautti et al., J Biol Chem 2005*, Xie et al., J Biol Chem 2007
Evidence: assay
-
NCI Pathway Database Atypical NF-kappaB pathway:
p110-alpha (PIK3CA)
→
I kappa B alpha/PIK3R1 complex (NFKBIA-PIK3R1)
(modification, collaborate)
Kang et al., Mol Cell Biochem 2003, Béraud et al., Proc Natl Acad Sci U S A 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Atypical NF-kappaB pathway:
p110-alpha (PIK3CA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Kang et al., Mol Cell Biochem 2003, Béraud et al., Proc Natl Acad Sci U S A 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Atypical NF-kappaB pathway:
NF kappa B1 p50/RelA complex (NFKB1-RELA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Kang et al., Mol Cell Biochem 2003, Béraud et al., Proc Natl Acad Sci U S A 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Atypical NF-kappaB pathway:
I kappa B alpha/PIK3R1 complex (NFKBIA-PIK3R1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Kang et al., Mol Cell Biochem 2003, Béraud et al., Proc Natl Acad Sci U S A 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Atypical NF-kappaB pathway:
NF kappa B1 p50/RelA/I kappa B alpha complex (NFKB1-NFKBIA-RELA)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Kang et al., Mol Cell Biochem 2003, Béraud et al., Proc Natl Acad Sci U S A 1999
Evidence: assay, physical interaction
-
NCI Pathway Database Angiopoietin receptor Tie2-mediated signaling:
FES (FES)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Mochizuki et al., J Cell Sci 2002*, Kanda et al., Cancer Res 2005*
Evidence: mutant phenotype, assay, other species
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
None
(modification, activates)
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
None
(modification, activates)
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SYK complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SYK)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Jiang et al., Blood 2003
Evidence: mutant phenotype
-
NCI Pathway Database E-cadherin signaling in the nascent adherens junction:
Src (SRC)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Fukuyama et al., Oncogene 2006
Evidence: mutant phenotype, assay, other species
-
NCI Pathway Database Netrin-mediated signaling events:
netrin 1/UNC5B/PIKE-L/GTP complex (NTN1-UNC5B-AGAP2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Tang et al., Nat Cell Biol 2008
Evidence: mutant phenotype
-
NCI Pathway Database EPHA2 forward signaling:
None
→
Ephrin A1/EPHA2/PI3K complex (EFNA1-EPHA2-PIK3CA-PIK3R1)
(modification, collaborate)
Pandey et al., J Biol Chem 1994
Evidence: assay
-
NCI Pathway Database IL4-mediated signaling events:
CBL (CBL)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Ueno et al., Blood 1998*
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Signaling events mediated by the Hedgehog family:
SMO (SMO)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Riobó et al., Proc Natl Acad Sci U S A 2006*
Evidence: mutant phenotype, other species
-
NCI Pathway Database SHP2 signaling:
RAF1 (RAF1)
→
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC/GRB2/SOS1/GAB2/SHP2/PI3K complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1-GRB2-SOS1-GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, activates)
Blanchard et al., Oncogene 2000, Lundin Brockdorff et al., Cytokine 2002, Karnitz et al., Mol Cell Biol 1995
Evidence: mutant phenotype
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Jiang et al., Blood 2003
Evidence: mutant phenotype
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Jiang et al., Blood 2003
Evidence: mutant phenotype
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Jiang et al., Blood 2003
Evidence: mutant phenotype
-
NCI Pathway Database Insulin Pathway:
Insulin Receptor/Insulin/IRS3 complex (INSR-INS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Xu et al., J Biol Chem 1999*
Evidence: assay, other species
-
NCI Pathway Database IFN-gamma pathway:
IFN-gamma/IFN-gammaR/JAK1/JAK1/JAK2/JAK2 complex (IFNGR1-JAK1-JAK2-IFNG)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Nguyen et al., J Biol Chem 2001, Deb et al., J Immunol 2003
Evidence: mutant phenotype
-
NCI Pathway Database IL2 signaling events mediated by PI3K:
IL2/IL2R beta/gamma/JAK1/LCK/JAK3/PI3K complex (IL2RB-JAK1-LCK-IL2-IL2RG-JAK3-PIK3CA-PIK3R1)
→
BCL-X (BCL2L1)
(transcription, activates)
González-García et al., J Biol Chem 1997
Evidence: mutant phenotype, other species
-
NCI Pathway Database BCR signaling pathway:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
-
NCI Pathway Database BCR signaling pathway:
PTEN (PTEN)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, inhibits)
-
NCI Pathway Database Osteopontin-mediated events:
Rho Family GTPase-active (RHOA/CDC42/RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Biswas et al., BMC cell biology 2004*, Chellaiah et al., Mol Biol Cell 1996
Evidence: mutant phenotype, assay
-
NCI Pathway Database IL6-mediated signaling events:
GRB2/SOS1/GAB family/SHP2 complex (GRB2-SOS1-GAB1_GAB2-PTPN11)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Takahashi-Tezuka et al., Mol Cell Biol 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL6-mediated signaling events:
GRB2/SOS1/GAB family/SHP2 complex (GRB2-SOS1-GAB1_GAB2-PTPN11)
→
GRB2/SOS1/GAB family/SHP2/PI3K complex (GRB2-SOS1-GAB1_GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, collaborate)
Takahashi-Tezuka et al., Mol Cell Biol 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL6-mediated signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
GRB2/SOS1/GAB family/SHP2/PI3K complex (GRB2-SOS1-GAB1_GAB2-PTPN11-PIK3CA-PIK3R1)
(modification, collaborate)
Takahashi-Tezuka et al., Mol Cell Biol 1998
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database IL4-mediated signaling events:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Aronica et al., Cytokine 2000*
Evidence: mutant phenotype, other species
-
NCI Pathway Database Ephrin B reverse signaling:
Fibrinogen complex (FGA-FGG-FGB)
→
PI3K complex (PIK3CA-PIK3R1)
(cell adhesion, collaborate)
Prévost et al., Blood 2004
Evidence: mutant phenotype
-
NCI Pathway Database Ephrin B reverse signaling:
alphaIIb/beta3 Integrin complex (ITGA2B-ITGB3)
→
PI3K complex (PIK3CA-PIK3R1)
(cell adhesion, activates)
Prévost et al., Blood 2004
Evidence: mutant phenotype
-
NCI Pathway Database Reelin signaling pathway:
RELN/VLDLR/DAB1/PI3K complex (RELN-VLDLR-DAB1-PIK3CA-PIK3R1)
→
AKT1 (AKT1)
(modification, activates)
Beffert et al., J Biol Chem 2002
Evidence: assay, other species
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
NGF (dimer)/TRKA complex (NTRK1-NGF)
→
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
(modification, activates)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
NGF (dimer)/TRKA complex (NTRK1-NGF)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K/PIKE/GTP complex (PIK3CA-PIK3R1-AGAP2)
→
PIKE/GTP complex (AGAP2)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Trk receptor signaling mediated by PI3K and PLC-gamma:
PI3K complex (PIK3CA-PIK3R1)
→
PIKE/GTP complex (AGAP2)
(modification, collaborate)
Ye et al., Cell 2000
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
RAS family/GTP/PI3K complex (PIK3CA-PIK3R1-HRAS_KRAS_HRAS_KRAS_NRAS)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database Neurotrophic factor-mediated Trk receptor signaling:
PI3K complex (PIK3CA-PIK3R1)
→
RAS family/GTP complex (HRAS_KRAS_HRAS_KRAS_NRAS)
(modification, collaborate)
Rodriguez-Viciana et al., Nature 1994
Evidence: mutant phenotype, physical interaction
-
NCI Pathway Database N-cadherin signaling events:
None
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Gavard et al., J Cell Sci 2004
Evidence: mutant phenotype, assay
-
NCI Pathway Database N-cadherin signaling events:
RAC1/GDP complex (RAC1)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, collaborate)
Gavard et al., J Cell Sci 2004
Evidence: mutant phenotype, assay
-
NCI Pathway Database N-cadherin signaling events:
PI3K complex (PIK3CA-PIK3R1)
→
None
(modification, activates)
Gavard et al., J Cell Sci 2004
Evidence: mutant phenotype, assay
-
NCI Pathway Database a6b1 and a6b4 Integrin signaling:
alpha6/beta4 Integrin/Laminin complex (ITGA6-ITGB4)
→
PI3K complex (PIK3CA-PIK3R1)
(modification, activates)
Chartier et al., J Cell Sci 2006, Shaw et al., Cell 1997*
Evidence: assay
-
Reactome Reaction:
PIK3CA
→
PIK3R1
(reaction)
Rodrigues et al., Mol Cell Biol 2000, Kainulainen et al., J Biol Chem 2000, Ong et al., Proc Natl Acad Sci U S A 2001, Guasch et al., Mol Cell Biol 2001, Demiroglu et al., Blood 2001, Agazie et al., Oncogene 2003, Jackson et al., Cancer Res 2004, Sordella et al., Science 2004, Chen et al., Proc Natl Acad Sci U S A 2004, Eswarakumar et al., Cytokine Growth Factor Rev 2005, Takeda et al., Clin Cancer Res 2007, Byron et al., Cancer Res 2008, Junttila et al., Cancer Cell 2009*, Jackson et al., Hum Pathol 2010, Wesche et al., Biochem J 2011, Odai et al., J Biol Chem 1995, Feshchenko et al., J Biol Chem 1998
-
Reactome Reaction:
PIK3CA
→
PIK3R1
(indirect_complex)
Kainulainen et al., J Biol Chem 2000, Ong et al., Proc Natl Acad Sci U S A 2001, Guasch et al., Mol Cell Biol 2001, Demiroglu et al., Blood 2001, Agazie et al., Oncogene 2003, Jackson et al., Cancer Res 2004, Sordella et al., Science 2004, Chen et al., Proc Natl Acad Sci U S A 2004, Eswarakumar et al., Cytokine Growth Factor Rev 2005, Takeda et al., Clin Cancer Res 2007, Byron et al., Cancer Res 2008, Junttila et al., Cancer Cell 2009*, Jackson et al., Hum Pathol 2010, Wesche et al., Biochem J 2011
-
Reactome Reaction:
PIK3CA
→
PIK3R1
(direct_complex)
Rodrigues et al., Mol Cell Biol 2000
-
WikiPathways AMP-activated Protein Kinase (AMPK) Signaling:
INS-IGF2
→
Complex of PIK3R3-PIK3R1-PIK3CB-PIK3CA-PIK3CG-PIK3CD-PIK3R2
(activation)
-
WikiPathways Insulin Signaling:
PIK3CD/PIK3C3/PIK3R3/PIK3R1/PIK3C2G/PIK3R2/PIK3CG/PIK3CB/PIK3R4/PIK3C2A/PIK3CA
→
Complex of IRS1-PIK3CA
(activation)
-
WikiPathways PI3K-AKT-mTOR signaling pathway and therapeutic opportunities:
HRAS/NRAS/KRAS
→
Complex of PIK3CA-PIK3CB-PIK3R1-PIK3R2-PIK3R3-PIK3CG
(activation)
-
WikiPathways Signaling Pathways in Glioblastoma:
GAB1
→
Complex of PIK3R1-PIK3R2-PIK3CA-PIK3CB-PIK3CD
(mim-stimulation)
-
WikiPathways Signaling Pathways in Glioblastoma:
SRC
→
Complex of PIK3R1-PIK3R2-PIK3CA-PIK3CB-PIK3CD
(mim-stimulation)
-
WikiPathways Signaling Pathways in Glioblastoma:
IRS1
→
Complex of PIK3R1-PIK3R2-PIK3CA-PIK3CB-PIK3CD
(mim-stimulation)
-
WikiPathways AMP-activated Protein Kinase (AMPK) Signaling:
Complex of PIK3R3-PIK3R1-PIK3CB-PIK3CA-PIK3CG-PIK3CD-PIK3R2
→
AKT1
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Bind Interaction:
PIK3CA
—
PIK3R1
Fruman et al., Annu Rev Biochem 1998*
-
IRef Biogrid Interaction:
PIK3CA
—
PIK3R1
(direct interaction, pull down)
Woscholski et al., J Biol Chem 1994*
-
IRef Biogrid Interaction:
PIK3CA
—
PIK3R1
(physical association, affinity chromatography technology)
Chamberlain et al., J Biol Chem 2004*
-
IRef Biogrid Interaction:
PIK3CA
—
PIK3R1
(direct interaction, pull down)
Ren et al., Mol Cell Biol 2005*
-
IRef Biogrid Interaction:
PIK3CA
—
PIK3R1
(physical association, affinity chromatography technology)
Kamal et al., FEBS Lett 2010*
-
MIPS CORUM Phosphatidylinositol 3-kinase (PIK3CA, PIK3R1):
Phosphatidylinositol 3-kinase (PIK3CA, PIK3R1) complex (PIK3CA-PIK3R1)
Huang et al., Science 2007*
-
IRef Corum Interaction:
PIK3CA
—
PIK3R1
(association, x-ray crystallography)
Huang et al., Science 2007*
-
IRef Hprd Interaction:
PIK3CA
—
PIK3R1
(in vivo)
Luo et al., J Cell Biol 2005*, Woscholski et al., J Biol Chem 1994*
-
IRef Hprd Interaction:
PIK3CA
—
PIK3R1
(in vitro)
Luo et al., J Cell Biol 2005*, Woscholski et al., J Biol Chem 1994*
-
IRef Intact Interaction:
PIK3CA
—
PIK3R1
(physical association, anti bait coimmunoprecipitation)
Kamal et al., FEBS Lett 2010*
-
IRef Intact Interaction:
PIK3CA
—
PIK3R1
(physical association, anti bait coimmunoprecipitation)
Beauséjour et al., Apoptosis 2012
-
IRef Intact Interaction:
PIK3CA
—
PIK3R1
(physical association, anti tag coimmunoprecipitation)
Hao et al., Cancer Cell 2013*
-
IRef Intact Interaction:
PIK3CA
—
PIK3R1
(physical association, anti tag coimmunoprecipitation)
Santos-Sierra et al., EMBO J 2009*
-
IRef Intact Interaction:
Complex of 81 proteins
(association, tandem affinity purification)
Pichlmair et al., Nature 2012
-
IRef Intact Interaction:
Complex of 43 proteins
(association, tandem affinity purification)
Pichlmair et al., Nature 2012
-
IRef Intact Interaction:
Complex of 18 proteins
(association, tandem affinity purification)
Pichlmair et al., Nature 2012
-
IRef Intact Interaction:
Complex of 20 proteins
(association, tandem affinity purification)
Pichlmair et al., Nature 2012
-
IRef Intact Interaction:
Complex of PIK3R1-PIK3R2-PIK3CA-PIK3R3
(association, anti bait coimmunoprecipitation)
Beauséjour et al., Apoptosis 2012
-
IRef Intact Interaction:
Complex of 111 proteins
(association, tandem affinity purification)
Pichlmair et al., Nature 2012
-
IRef Intact Interaction:
Complex of 29 proteins
(association, tandem affinity purification)
Li et al., Molecular systems biology 2013
-
IRef Intact Interaction:
Complex of 40 proteins
(association, tandem affinity purification)
Li et al., Molecular systems biology 2013
-
IRef Intact Interaction:
Complex of 25 proteins
(association, anti bait coimmunoprecipitation)
Hao et al., Cancer Cell 2013*
-
IRef Intact Interaction:
Complex of 12 proteins
(association, tandem affinity purification)
Brehme et al., Proc Natl Acad Sci U S A 2009
-
IRef Intact Interaction:
Complex of PIK3R1-PIK3CA
(association, anti bait coimmunoprecipitation)
Luo et al., J Cell Biol 2005*
-
IRef Ophid Interaction:
PIK3CA
—
PIK3R1
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
-
IRef Ophid Interaction:
PIK3CA
—
PIK3R1
(aggregation, confirmational text mining)
Woscholski et al., J Biol Chem 1994*
Text-mined interactions from Literome
Sutor et al., J Biol Chem 1999
:
Analysis of the upstream pathway leading to MEK activation revealed that inhibition of
PI3-K did not
block c-Raf activation, whereas MEK activation was effectively blocked under these conditions ... Because
c-Raf activation and MEK activation were inversely
affected by
PI3-K- and cAMP dependent pathways, we examined whether IL-3 activated the alternative Raf isoforms A-Raf and B-Raf ... Moreover,
A-Raf activation , like MEK activation, was blocked by inhibition of
PI3-K but was insensitive to cAMP
Uehara et al., Eur J Biochem 1999
:
We previously discovered that
insulin activates Ras and that this is
mediated by wortmannin-sensitive
PI 3-K ... Interestingly, treating 3T3-L1 cells with PTX attenuates the
activation by
insulin of both the Ras-MAPK cascade and
PI 3-K
Craddock et al., J Biol Chem 1999
:
Using regulated expression of dominant negative p85 ( Deltap85 ) in stably transfected IL-3 dependent BaF/3 cells, we have specifically investigated the
role of class IA
PI3K in
IL-3 signaling
Tan et al., Cancer Res 1999
(Breast Neoplasms) :
HRG-beta also
increased the kinase activities of extracellular signal regulated protein kinase ( ERK ) and
PI3K in these cells
Liu et al., Genes Dev 1999
:
Engagement of IL3-R and GM-CSF-R in these cells leads to increased and prolonged
PI3'K dependent PI ( 3,4,5 ) P3 accumulation and
PKB activation
Miura et al., Biochim Biophys Acta 1999
(Insulin Resistance) :
We have examined the effect of TNF-alpha on
insulin induced glucose uptake and activations of tyrosine kinase, IRS-1,
PI3K and PKC in rat adipocytes ... We have examined the
effect of
TNF-alpha on insulin induced glucose uptake and activations of tyrosine kinase, IRS-1,
PI3K and PKC in rat adipocytes
Ciprés et al., Eur J Immunol 1999
:
The requirement for
IL-2 induced
PI3K activity in suppressing the onset of apoptotic cell death is discussed
Takahashi et al., Am J Physiol 1999
:
These results indicate that ANG II stimulates
Akt/PKB activity via AT1 receptors in VSMC and that the activities of tyrosine kinase and
PI3K are
required for this activation ... These results indicate that ANG II stimulates
Akt/PKB activity via AT1 receptors in VSMC and that the activities of tyrosine kinase and
PI3K are
required for this activation
Li et al., Am J Physiol 1999
:
IGF-I activated a wortmannin-sensitive
PI3K and its purported effector, the atypical protein kinase C (PKC)-zeta
Sizemore et al., Mol Cell Biol 1999
:
In contrast,
PI3K inhibitors
block the IL-1 stimulated phosphorylation of
NF-kappaB itself, especially the p65/RelA subunit
Astoul et al., J Cell Biol 1999
:
Moreover,
PI3K signals are both necessary and
sufficient for sustained activation of
PKB in B lymphocytes
Campana et al., J Neurosci Res 1999
:
Phosphatidylinositol 3-kinase and Akt protein kinase
mediate IGF-I- and prosaptide induced survival in Schwann cells
Bhanot et al., Am J Physiol 1999
(Hyperinsulinism...) :
Basal and
insulin activated
PI3K activities were further enhanced up to 2-fold and 1.3-fold, respectively, in FF rats ... In summary, 1 ) the PI3K -- > PKB -- > S6K pathway was upregulated under basal conditions, and 2 ) insulin stimulation of
PI3K and S6K activities was
enhanced , but both
PKB and GSK-3 were refractory to the effects of insulin in FF rats
Kelley et al., J Biol Chem 1999
:
In normal human monocytes,
M-CSF increased the levels of tyrosine phosphorylated proteins and induced Akt activation in a
PI3K dependent manner ... In normal human monocytes, M-CSF increased the levels of tyrosine phosphorylated proteins and induced
Akt activation in a
PI3K dependent manner
Higaki et al., Arterioscler Thromb Vasc Biol 1999
:
We also found that
transforming growth factor-beta stimulated
PI3K activity and the phosphorylation of Akt, a downstream signaling molecule of PI3K
Ozes et al., Nature 1999
:
Wortmannin ( a PI(3)K inhibitor ), dominant negative
PI(3)K or kinase-dead Akt
inhibits TNF mediated
NF-kappaB activation ... Wortmannin ( a
PI(3)K inhibitor ), dominant negative PI(3)K or kinase-dead
Akt inhibits TNF mediated NF-kappaB activation
Lee-Fruman et al., Oncogene 1999
:
Similar to S6K1,
S6K2 is
activated by mitogens and by constitutively active
PI3K , and is inhibited by rapamycin as well as wortmannin
Gottschalk et al., Learn Mem 1999
:
Neurotrophin-3 (NT-3) , a close relative of BDNF, did not
activate MAPK or
PI3K and had no effect on synaptic fatigue in the neonatal hippocampus
Mounho et al., Toxicol Appl Pharmacol 1999
:
The pathway leading to peroxisome proliferator induced ERK activation is different than that induced by phorbol ester or EGF, since the
PI3K inhibitors
had no effect on
ERK phosphorylation induced by these agents
Hawkins et al., J Biol Chem 1999
:
To determine the time course of GlcN induced defects in
insulin stimulated
PI3K activity and peripheral insulin action, GlcN was administered for 30, 60, 90, or 120 min during 2-h euglycemic, hyperinsulinemic clamp studies ...
Activation of muscle
PI3K by
insulin was attenuated following only 30 min of GlcN infusion ( GlcN 30 min = 1.5-fold versus saline = 2.5-fold stimulation ; p < 0.05 )
Altiok et al., J Biol Chem 1999
(Breast Neoplasms) :
In the absence of heregulin, the ectopic expression of the constitutively active p110 subunit of
PI3K was
sufficient to induce
BRCA1 phosphorylation
Beitz et al., J Biol Chem 1999
:
Whereas CD19 does not appear to be involved in this SYK dependent pathway, the SYK substrate CBL is likely involved as the dominant negative SYK markedly attenuates CBL tyrosine phosphorylation and completely blocks the
BCR dependent association of CBL with p85
PI3K
Laffargue et al., J Biol Chem 1999
:
We have identified adherent cell lines where
lysophosphatidic acid (LPA) strongly and rapidly
activates the accumulation of
PI3K lipid products ... Finally, we show that
LPA can not
activate PI3K in cell lines lacking the EGFR/Gab1 pathway, including cells that transactivate the PDGF receptor ... Altogether, these results demonstrate that
activation of
PI3K by
LPA is conditioned by the ability of LPA to transactivate an EGFR/Gab1 signaling pathway
Sánchez-Margalet et al., J Cell Physiol 2000
:
In order to study the role of phosphatidylinositol-3-kinase (PI3K), PKB, FRAP, S6 kinase, and MAP kinase in insulin stimulated glycogen synthesis, we used a specific inhibitor of
PI3K , LY294002, the immunosuppressant
inhibitor of
FRAP , rapamycin, and the inhibitor of MAPK kinase ( MEK ) /MAPK, PD98059, in rat HTC hepatoma cells overexpressing human insulin receptors ... In order to study the role of phosphatidylinositol-3-kinase (PI3K), PKB, FRAP, S6 kinase, and MAP kinase in insulin stimulated glycogen synthesis, we used a specific inhibitor of
PI3K , LY294002, the immunosuppressant
inhibitor of FRAP, rapamycin, and the inhibitor of MAPK kinase ( MEK )
/MAPK , PD98059, in rat HTC hepatoma cells overexpressing human insulin receptors
Goswami et al., J Neurosci Res 2000
:
Inhibitors of
PI3K , wortmannin, and LY294002,
induced a time dependent activation of caspase-3 (
CPP32 ), with a peak at 6 hr, leading to subsequent cell death by apoptosis in a dorsal root ganglion cell line ( F-11 ) ... Lowering cyclic AMP ( cAMP ) levels enhanced both
caspase-3 activation and cell death
induced by
PI3K inhibitors, whereas a nonhydrolyzable cAMP analog ( Bt2cAMP ), lowered CPP32 and was protective
Zundel et al., Mol Cell Biol 2000
:
Overexpression of
caveolin 1 alone is
sufficient to alter
PI(3)K activity and sensitizes fibroblasts to ceramide induced cell death
Madrid et al., Mol Cell Biol 2000
:
In this study, we show that oncogenic
H-Ras requires
PI3K and Akt to stimulate the transcriptional activity of NF-kappaB ... In this study, we show that oncogenic H-Ras
requires PI3K and Akt to stimulate the transcriptional activity of
NF-kappaB
Desbois-Mouthon et al., Endocrinology 2000
:
Insulin inhibition of JNKs was
mediated by
PI 3-K , as it was blocked by wortmannin and LY294002 and required the de novo synthesis of a phosphatase ( s ), as it was abolished by orthovanadate and actinomycin D. MKP-1 was a good candidate because 1 ) insulin stimulation of MKP-1 expression correlated with insulin inhibition of JNKs ; 2 ) insulin stimulation of MKP-1 expression, like insulin inhibition of JNKs, was mediated by PI 3-K ; and 3 ) the transient expression of an antisense MKP-1 RNA reduced the insulin inhibitory effect on JNKs
Krasilnikov et al., Biochemistry (Mosc) 2000
(Cell Transformation, Neoplastic...) :
The transforming effect of PI3K is supposed to occur on the basis of complex alterations in cellular signaling pathways : appearance of constitutively generated
PI3K dependent mitogen signal and
activation of some protooncogenes ( src, ras, rac, etc. ),
PI3K/PKB-pathway stimulation resulting in delay of apoptosis and increase of cell survival, and actin cytoskeleton reorganization ... The transforming effect of PI3K is supposed to occur on the basis of complex alterations in cellular signaling pathways : appearance of constitutively generated
PI3K dependent mitogen signal and
activation of some protooncogenes ( src, ras, rac, etc. ),
PI3K/PKB-pathway stimulation resulting in delay of apoptosis and increase of cell survival, and actin cytoskeleton reorganization
Chandrasekher et al., Invest Ophthalmol Vis Sci 2000
:
Phosphatidylinositol 3-kinase in bovine lens and its
stimulation by insulin and
IGF-1 ...
Phosphatidylinositol 3-kinase in bovine lens and its
stimulation by
insulin and IGF-1
Ling et al., J Cell Biochem 1999
(Astrocytoma) :
Our data suggest a
role for PI3-K and
p125FAK complex formation in
PI3-K activation
Zhong et al., Cancer Res 2000
(Anoxia...) :
Here we demonstrate that in human prostate cancer cells, basal-, growth factor-, and mitogen induced expression of
hypoxia-inducible factor 1 (HIF-1) alpha , the regulated subunit of the transcription factor HIF-1, is
blocked by LY294002 and rapamycin, inhibitors of
PI3K and FRAP, respectively
Herbert et al., J Biol Chem 2000
:
Phosphatidylinositol 3-kinase and protein kinase B were
activated by
insulin but not by TPA
Gold et al., Immunity 2000
:
We define a signaling cascade in which
PI3K is
required to recruit
amphiphysin II to the phagosome, and amphiphysin II in turn recruits dynamin
Andreelli et al., Diabetologia 2000
(Diabetes Mellitus, Type 2) :
Because we have shown in an earlier study that there is also a defective regulation of p85 alpha
PI3K gene expression in
response to
insulin , these data support the hypothesis that alterations in the regulation of gene expression could be involved in the pathogenesis of Type II diabetes
Tang et al., J Biol Chem 2000
:
Activation of
PI3K leads to enhanced activity of
PKB and increased levels of the anti-apoptotic protein Bcl-X ( L )
Kim et al., FEBS Lett 2000
:
This study shows a direct evidence that the SH2-SH2-SH3 region of PLCgamma1 contributes to the NF-kappaB signaling and that MAPK, but not
PI3K and PKC, is
involved in SH2-SH2-SH3 mediated
NF-kappaB activation in these cells
Zheng et al., J Biol Chem 2000
(MAP Kinase Signaling System) :
PMA also decreased
IGF-1 induced tyrosine phosphorylation of insulin receptor substrate-1 and its association with
PI3K
Ram et al., J Cell Physiol 2000
(Breast Neoplasms) :
Phosphatidylinositol 3-kinase (PI3K) is activated by
p185(erbB-2) /erbB-3 heterodimers in cells stimulated by HRG, and
PI3K is constitutively
activated by p185(erbB-2) /erbB-3 in breast carcinoma cells that overexpress c-erbB-2 ... Furthermore, erbB-3 principally mediated the direct recruitment of p85 in cells stimulated by HRG or EGF, indicating that, in addition to the high-level
activation of
PI3K by
p185(erbB-2) / erbB-3, EGFR/erbB-3 heterodimer interaction is essential for the weak but significant level of PI3K activated by EGF in cells that express normal EGFR levels ... Furthermore, erbB-3 principally mediated the direct recruitment of p85 in cells stimulated by HRG or EGF, indicating that, in addition to the high-level activation of PI3K by p185(erbB-2) / erbB-3,
EGFR/erbB-3 heterodimer interaction is
essential for the weak but significant level of
PI3K activated by EGF in cells that express normal EGFR levels ... Finally,
HRG-beta was also an especially potent
inducer of
PI3K in the nontransformed MCF-10A cells, which were derived spontaneously from normal reduction mammoplasty tissue
Burow et al., Biochem Biophys Res Commun 2000
:
PI3K and Akt
stimulated NF-kappaB activation in a dose dependent manner, suggesting a common link between these two pathways ...
PI3K-Akt signaling
activated NF-kappaB through both TNFR signaling dependent and -independent mechanisms, potentially representing a mechanism by which Akt functions to suppress apoptosis in cancer
Ueki et al., J Clin Invest 2000
(Insulin Resistance) :
In primary hepatocytes isolated from null mice, expression of IRS-1 enhanced both
PI3K and PKB activities, but expression of
IRS-1Deltap85 enhanced only PKB
Grey et al., Endocrinology 2000
:
Taken together, the current data suggest that c-src, via its SH3 domain, may participate in
CSF-1 induced activation of
PI3-K and that PI3-K and c-src are in the signaling pathway that subserves CSF-1 induced cytoskeletal changes in osteoclasts
Wooten et al., Mol Cell Biol 2000
:
Inhibitors of PKC-iota activity and
PI3K had no effect on NGF induced MAPK or p38 activation but
reduced NGF stimulated
c-Jun N-terminal kinase activity ... Src,
PI3K , and PKC-iota were likewise
required for NGF induced
NF-kappaB activation and cell survival, whereas Ras was not required for either survival or NF-kappaB activation but was required for differentiation
Pham et al., Circ Res 2000
:
One mechanism involves
PI3K/PKB dependent phosphorylation of
4E-BP1 , which dissociates from eIF4E, allowing initiation of translation from the 7-methylGTP cap of mRNAs ...
Insulin or H ( 2 ) O ( 2 )
increased the phosphorylation ( activation ) of PKB through
PI3K , but, whereas insulin induced a sustained response, the response to H ( 2 ) O ( 2 ) was transient
Ceponis et al., J Biol Chem 2000
:
In contrast, although the
PI3K inhibitors wortmannin and LY294002 did not
affect IL-4 or IL-13
STAT 6 activation, they significantly inhibited the ability of either cytokine to lower TER ... In contrast, although the
PI3K inhibitors wortmannin and LY294002 did not
affect IL-4 or
IL-13 STAT 6 activation, they significantly inhibited the ability of either cytokine to lower TER ... In contrast, although the
PI3K inhibitors wortmannin and LY294002 did not
affect IL-4 or IL-13 STAT 6 activation, they significantly inhibited the ability of either cytokine to lower TER
Suzuki et al., Biochem Biophys Res Commun 2000
(Breast Neoplasms) :
While the IGF-I induced activation of
PKB/Akt was
inhibited by
PI3-K inhibitor LY294002 but not by MEK inhibitor PD98059, the activation of both MEK and ERK by IGF-I was inhibited by both ... While the IGF-I induced activation of
PKB/Akt was
inhibited by
PI3-K inhibitor LY294002 but not by MEK inhibitor PD98059, the activation of both MEK and ERK by IGF-I was inhibited by both
Lizcano et al., Biochem J 2000
:
However insulin-like growth factor 1, a potent activator of PI3K and
PKB does not increase the phosphorylation of Ser ( 136 ) in BAD transfected HEK-293 cells, and nor is the basal level of Ser ( 136 ) phosphorylation
suppressed by inhibitors of
PI3K
Li et al., Eur J Immunol 2000
(MAP Kinase Signaling System) :
Thus, in normal human B cells, PI3K is upstream of the Ca2+ response while
PI3K , Ca2+ release and protein kinase C are all
required for
ERK2 activation, and CD19 enhances the MAPK cascade at multiple levels, depending on the state of differentiation
Kim et al., Diabetes 2000
(Obesity) :
In adipose tissue of obese rats, in spite of an 86 % reduction in
insulin stimulated
PI3K activity, activation of Akt2 was increased
Okano et al., J Biol Chem 2000
(Esophageal Neoplasms) :
PI3K inhibitors, wortmannin or LY294002, significantly
blocked the
Akt kinase activity induced by EGF ... Robust activation of Akt2 by
EGF was observed in some cell lines in a
PI3K dependent manner ... Robust activation of
Akt2 by EGF was observed in some cell lines in a
PI3K dependent manner
Dufourny et al., J Endocrinol 2000
(Breast Neoplasms) :
Since transcriptional activation of the cyclin D1 promoter by EGF, E2 and TPA is independent of PI3-K activity, these findings suggest a post-transcriptional
role for
PI3-K in the regulation of
cyclin D1 expression ... Since transcriptional activation of the cyclin D1 promoter by
EGF , E2 and TPA is
independent of
PI3-K activity, these findings suggest a post-transcriptional role for PI3-K in the regulation of cyclin D1 expression
Sachinidis et al., Br J Pharmacol 2000
:
Furthermore CTX attenuated the
PDGF-BB induced tyrosine phosphorylation of the PDGF-Rbeta,
PI 3'-K , PLC-gamma1 and ERK1/2 indicating an action of cyclic AMP on PDGF-beta receptor
Sui et al., Br J Haematol 2000
:
Interestingly, both
EPO and SCF
induced activation of
PI3K ... Interestingly, both EPO and
SCF induced activation of
PI3K ... However, through
PI3K , SCF
caused activation of
protein kinase B (PKB) , an anti-apoptosis signal, whereas EPO led to activation of ERKs
Gonzalez-Robayna et al., Mol Endocrinol 2000
:
Lastly, FSH mediated phosphorylation of
p38MAPK is negatively
affected by A kinase and
PI3-K , suggesting that it may be downstream of specific members of the cAMP-GEF/Rap/Raf pathway ... Lastly, FSH mediated phosphorylation of
p38MAPK is negatively
affected by A kinase and
PI3-K , suggesting that it may be downstream of specific members of the cAMP-GEF/Rap/Raf pathway
Peyrollier et al., Biochem J 2000
:
PI3K activation was inhibited by wortmannin and was not
dependent upon
insulin receptor substrate-1 activation
Wu et al., Oncogene 2000
(Brain Neoplasms...) :
Reduced
EGF stimulated activation of
PI3-K was mediated by interactions between carboxyl terminus of SIRPalpha1 and the Src homology-2 (SH2) containing phosphotyrosine phosphatase, SHP2 ... Reduced EGF stimulated activation of
PI3-K was
mediated by interactions between carboxyl terminus of SIRPalpha1 and the Src homology-2 (SH2) containing phosphotyrosine phosphatase,
SHP2 ... These data reveal a pathway that negatively regulates
EGFR induced
PI3-K activation in glioblastoma cells and involves interactions between SHP2 and tyrosine phosphorylated SIRPalpha1 ... These data reveal a pathway that negatively regulates EGFR induced
PI3-K activation in glioblastoma cells and
involves interactions between
SHP2 and tyrosine phosphorylated SIRPalpha1 ... These data reveal a pathway that negatively regulates EGFR induced
PI3-K activation in glioblastoma cells and
involves interactions between SHP2 and tyrosine phosphorylated
SIRPalpha1
Sasaki et al., Nature 2000
(Adenocarcinoma...) :
PI(3)K mediated activation of the cell survival kinase
PKB/Akt , and negative regulation of PI(3)K signalling by the tumour suppressor PTEN ( refs 3, 4 ) are key regulatory events in tumorigenesis ...
PI(3)K mediated
activation of the cell survival kinase
PKB/Akt , and negative regulation of PI(3)K signalling by the tumour suppressor PTEN ( refs 3, 4 ) are key regulatory events in tumorigenesis ... PI(3)K mediated activation of the cell survival kinase PKB/Akt, and negative
regulation of
PI(3)K signalling by the tumour suppressor
PTEN ( refs 3, 4 ) are key regulatory events in tumorigenesis
Martelli et al., J Bone Miner Res 2000
:
In contrast, intranuclear translocation of
PI 3-K did not occur in
response to the proapoptotic cytokine
tumor necrosis factor alpha (TNF-alpha)
Kusch et al., J Biol Chem 2000
:
We demonstrate that
uPA induces
PI3-K activation, which is abolished in VSMC expressing the dominant negative form of Tyk2 ... The regulatory subunit
p85 of PI3-K co-immunoprecipitates with Tyk2 but not with Jak1, Jak2, or Jak3, and uPA stimulation
increases the
PI3-K activity in Tyk2 immunoprecipitates ... The regulatory subunit p85 of PI3-K co-immunoprecipitates with Tyk2 but not with Jak1, Jak2, or Jak3, and
uPA stimulation
increases the
PI3-K activity in Tyk2 immunoprecipitates ... We provide evidence that the
Tyk2 mediated
PI3-K activation in response to uPA is required for VSMC migration ... We provide evidence that the Tyk2 mediated
PI3-K activation in
response to
uPA is required for VSMC migration
Besset et al., J Biol Chem 2000
:
In agreement with Ras independent
activation of
PI3K by
GDNF in neuronal cells, survival of sympathetic neurons induced by GDNF was dependent on PI3K but was not affected by microinjection of blocking anti-Ras antibodies, which did compromise neuronal survival by nerve growth factor, suggesting that Ras is not required for GDNF induced survival of sympathetic neurons ... This latter complex can also assemble directly onto phosphorylated Tyr-1096, offering an alternative route to
PI3K activation by
GDNF
Gesbert et al., J Biol Chem 2000
:
The
PI3K inhibitor LY-294002
blocks the ability of BCR/ABL to induce
p27 ( Kip1 ) down-regulation and inhibits BCR/ABL induced entry into S phase
Demoulin et al., FEBS Lett 2000
:
We observed a
PI 3-K dependent phosphorylation of protein kinase B (PKB) in TS1 cells, but not in
BaF/9R , nor in other IL-9 dependent cell lines ... We observed a
PI 3-K dependent phosphorylation of
protein kinase B (PKB) in TS1 cells, but not in BaF/9R, nor in other IL-9 dependent cell lines
York et al., Mol Cell Biol 2000
:
We show here that
Rap1 activation
requires both TrkA internalization and
PI3-K , whereas Ras activation requires neither TrkA internalization nor PI3-K ... Both inhibitors of
PI3-K and inhibitors of endocytosis prevent GTP loading of Rap1 and
block sustained
ERK activation by NGF ... PI3-K and endocytosis may also regulate ERK signaling at a second site downstream of Ras, since both rapid ERK activation and the Ras dependent
activation of the MAP kinase kinase kinase
B-Raf are blocked by inhibition of either
PI3-K or endocytosis ... PI3-K and endocytosis may also regulate ERK signaling at a second site downstream of Ras, since both rapid
ERK activation and the Ras dependent activation of the MAP kinase kinase kinase B-Raf are blocked by inhibition of either
PI3-K or endocytosis
Ahmad et al., Cell Signal 2000
:
We report here that the
PI3K inhibitor, wortmannin,
prevented the IGF-1 dependent stimulation of
PDE3B activity
Mitsuuchi et al., Cancer Res 2000
(Ovarian Neoplasms) :
Experiments with additional ovarian carcinoma cell lines revealed that
PI3K is
involved in the expression of
p21 induced by cisplatin or paclitaxel in OVCAR-10 cells, which have wild-type p53, but not in OVCAR-5 cells, which lack functional p53
Otero et al., J Biol Chem 2001
(Lymphoma, B-Cell) :
A prominent feature of CD19 signaling is the binding and activation of phosphoinositide 3-kinase ( P13K ), which accounts for the majority of
PI3K activity
induced by
BCR ligation
Miyakawa et al., J Biol Chem 2001
:
In primary murine MKs,
TPO also
induced phosphorylation of SHP2, its association with p85 and enhanced
PI3K activity, but in contrast to the results in cell lines, neither Gab2 nor IRS2 are phosphorylated in MKs
Ebner et al., J Neurosci Res 2000
:
We demonstrate that
PI3K and Akt ( Ser-473 phosphorylation ) are activated in
response to platelet derived growth factor but not basic
fibroblast growth factor-2 ( FGF2 ) and that distinct forms of PI3K are activated in early progenitors and later-maturation pro-oligodendroblasts as identified by their sensitivity to wortmannin ... Our results therefore demonstrate that
PI3K-Akt signaling independently regulates proliferation and survival, that the form of PI3K is distinct in early progenitors and pro-oligodendroblasts, and that
FGF2 does not
activate this pathway in either primary glial cell population
Kawabe et al., J Hypertens 2000
(Insulin Resistance) :
Insulin stimulated activities of IRS-1 and
PI3-K , but not MAPK activity, were also attenuated in the presence of high concentrations of glucose
Birkenkamp et al., Exp Hematol 2000
(Acute Disease...) :
An inhibitor of
PI3-K differentially
affects proliferation and
IL-6 protein secretion in normal and leukemic myeloid cells depending on the stage of differentiation
van Dijk et al., Blood 2000
:
The
PI3-K dependent activation and phosphorylation of the tyrosine kinase
Tec and the adapter molecule p62Dok-1 are reported ... The
PI3-K dependent activation and phosphorylation of the tyrosine kinase Tec and the adapter molecule
p62Dok-1 are reported
Bracke et al., J Leukoc Biol 2000
(Asthma...) :
Moreover, inhibition of
PI3K in these cells
blocked the background and the TNF-alpha induced
IgA binding completely
Dijkers et al., Mol Cell Biol 2000
:
This transcriptional regulation occurs through modulation of the forkhead transcription factor FKHR-L1, and IL-3 inhibited
FKHR-L1 activity in a
PI3K dependent manner ... Taken together, these observations indicate that inhibition of p27 ( KIP1 ) transcription through
PI3K induced
FKHR-L1 phosphorylation provides a novel mechanism of regulating cytokine mediated survival and proliferation
Aikawa et al., Circulation 2000
:
Insulin strongly
activated both
PI3K and the putative downstream effector AKT : Moreover, a proapoptotic protein, BAD :, was significantly phosphorylated and inactivated by insulin through PI3K
Sumitomo et al., J Clin Invest 2000
:
Coimmunoprecipitation experiments show that
NEP associates with tyrosine phosphorylated Lyn kinase, which then binds the p85 subunit of phosphatidylinositol 3-kinase (PI3-K)
resulting in an
NEP-Lyn-PI3-K protein complex
Harada et al., J Biol Chem 2001
:
In contrast, the N191A mutant, which retains PI3K binding ability, resulted in a complete abrogation of activity, suggesting that
PI3K mediates a negative effect upon transcriptional activation of the
IL-2 gene ... Taken together, these data indicate that
PI3K , when associated with the YMNM motif, may
act as a negative mediator in CD28 mediated
IL-2 gene transcription
Tu et al., Cancer Res 2000
(MAP Kinase Signaling System...) :
IGF-I effectively
activated PI 3-K in 8226 and OCI-My5 MM cells, but IL-6 was ineffective ... However,
IL-6 successfully
activated PI 3-K in AF-10 MM cells and IL-6 dependent MH.60 plasmacytoma/hybridoma cells ...
IGF-I also successfully activated PI 3-K in four of four MM patient specimens, and IL-6
activated PI 3-K in three of four specimens ... IGF-I also successfully activated
PI 3-K in four of four MM patient specimens, and
IL-6 activated PI 3-K in three of four specimens
Lazaar et al., J Immunol 2001
:
VCAM-1 engagement also
stimulated a rapid increase in
PI3K activity
Yart et al., J Biol Chem 2001
:
Indeed, the association of
Gab1 with SHP2 was
blocked by
PI3K inhibitors, and expression of Gab1 mutant deficient for binding to SHP2 was found to inhibit Ras stimulation without interfering with PI3K activation ... Indeed, the association of Gab1 with
SHP2 was
blocked by
PI3K inhibitors, and expression of Gab1 mutant deficient for binding to SHP2 was found to inhibit Ras stimulation without interfering with PI3K activation
Ye et al., Cell 2000
:
Dominant negative
PIKE prevents the NGF enhancement of
PI3K and upregulation of cyclin D1 ... Overexpression of 4.1N abolishes
PIKE effects on
PI3K ...
Activation of nuclear
PI3K by
PIKE is inhibited by the NGF stimulated 4.1N translocation to the nucleus ... Thus, PIKE physiologically modulates the
activation by
NGF of nuclear
PI3K
Gagnon et al., Endocrinology 2001
:
Exogenous PI ( 3,4,5 ) P3 ( 10 microM ), the principal product of
IGF-1 stimulated
PI3K in 3T3-L1 preadipocytes, had a modest survival effect on its own, reducing cell death from 47.9 +/- 3.4 % to 35.6 +/- 3.5 %
Bobe et al., Blood 2001
(Agammaglobulinemia) :
Phosphatidylinositol 3-kinase dependent translocation of
phospholipase Cgamma2 in mouse megakaryocytes is independent of Bruton tyrosine kinase translocation
Zubilewicz et al., Invest Ophthalmol Vis Sci 2001
:
Inhibition of
PI 3-K/p70 ( S6K ) activities also unexpectedly
inhibited ERK activity, whereas the converse was not observed, suggesting that PI 3-K acted upstream from ERK and controlled this pathway for CEC proliferation
Hii et al., Immunology 2001
:
Incubation of neutrophils with cartilage resulted in the activation of PI3-K in neutrophils, consistent with a
role for
PI3-K in
proteoglycan degradation ... These data demonstrate that the
proteoglycan degradative activity of neutrophils
required PI3-K but not PKC or the ERK1/ERK2/ERK5 cascades and was insensitive to increases in intracellular cAMP concentrations
Carrillo et al., Endocrinology 2001
:
However, this
PI 3-K inhibitor also
reduced insulin mediated phosphorylation of p44/p42
MAPK in cultured rat hepatocytes, indicating that both the PI 3-K and MAPK pathways could be involved in PK-L activation by insulin ... From these findings it can be concluded that both
PI 3-K and MAPK pathways, but not p70 S6-kinase, are
involved in the short-term activation of PK-L by
insulin in rat hepatocytes
Trümper et al., Ann N Y Acad Sci 2000
:
Insulin and
IGF-1 stimulated
PI 3-K activity was mainly associated with insulin receptor substrate (IRS) isoforms IRS-1 and IRS-2 and less so with the IRS-isoform Grb-2 associated binder-1 (Gab-1) ...
Insulin and IGF-1
stimulated PI 3-K activity was mainly associated with insulin receptor substrate (IRS) isoforms IRS-1 and IRS-2 and less so with the IRS-isoform Grb-2 associated binder-1 (Gab-1) ... In contrast,
GLP-1 induced
PI 3-K activity mainly in Gab-1 and also in IRS-2 immunoprecipitates, although in an attenuated kinetic ... In contrast,
GLP-1 induced
PI 3-K activity mainly in Gab-1 and also in IRS-2 immunoprecipitates, although in an attenuated kinetic
Al-Okla et al., Cell Microbiol 1999
:
However,
PI-3K activation is not
involved in
IL-8 release
Baumgartner et al., Cell Microbiol 2000
:
PI3-K induction of
GM-CSF appears to be at the transcriptional level and, consistently, we demonstrate that PI3-K is also involved in the constitutive induction of AP-1 and NF-kappaB, which characterizes Theileria infected leucocytes ... PI3-K induction of GM-CSF appears to be at the transcriptional level and, consistently, we demonstrate that
PI3-K is also
involved in the constitutive induction of
AP-1 and NF-kappaB, which characterizes Theileria infected leucocytes ... PI3-K induction of GM-CSF appears to be at the transcriptional level and, consistently, we demonstrate that
PI3-K is also
involved in the constitutive induction of AP-1 and
NF-kappaB , which characterizes Theileria infected leucocytes
Wang et al., American journal of physiology. Renal physiology 2001
:
In A6 kidney cells, mineralocorticoid induction of the phosphorylated form of SGK preceded the increase in Na+ transport, and specific inhibition of
PI3K inhibited both phosphorylation of
SGK and mineralocorticoid induced Na+ transport
Hirose et al., Metabolism 2001
(Insulin Resistance) :
Denervation caused a decline in the
insulin induced binding of p85 regulatory subunit of PI 3-K to IRS-1 to 61 % ( P < .001 ) and IRS-1 associated
PI 3-K activity to 57 % ( P < .01 ) ... These results provide evidence that long-term denervation results in insulin resistance because of derangements at multiple points, including tyrosine phosphorylation of insulin receptor and its downstream signaling molecule,
IRS-1 , protein expression of IRS-1, and
activation of
PI 3-K
Chaudhary et al., J Cell Biochem 2001
:
Wortmannin ( 500 nM ), a specific inhibitor of phosphatidylinositol 3-kinase ( PI 3-K), inhibited the activation of ERK1 and ERK2 by PDGF-BB but not by FGF-2 suggesting that
PI 3-K mediated the activation of ERK MAPK pathway by PDGF-BB but not by
FGF-2 ... Wortmannin ( 500 nM ), a specific inhibitor of phosphatidylinositol 3-kinase ( PI 3-K), inhibited the activation of ERK1 and ERK2 by PDGF-BB but not by FGF-2 suggesting that
PI 3-K mediated the activation of ERK MAPK pathway by
PDGF-BB but not by FGF-2 ... Taken together, our data for the first time revealed that the activation of
ERK1/2 by PDGF-BB is
mediated by
PI 3-K , and secondly, Akt is activated by PDGF-BB and EGF but not by FGF-2 in human and mouse osteoblastic cells ... Taken together, our data for the first time revealed that the activation of ERK1/2 by
PDGF-BB is
mediated by
PI 3-K , and secondly, Akt is activated by PDGF-BB and EGF but not by FGF-2 in human and mouse osteoblastic cells
Shafrir et al., Diabetes Metab Res Rev 2001
(Diabetes Mellitus, Experimental...) :
Although evidence has been provided that the insulin receptor is activated, the possibility exists that cytosolic non-receptor tyrosine kinase, direct phosphorylation of
IRS-1 and
activation of
PI3-K , leading to GLUT4 translocation, are involved
Chen et al., EMBO Rep 2001
:
However, in this report we demonstrate that inhibition of epidermal growth factor (EGF) stimulated
PI3K activity by expression of the kinase-deficient PI3K p110 subunit ( p110delta kin ) does not
block the lysosomal targeting and degradation of the
EGF receptor (EGFR)
von Gise et al., Mol Cell Biol 2001
:
The survival effect of activated MEK in 32D cells is achieved by both MEK- and
PI3K dependent mechanisms and
results in the activation of PI3K and in the phosphorylation of
AKT
Santiago-Pérez et al., J Cell Physiol 2001
(MAP Kinase Signaling System) :
Accordingly,
ERK1/2 phosphorylation induced by UTP was
inhibited by the
PI3K inhibitors, wortmannin and LY294002, and the c-src inhibitors, radicicol and PP2, but not by inhibitors of protein kinase C ( PKC ) ... Accordingly,
ERK1/2 phosphorylation induced by UTP was
inhibited by the
PI3K inhibitors, wortmannin and LY294002, and the c-src inhibitors, radicicol and PP2, but not by inhibitors of protein kinase C ( PKC )
Palacio et al., Eur J Endocrinol 2001
:
In murine osteoclast-like cells grown from bone marrow cells co-cultured with osteoblasts, the
activation of the
PI 3-K by
CSF-1 was determined both in vivo and in vitro ... In osteoclast-like cells,
CSF-1 stimulated
PI 3-K activity ... In osteoclast-like cells,
CSF-1 stimulated
PI 3-K activity
Belletti et al., J Biol Chem 2001
:
The
role of
PI3K activity in the up-regulation of
Id2 gene expression by the IGF-IR was confirmed by different methods and in different cell types
Ingham et al., J Biol Chem 2001
:
Moreover, using confocal microscopy, we show that
BCR ligation can induce the translocation of Gab1 from the cytosol to the plasma membrane and that this
requires the Gab1 PH domain as well as
PI3K activity ... Moreover, using confocal microscopy, we show that BCR ligation can induce the translocation of
Gab1 from the cytosol to the plasma membrane and that this
requires the Gab1 PH domain as well as
PI3K activity
Lee et al., J Biol Chem 2001
:
We also demonstrated that HBx inhibits caspase 3 activity and HBx down-regulation of
caspase 3 activity was
blocked by the
PI3K inhibitor
Ellerbroek et al., Cancer Res 2001
(MAP Kinase Signaling System...) :
Inhibition of
PI3K and MAPK activity
impairs EGF stimulated cell migration, in vitro invasion, and
MMP-9 production
Reyes-Reyes et al., J Cell Sci 2001
(Leukemia) :
We found that integrins activated both NF-kappaB and
MAPK in a
PI 3-K dependent manner, as wortmannin and LY294002 blocked these responses ... We found that integrins activated both
NF-kappaB and MAPK in a
PI 3-K dependent manner, as wortmannin and LY294002 blocked these responses
Chen et al., Cancer Res 2001
(Fibrosarcoma) :
Hypoxia induced signaling also resulted in
PI 3-K dependent phosphorylation of
Akt on Ser-473, a modification of Akt that is important for its activation
Sheng et al., Cancer Res 2001
(MAP Kinase Signaling System) :
Inhibition of MAPK/ERK kinase activity by PD 98059 completely blocked the K-Ras mediated induction of COX-2, whereas inhibition of
PI3K/Akt/PKB activity with LY 294002 or by expressing a dominant negative Akt ( Akt-K179M ) partially
blocked the induction of
COX-2 by K-Ras
Sidhu et al., Mol Pharmacol 2001
:
We investigated the dose dependence for this response and for the
effects of
insulin and extracellular matrix on
PI3K signaling and CYP2E1 mRNA expression levels using a highly defined rat primary hepatocyte culture system
Li et al., Mol Cell Neurosci 2001
:
PI3K inhibitors that blocked NRG mediated rescue also
blocked the phosphorylation of Akt,
MAPK , and Bad ...
PI3K inhibitors that blocked NRG mediated rescue also
blocked the phosphorylation of
Akt , MAPK, and Bad
Wang et al., Gastroenterology 2001
:
The
PI3K inhibitor, wortmannin, in combination with sodium butyrate, synergistically
induced IAP and sucrase enzyme activities and IAP messenger RNA levels in a time- and dose dependent fashion
Melillo et al., Oncogene 2001
:
We have examined the mechanisms by which
Ret stimulates
PI3-K ... All together, these findings suggest that IRS-1 is a component of the signaling pathway which leads to
Ret mediated
PI3-K activation, a pathway which can be targeted by Hirschsprung associated Ret mutations
Kuo et al., Oncogene 2001
:
The involvement of
PI 3-K/Akt dependent up-regulation of
Mcl-1 in the prevention of apoptosis of Hep3B cells by interleukin-6 ... Our previous works have demonstrated that both
PI 3-K/Akt and STAT3 pathways were concomitantly activated and cooperatively
mediated the anti-apoptotic effect of
IL-6 ... However, the IL-6 induced
Mcl-1 up-regulation was effectively attenuated in the
presence of
PI 3-K inhibitors, LY294002 and wortmannin
Buxadé et al., Immunology 2001
:
The increase in translation of TNF-alpha due to serum could be inhibited by the phosphatidylinositol (PI) 3-K inhibitors, wortmannin and LY294002, suggesting that
PI 3-K is
involved in the translational control of
TNF-alpha by serum
Jiang et al., J Immunol 2001
:
Whereas a calcineurin dependent pathway was essential for Bik mRNA induction, both the phosphatidylinositol 3-kinase
(PI3K)- and the calcineurin dependent pathways were
required for the sustained production of
Bik protein
Gauthier et al., Am J Physiol Cell Physiol 2001
(MAP Kinase Signaling System) :
To investigate whether human intestinal epithelial cell survival involves distinct control mechanisms depending on the state of differentiation, we analyzed the in vitro effects of
insulin , pharmacological
inhibitors of Fak, MEK/Erk, and
PI3-K/Akt , and integrin ( beta1, beta4 ) -blocking antibodies on the survival of the well established human Caco-2 enterocyte-like and HIEC-6 cryptlike cell models ... Herein, we report that 1 ) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125(Fak), p42 ( Erk-2 ), and p57 ( Akt ) activated levels ; 2 ) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated ( subconfluent Caco-2, confluent HIEC-6 ) and differentiated ( 30 days postconfluent Caco-2 ) cells ; 3 ) exposure to insulin and the inhibition of Fak, MEK, and
PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed ; and 4 ) Fak, beta1 and beta4 integrins, as well as the
MEK/Erk and PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation ... Herein, we report that 1 ) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125(Fak), p42 ( Erk-2 ), and p57 ( Akt ) activated levels ; 2 ) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated ( subconfluent Caco-2, confluent HIEC-6 ) and differentiated ( 30 days postconfluent Caco-2 ) cells ; 3 ) exposure to insulin and the inhibition of Fak, MEK, and
PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed ; and 4 ) Fak, beta1 and beta4 integrins, as well as the MEK/Erk and
PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation
Phu et al., J Leukoc Biol 2001
:
Anti-CD3 induced
CD8 ( + ) T-cell proliferation and CTL development were
inhibited dose dependently by both
PI3-K inhibitors ...
IL-2 synthesis by anti-CD3 activated CD8 ( + ) T cells was also
diminished by
PI3-K inhibition ...
PI3-K inhibition
resulted in a modest decrease in anti-CD3 induced
CD4 ( + ) T-cell proliferation but failed to affect IL-2 expression by anti-CD3 activated CD4 ( + ) T cells ...
PI3-K inhibition during CTL induction
resulted in decreased levels of mRNAs coding for granzyme B, perforin, and
Fas ligand ...
PI3-K inhibition during CTL induction
resulted in decreased levels of mRNAs coding for
granzyme B , perforin, and Fas ligand ... These results support the conclusion that
PI3-K activation is
involved in T-cell receptor,
CD28 , and IL-2 receptor signaling of CD8 ( + ) T cells ... These results support the conclusion that
PI3-K activation is
involved in T-cell receptor, CD28, and
IL-2 receptor signaling of CD8 ( + ) T cells
Simpson et al., Mol Cell Biol 2001
(Breast Neoplasms) :
In addition,
PTEN , LY294002, and rapamycin, an inhibitor of mammalian target of rapamycin,
caused a reduction in the molecular weight of IRS-2 and an increase in the association of IRS-2 with
PI3K
Farese et al., Experimental biology and medicine (Maywood, N.J.) 2001
:
These changes include : ( i ) activation of phosphatidylinositol 3-kinase (PI3K) and production of PIP3 ; ( ii ) PIP3 dependent activation of atypical protein kinase Cs ( PKCs ) ; ( iii ) PIP3 dependent activation of PKB ; ( iv )
PI3K dependent activation of
phospholipase D and hydrolysis of phosphatidylcholine with subsequent increases in phosphatidic acid ( PA ) and diacylglycerol ( DAG ) ; ( v ) PI3K independent activation of glycerol-3-phosphate acylytansferase and increases in de novo synthesis of PA and DAG ; and ( vi ) activation of DAG-sensitive PKCs
Kojima et al., Exp Hematol 2001
(MAP Kinase Signaling System) :
TPO induces the association of tyrosine phosphorylated Gab1 with
p85-PI3K ... TPO
induces the association of tyrosine phosphorylated
Gab1 with
p85-PI3K
Islam et al., Invest Ophthalmol Vis Sci 2001
:
The data also show that
PLCgamma1 activation and cell proliferation were
inhibited by
PI3K inhibitors, suggesting a role for PI3K in EGF stimulated proliferation of corneal epithelial cells
Carrillo et al., Life Sci 2001
(Diabetes Mellitus, Experimental) :
In conclusion, increased expression of IR and
IRS-1 leads to increased association of
PI3K in vivo in diabetic regenerating rats
Johnson et al., J Virol 2001
:
The cellular kinases Akt and p70S6K and the transcription factor
NF-kappaB were activated in a
PI3-K dependent manner at similar times following HCMV infection
Honda et al., J Neurosci Res 2001
(Alzheimer Disease...) :
Furthermore, 17beta-estradiol induced phosphorylation of the cAMP response element binding protein ( CREB ) at Ser ( 133 ) within 15 min and then upregulated
Bcl-2 in a
PI3-K/Akt dependent manner
Zhong et al., Biochem Biophys Res Commun 2001
(Prostatic Neoplasms) :
Compared to that of HIF-1alpha, the constitutive, serum-,
EGF- , and PMA increased HIF-1beta protein expression were also
inhibited by selective
PI3K or FRAP/TOR inhibitors but in higher doses ... Compared to that of HIF-1alpha, the constitutive, serum-, EGF-, and PMA increased
HIF-1beta protein expression were also
inhibited by selective
PI3K or FRAP/TOR inhibitors but in higher doses
Weber et al., Comp Biochem Physiol B Biochem Mol Biol 2001
:
These data suggest that
PI 3-K activity is
required for GtH-
MIS- and IGF-I induction of GVBD in striped bass ... These data suggest that
PI 3-K activity is
required for GtH- MIS- and
IGF-I induction of GVBD in striped bass
Osawa et al., J Immunol 2001
:
TNF-alpha induced
activations of
PI3K and Akt were inhibited by DMS
Nguyen et al., J Biol Chem 2001
:
IFN gamma activates
PI3K as well as Akt in a variety of cell lines ... Constitutively active forms of
PI3K or Akt activate and their dominant negative derivatives
inhibit STAT1-driven transactivation in response to IFN gamma
Shaw et al., Mol Cell Biol 2001
(Neoplasm Invasiveness) :
In the present study, we investigated the signaling pathway by which the
alpha6beta4 integrin activates
PI3K ... We identified insulin receptor substrate 1 (IRS-1) and IRS-2 as signaling intermediates in the
activation of
PI3K by the
alpha6beta4 integrin ... Moreover, we identified a tyrosine residue in the cytoplasmic domain of the beta4 subunit, Y1494, that is required for alpha6beta4 dependent phosphorylation of
IRS-2 and
activation of
PI3K in response to receptor ligation
von Lindern et al., Oncogene 2001
(Cell Transformation, Neoplastic...) :
However, while v-ErbB transformed cells and normal progenitors depended on
PI3K signaling for renewal,
c-ErbB also
induces progenitor expansion by PI3K independent mechanisms
Nishimatsu et al., Circ Res 2001
:
AM-induced Akt phosphorylation was inhibited by pretreatment with a
calmodulin dependent protein kinase inhibitor as well as with
PI3K inhibitors
Fresno Vara et al., Mol Biol Cell 2001
:
In contrast, they inhibited the PRL dependent stimulation of the SFKs substrate Sam68, the phosphorylation of the tyrosine phosphatase Shp2, and the
PI3K dependent
Akt and p70S6k serine kinases ... In contrast, they inhibited the PRL dependent stimulation of the SFKs substrate Sam68, the phosphorylation of the tyrosine phosphatase Shp2, and the
PI3K dependent Akt and
p70S6k serine kinases
Nosaka et al., Biochem Biophys Res Commun 2001
(Fibrosarcoma) :
The
PI3K inhibitor LY294002 significantly
inhibited TNFalpha activation of Rac as well as Erk and abolished that of the PI3K target Akt, without showing any inhibitory effects on JNK and p38 activation ... The
PI3K inhibitor LY294002 significantly
inhibited TNFalpha activation of Rac as well as
Erk and abolished that of the PI3K target Akt, without showing any inhibitory effects on JNK and p38 activation ... The
PI3K inhibitor LY294002 significantly
inhibited TNFalpha activation of
Rac as well as Erk and abolished that of the PI3K target Akt, without showing any inhibitory effects on JNK and p38 activation
Terada et al., Kidney Int 2001
(Dehydration) :
PI3-K inhibitors and the dominant negative mutant of
PI3-K inhibited the hyperosmolality induced phosphorylation of
Akt
Sbrissa et al., Mol Cell Endocrinol 2001
:
Insulin but not PDGF or EGF stimulation of 3T3-L1 adipocytes markedly increased the PtdIns 3-P production ( 4.2-fold ) in
PIKfyve immune complexes, primarily as a
result of increased
PI 3-K intrinsic enzymatic activity ... Insulin but not PDGF or
EGF stimulation of 3T3-L1 adipocytes markedly increased the PtdIns 3-P production ( 4.2-fold ) in PIKfyve immune complexes, primarily as a
result of increased
PI 3-K intrinsic enzymatic activity ...
Insulin but not PDGF or EGF stimulation of 3T3-L1 adipocytes markedly increased the PtdIns 3-P production ( 4.2-fold ) in PIKfyve immune complexes, primarily as a
result of increased
PI 3-K intrinsic enzymatic activity ... Intriguingly, while both
insulin and PDGF
caused an increase of class I ( A )
PI 3-K activity co-immunoprecipitated with tyrosine phosphorylated proteins, only insulin treatment yielded an activation of class I(A) PI 3-K in PIKfyve immune complexes
Dong et al., Cancer Res 2001
(Carcinoma, Squamous Cell...) :
Hepatocyte growth factor/scatter factor induced activation of MEK and
PI3K signal pathways
contributes to expression of proangiogenic cytokines
interleukin-8 and vascular endothelial growth factor in head and neck squamous cell carcinoma ... Hepatocyte growth
factor/scatter factor induced activation of MEK and
PI3K signal pathways contributes to expression of proangiogenic cytokines interleukin-8 and vascular endothelial growth factor in head and neck squamous cell carcinoma ... Inhibitors of MEK ( U0126 ) and
PI3K ( LY294002 )
blocked p42/p44 ( erk ) and Akt, respectively, and partially blocked HGF induced production of IL-8 and VEGF, whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A ... Hepatocyte growth factor/scatter factor induced activation of MEK and
PI3K signal pathways
contributes to expression of proangiogenic cytokines interleukin-8 and
vascular endothelial growth factor in head and neck squamous cell carcinoma ... Inhibitors of MEK ( U0126 ) and
PI3K ( LY294002 ) blocked p42/p44 ( erk ) and Akt, respectively, and partially
blocked HGF induced production of IL-8 and
VEGF , whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A ... Inhibitors of MEK ( U0126 ) and
PI3K ( LY294002 )
blocked p42/p44 ( erk ) and Akt, respectively, and partially blocked HGF induced production of IL-8 and VEGF, whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A ... Inhibitors of MEK ( U0126 ) and
PI3K ( LY294002 )
blocked p42/p44 ( erk ) and
Akt , respectively, and partially blocked HGF induced production of IL-8 and VEGF, whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A ... Inhibitors of MEK ( U0126 ) and
PI3K ( LY294002 ) blocked p42/p44 ( erk ) and Akt, respectively, and partially
blocked HGF induced production of
IL-8 and VEGF, whereas the combination of U0126 and LY294002 completely inhibited expression of IL-8 and VEGF by UMSCC-11A
Chuenkova et al., Proc Natl Acad Sci U S A 2001
(Chagas Disease) :
In contrast, the Cys-rich domain of TS did not block apoptosis in Schwann cells overexpressing dominant negative
Akt or constitutively active PTEN, a negative
regulator of
PI3K/Akt signaling ... In contrast, the Cys-rich domain of TS did not block apoptosis in Schwann cells overexpressing dominant negative Akt or constitutively active
PTEN , a negative
regulator of
PI3K/Akt signaling
Guillemot et al., J Biol Chem 2001
(MAP Kinase Signaling System) :
Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of
Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also
involves PI3K and SHP-2 ... Taken together, these findings demonstrate that Ang II-induced
cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a p21(ras)/Raf-1/MEK/ERK dependent manner, and also
involves PI3K and SHP-2 ... Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a
p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves
PI3K and SHP-2 ... Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a
p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves
PI3K and SHP-2 ... Taken together, these findings demonstrate that Ang II-induced cyclin D1 up-regulation is mediated by the activation and specific interaction of Egr-1 with the -136 to -96 bp region of the cyclin D1 promoter and by activation of the -29 to +139 bp region, both in a
p21(ras)/Raf-1/MEK/ERK dependent manner, and also involves
PI3K and SHP-2
Sun et al., Cancer Res 2001
(Breast Neoplasms) :
Moreover, we found that
ERalpha binds to the p85alpha regulatory subunit of PI3K in the absence or presence of estradiol in epithelial cells and subsequently
activates PI3K/AKT2 , suggesting ERalpha regulation of PI3K/AKT2 through a nontranscriptional and ligand independent mechanism
Gooch et al., J Biol Chem 2001
(Hypertrophy) :
Inhibition of either MAPK or
PI3K , however,
had no effect on IGF-I induced hypertrophy or
ECM production
Richards et al., Endocrinology 2001
:
Collectively, these data suggest that the E2-induced decrease in uterine
insulin receptor substrate-2 requires IGF-I signaling, is not
dependent solely on insulin receptor substrate-1 and
PI3K , and is blocked by progesterone as well as by pharmacological inhibition of proteasomal protease activity ... Collectively, these data suggest that the E2-induced decrease in uterine insulin receptor substrate-2 requires
IGF-I signaling, is not
dependent solely on insulin receptor substrate-1 and
PI3K , and is blocked by progesterone as well as by pharmacological inhibition of proteasomal protease activity
Boileau et al., Endocrinology 2001
:
Phosphatidylinositol 3-kinase- dependent
protein kinase B activation is not sufficient to stimulate glucose transport and glycogen synthesis, highlighting the placenta as a nonclassic target of insulin for the regulation of glucose metabolism
Chian et al., Blood 2001
(Cell Transformation, Neoplastic) :
SCF stimulates association of
p85PI3K with phosphorylated tyrosine 721 of wild-type c-Kit
Lenferink et al., Cancer Res 2001
(Breast Neoplasms...) :
The inhibition of
PI3K/Akt resulted in increased activity of
glycogen synthase kinase-3beta , which phosphorylated cyclin D1, potentially reducing its steady-state levels
Stephens et al., J Biol Chem 2001
:
In endothelial cells overexpressing wild-type platelet derived growth factor beta ( PDGFbeta ) receptors, which express Bmx and Src as their major Btk ( Bruton 's tyrosine kinase ) family and Src family tyrosine kinases, respectively, PDGF can stimulate
PI3K dependent tyrosine phosphorylation of
DAPP-1 ... We show that in DT40 chicken B cell lines, antibody stimulation leads to
PI3K dependent tyrosine phosphorylation of
DAPP-1 that is lost in Lyn- or Syk-deficient cell lines but not Btk-deficient cell lines ...
PI3K dependent activation of
PKB is only lost in Syk-deficient lines
Fang et al., Nat Immunol 2001
:
Proteolysis independent
regulation of
PI3K by
Cbl-b mediated ubiquitination in T cells
Bretland et al., Cell Prolif 2001
(Carcinoma...) :
The effects of specific kinase inhibitors indicated that both Janus kinase 2 and protein kinase C partially protect HaCaT cells from anoikis through inducing cell cycle arrest of surviving nonadherent cells ; inhibition of
Phosphatidylinositol 3-kinase did not
induce cycling in HaCaTs prevented from adhesion but did stimulate anoikis
Wheeler et al., Mol Cell Biol 2001
:
Interaction with
Grb2 dramatically
increased the catalytic activity of this
PI3K
Mograbi et al., J Biol Chem 2001
:
Thus, both
PI3K and Akt act in concert to finely
regulate the level of
ERK
Rojnuckarin et al., J Biol Chem 2001
:
PKCzeta and
PI3K also
contribute to TPO induced
ERK activation in MKs, confirming their physiological relevance
Martín et al., J Neurochem 2001
:
Akt1 activation was blocked by the
PI3K inhibitor wortmannin ... The present findings demonstrate that
Akt1 is activated in response to Abeta ( 25-35 ) in a
PI3K dependent manner and that active Akt1 protects PC12 cells against the pro-apoptotic action of this peptide
Chen et al., EMBO Rep 2001
:
We conclude that wortmannin alters intracellular trafficking of EGFR by activating
Rab5 rather than by
inhibiting PI3K
Che et al., Circulation 2001
:
Because phosphatidylinositol 3'-kinase (PI3-K) is essential for Bcr/Abl leukemogenesis, we evaluated the
role of mouse PDGF-beta-receptor binding sites for
PI3-K ( Y708, Y719 ) and for phospholipase C-gamma ( Y977, Y989 ) in PDGF mediated
Bcr kinase activation
Goetze et al., Biochem Biophys Res Commun 2001
:
Insulin induced rapid tyrosine-phosphorylation of the IR and IRS-1 and
caused a 2.8-fold increase of IRS-1 bound
PI3K ...
TNFalpha had no effect on insulin induced tyrosine-phosphorylation of IR or IRS-1, but
inhibited insulin stimulated
IRS-1/PI3K-association by 84 % ... TNFalpha had no effect on insulin induced tyrosine-phosphorylation of IR or IRS-1, but inhibited
insulin stimulated
IRS-1/PI3K-association by 84 % ... Thus, TNFalpha selectively interferes with insulin 's antiapoptotic signaling in VSMC by inhibiting the association of
IRS-1/PI3K and the downstream
activation of
Akt
Komalavilas et al., J Appl Physiol 2001
:
Phosphatidylinositol 3-kinase ( PI3-kinase )
activates protein kinase B ( also known as Akt ), which phosphorylates and activates a cyclic nucleotide phosphodiesterase 3B
Bernabé et al., Exp Cell Res 2001
(MAP Kinase Signaling System) :
Thus, we propose that exposure to apoptotic concentrations of NO triggers ERK- and p38 dependent cytochrome c release,
caspase 3
activation , and
PI3K dependent Bcl-2 phosphorylation ... Thus, we propose that exposure to apoptotic concentrations of NO triggers ERK- and p38 dependent cytochrome c release, caspase 3 activation, and
PI3K dependent
Bcl-2 phosphorylation
Viñals et al., Mol Cell Biol 2001
:
We established that TGF-beta1 stimulated the expression of TGF-alpha mRNA and protein, the tyrosine phosphorylation of a 170-kDa membrane protein representing the
epidermal growth factor (EGF) receptor , and the delayed
activation of
PI3K/Akt and p42/p44 MAPK
Alonzi et al., Mol Cell Neurosci 2001
:
To assess the relative importance of these pathways in promoting the survival of cytokine dependent neurons, we conditionally inactivated
STAT3 in mice and
inhibited MEK,
PI3K , and Akt in cultured neurons using pharmacological reagents and by expressing specific inhibitory proteins
Riley et al., Oncogene 2001
:
This was because reduced
PI3-K activity
lead to proteolytic degradation of
p27
Hideshima et al., Oncogene 2001
(MAP Kinase Signaling System...) :
We demonstrate that Dex induced apoptosis in MM.1S cells is
mediated by downstream activation of
caspase-9 , with resultant caspase-3 cleavage ; and conversely, that IL-6 triggers activation of
PI3-K and its association with SHP2, inactivates caspase-9, and protects against Dex induced apoptosis ... We demonstrate that Dex induced apoptosis in MM.1S cells is mediated by downstream activation of caspase-9, with resultant caspase-3 cleavage ; and conversely, that
IL-6 triggers activation of
PI3-K and its association with SHP2, inactivates caspase-9, and protects against Dex induced apoptosis ... Finally, we show that
IL-6 triggered
PI3-K/Akt signaling in MM.1S cells inactivates forkhead transcriptional factor (FKHR), with related G1/S phase transition, whereas LY294002 blocks this signaling, resulting in upregulation of p27 ( KIP1 ) and G1 growth arrest
Wu et al., Oncogene 2001
(Glioblastoma) :
Based on these results, we conclude that SHP-2 is required for mediating PI3K/Akt activation, and the N-terminal SH2 domain is critically important for a `` positive ''
role of
SHP-2 in regulating
PI3K pathway activation
Niculescu et al., Immunol Res 2001
:
PI3-K activation by C5b-9 induced
STAT3 phosphorylation and translocation from cytoplasm to nucleus
Weber et al., Mol Biol Cell 2001
:
Our data suggest that inhibition of initial
PI3-K activation by inactive
H-Ras or sustained activation of an inhibitory ERK pathway by active H-Ras prevail to abolish LFA-1 regulation and transendothelial migration induced by SDF-1alpha in leukocytes, establishing a complex and bimodal involvement of H-Ras
Murillo et al., Endocrinology 2001
(Disease Progression...) :
At this stage,
PI3K inhibition rapidly
triggered accumulation of
p27 ( kip1 ), cell cycle arrest, and cell death
Mehrhof et al., Circulation 2001
:
IGF-I-stimulation was followed by a
PI3K dependent phosphorylation of
AKT and BAD and an MEK1 dependent phosphorylation of extracellular signal regulated kinase ( ERK ) 1 and ERK2 ... IGF-I-stimulation was followed by a
PI3K dependent phosphorylation of AKT and
BAD and an MEK1 dependent phosphorylation of extracellular signal regulated kinase ( ERK ) 1 and ERK2 ... In summary, our data demonstrate that in cardiomyocytes, the antiapoptotic effect of
IGF-I requires both
PI3K- and MEK1 dependent pathways leading to the activation of the transcription factor CREB, which then induces the expression of the antiapoptotic factor bcl-2
Gonzalez-Garcia et al., J Biol Chem 2002
:
The p85 C-terminal SH2 domain is responsible for p85 coupling to p70S6K and FRAP, because deletion of the C-terminal SH2 domain inhibits complex formation and impairs
p70S6K activation by
PI3K
Thomas et al., J Biol Chem 2002
:
Finally, both
PI 3-K inhibition by LY294002 and
AKT inhibition by transfection of a dominant negative enzyme blocked RSV induced NF-kappaB transcriptional activity ... Finally, both
PI 3-K inhibition by LY294002 and AKT inhibition by transfection of a dominant negative enzyme
blocked RSV induced
NF-kappaB transcriptional activity
King et al., Brain Res 2001
:
MPP induced
caspase-3 activation was
increased by inhibition of
PI3K , and decreased by stimulation of PI3K, indicative of anti-apoptotic signaling by the PI3K/Akt pathway ... Rotenone induced activation of
caspase-3 was
enhanced by inhibition of
PI3K or increased GSK3beta activity, and was attenuated by inhibiting GSK3beta with lithium
Nadler et al., Am J Physiol Endocrinol Metab 2001
(Insulin Resistance) :
Thus BtB6 mice demonstrate the dissociation of insulin stimulated
PI3K activity and
Akt/PKB activation and represent a useful model to investigate the causes of insulin resistance in humans ... Thus BtB6 mice demonstrate the dissociation of insulin stimulated
PI3K activity and
Akt/PKB activation and represent a useful model to investigate the causes of insulin resistance in humans ... Thus BtB6 mice demonstrate the dissociation of
insulin stimulated
PI3K activity and Akt/PKB activation and represent a useful model to investigate the causes of insulin resistance in humans
Banerji et al., Oncogene 2001
(Lymphoma, B-Cell...) :
Inhibition of
PI3-K signalling by LY294002
down-regulated cyclin D2 and up-regulated p27 ( Kip1 ) expression at both protein and RNA levels, mimicking the effects of BCR-stimulation ... Inhibition of
PI3-K signalling by LY294002
down-regulated cyclin D2 and up-regulated
p27 ( Kip1 ) expression at both protein and RNA levels, mimicking the effects of BCR-stimulation
Hatano et al., Am J Physiol Gastrointest Liver Physiol 2001
:
The
PI3K inhibitor LY-294002
blocks TNF-alpha- and Fas mediated Akt phosphorylation ... The
PI3K inhibitor LY-294002
blocks TNF-alpha- and Fas mediated
Akt phosphorylation
Zeng et al., J Biol Chem 2002
:
As expected,
CDC42 and Rac1 activation mediated by EGLT can be completely
inhibited by
PI3K inhibitors, wortmannin and LY294002, and the p85 dominant negative mutant but not by either the phospholipase C inhibitor, or an intracellular Ca ( 2+ ) chilator BAPTA/AM ... As expected,
CDC42 and Rac1 activation mediated by EGLT can be completely
inhibited by
PI3K inhibitors, wortmannin and LY294002, and the p85 dominant negative mutant but not by either the phospholipase C inhibitor, or an intracellular Ca ( 2+ ) chilator BAPTA/AM ... As expected, CDC42 and
Rac1 activation mediated by EGLT can be completely
inhibited by
PI3K inhibitors, wortmannin and LY294002, and the p85 dominant negative mutant but not by either the phospholipase C inhibitor, or an intracellular Ca ( 2+ ) chilator BAPTA/AM
Ivanov et al., J Biol Chem 2002
:
Conversely, inhibition of
PI3K-AKT signaling via the specific pharmacological inhibitor LY294002
up-regulated AP1/Jun- and STAT dependent transcriptional activities, resulting in suppression of the FasR promoter activities and decreased FasR surface expression
Stroppolo et al., J Neurochem 2001
:
We also found that inhibition of
PI3K reduces BDNF induced
Erk phosphorylation, indicating that cross-talk between these pathways may play a prominent role in MSNs
Thomas et al., J Biol Chem 2002
(Calcium Signaling) :
Together, these data indicate that H ( 2 ) O ( 2 ) promotes calcium dependent eNOS activity through a coordinated change in the phosphorylation status of the enzyme mediated by Src- and
ErbB receptor
dependent PI 3-K activation ... In turn,
PI 3-K mediates
eNOS Ser-1177 phosphorylation via a calcium- and Akt dependent pathway, whereas eNOS Thr-495 dephosphorylation does not involve calcium or Akt
Kralik et al., Endocrinology 2002
:
Insulin , but not hyperosmolarity, clearly
increased the activities of
PI3K and Akt ... C2-ceramide did not alter
insulin stimulated
PI3K activity, but did decrease the ability of insulin to activate Akt and GLUT4 translocation
Park et al., J Immunol 2002
(MAP Kinase Signaling System) :
Moreover, while the expression of Bcl-2 and Bcl-x ( L ) depends on both PI3K and p38 mitogen activated protein kinase, the up-regulation of cIAPs and the down-regulation of
active caspase-3 by CpG DNA
require PI3K activation, suggesting PI3K dependent up-regulation of cIAPs in the antiapoptotic activity of CpG DNA in DCs
Laprise et al., J Biol Chem 2002
:
We showed that inhibition of
PI3K signaling in Caco-2/15 cells
repressed sucrase-isomaltase and villin protein expression
Fujita et al., J Biol Chem 2002
:
Hsp90 inhibitors
had no effect on
PI3K protein expression
Yao et al., Oncogene 2001
(Breast Neoplasms...) :
MEK-1 inhibitor PD098059 partially blocked MMP-9 activation, whereas
PI3-K inhibitor wortmannin
had no effect on heregulin-beta1 mediated
MMP-9 activation
Li et al., Oncogene 2001
(Melanoma) :
All melanocytic cells expressed the HGF receptor c-Met, and autocrine
HGF caused constitutive activation of c-Met, MAPK and
PI3K
Huang et al., J Biol Chem 2002
:
Phosphatidylinositol 3-kinase is
activated by
vascular endothelial growth factor ( VEGF ), and many of the angiogenic cellular responses of VEGF are regulated by the lipid products of phosphatidylinositol 3-kinase
Davidson et al., Am J Physiol Endocrinol Metab 2002
(Body Weight) :
With brief time matched CR, reduced visceral fat mass precedes increased insulin sensitivity ; transient reduction in fructose 6-phosphate may trigger more persistent changes but does not coincide with enhanced insulin action ; and PI3K is essential for insulin stimulated 3-O-methylglucose transport in CR as well as AL rats, although
insulin stimulated
PI3K is not significantly greater in CR compared with AL animals
Ricono et al., American journal of physiology. Renal physiology 2002
(MAP Kinase Signaling System) :
Although
PDGF AA stimulates
PI 3-K and MAPK activity, it is not mitogenic and only modestly chemotactic
Rikitake et al., Arterioscler Thromb Vasc Biol 2002
:
S1P activated the phosphatidylinositol-3-kinase (PI3K)/Akt/endothelial NO synthase (eNOS) pathway in ECs, since S1P stimulated
eNOS phosphorylation and NO production were
blocked by inhibition of activities of
PI3K and Akt
Murphy et al., J Biol Chem 2002
:
In contrast, like Ras, expression of activated TC21 resulted in membrane translocation and an increase in the
PI3K dependent phosphorylation of
Akt , and inhibition of PI3K activity interfered with TC21 focus formation
Kruszynska et al., J Clin Endocrinol Metab 2002
(Insulin Resistance) :
The
insulin induced increase in IRS-1 associated
PI3K activity was impaired by elevated NEFA, so that activity at the end of the clamps with Intralipid was 35 % lower than in the control clamps ( P < 0.05 )
Pandey et al., Endocrinology 2002
:
Expression of a dominant negative mutant of Akt1 or class I
PI3K inhibited the insulin stimulation of
PI3K/Akt1 signaling without affecting phosphorylation of IkappaBalpha ... Expression of a dominant negative mutant of Akt1 or class I
PI3K inhibited the
insulin stimulation of PI3K/Akt1 signaling without affecting phosphorylation of IkappaBalpha
Sukumaran et al., J Biol Chem 2002
:
This is the first report of FAK- and
PI3K dependent
PKC-alpha activation in bacterial invasion related to cytoskeletal reorganization
Inabe et al., J Exp Med 2002
:
The functional interaction between PI3K and Rac1 was also demonstrated by increased
PI3K activity in the
presence of GTP bound
Rac1
Aoukaty et al., J Biol Chem 2002
(Lymphoproliferative Disorders) :
These data indicate that the cytotoxicity of activated NK cells is mediated by the association of 2B4 and
SAP/SH2D1A , and that this association is
dependent upon the activity of
PI3K ... These data indicate that the cytotoxicity of activated NK cells is mediated by the association of 2B4 and
SAP/SH2D1A , and that this association is
dependent upon the activity of
PI3K
Ikuno et al., Invest Ophthalmol Vis Sci 2002
(Disease Models, Animal...) :
PI3K and PLCgamma
play a central role in experimental
PVR
Park et al., J Leukoc Biol 2002
:
p43-Dependent activation of ERK was
inhibited by
PI3-K inhibitors, and the activation of p38 MAPK was not ... p43-Dependent activation of
ERK was
inhibited by
PI3-K inhibitors, and the activation of p38 MAPK was not ... Thus, the results of this work suggest that p43 should induce cell-cell adhesion via the
PI3-K/ERK- and p38
MAPK dependent up-regulation of ICAM-1
García et al., Mol Endocrinol 2002
:
PI3K is
involved in the IGF-I inhibition of TSH induced
sodium/iodide symporter gene expression ...
PI3K is
involved in the
IGF-I inhibition of TSH induced sodium/iodide symporter gene expression ... Interestingly, inhibition of
PI3K blocked
IGF-I repression of TSHinduced NIS mRNA and protein levels
Worrall et al., Mol Endocrinol 2002
:
A negative role for Ca ( 2+ ) is also indicated in proximal insulin signaling steps, in that, depletion of intracellular Ca ( 2+ ) blocks IRS1 serine/threonine phosphorylation and enhances
insulin stimulated protein-protein interaction and
PI3K activity
Ye et al., Nature 2002
:
PIKE is a nuclear GTPase that activates nuclear PI(3)K activity, and mediates the physiological
activation by
nerve growth factor (NGF) of nuclear
PI(3)K activity
Zhang et al., Brain Res Mol Brain Res 2002
:
The effects of DHEA on neural cell survival and activation of
Akt were not blocked by the steroid hormone antagonists flutamide and tamoxifen, but both were
blocked by a
PI3-K inhibitor, LY294002
Ramírez de Molina et al., Oncogene 2002
(Cell Transformation, Neoplastic...) :
Regulation of
choline kinase activity by Ras proteins
involves Ral-GDS and
PI3K
Recio et al., Oncogene 2002
(Melanoma) :
Activation of p38 kinase by
HGF/SF was partially blocked by the
PI3K-specific inhibitor as well
Sumitani et al., Endocrinology 2002
:
PI3K activity, but not mTOR, may
regulate transcriptional activity of
myogenin
Haimsohn et al., Endocrinology 2002
(Breast Neoplasms) :
4 ) The insulin receptor substrate-1/2 associated
PI3K , Shc proteins, and the kinases Akt and Erk1/2, downstream mediators of the antiapoptotic signaling by IGF-IR, were
activated to a higher extent and for a longer time period by
ATA , compared with IGF-I
Tu et al., J Pharmacol Exp Ther 2002
:
Inactivating
PI3K with wortmannin
prevented H2O2 from inducing Thr389 phosphorylation and
p70S6K1 activation ... Inactivating
PI3K with wortmannin
prevented H2O2 from inducing Thr389 phosphorylation and
p70S6K1 activation
Shi et al., J Biol Chem 2002
(MAP Kinase Signaling System...) :
Because activation of the
PI3-K/AKT as well as RAS-MEK-ERK pathways may
result in downstream stimulation of the
p70 ( S6K ) ( p70 ) and phosphorylation of the 4E-BP1 translational repressor, we assessed these potential molecular targets in IL-6 treated myeloma cells ... These results indicate that both ERK and PI3-K/AKT pathways are required for optimal IL-6 induced p70 activity, but
PI3-K/AKT is
sufficient for
4E-BP1 phosphorylation
Richards et al., Mol Endocrinol 2002
:
In naïve granulosa cells, both FSH and IGF-I stimulate rapid phosphorylation of
FKHR at multiple sites causing its redistribution from the nucleus to the cytoplasm in a
PI3K dependent manner
Appleman et al., J Immunol 2002
(MAP Kinase Signaling System) :
Decreased abundance of
cyclin dependent kinase inhibitor p27 ( kip1 ), which requires simultaneous TCR/CD3 and CD28 ligation, was
dependent upon both MEK and
PI3K activity
Kops et al., Mol Cell Biol 2002
(Colonic Neoplasms) :
As for the activity of the Forkheads, we also show that protein levels of
p130 are
controlled by endogenous
PI3K/PKB signaling upon cell cycle reentry
Fang et al., Mol Cell Biol 2002
:
PI3K inhibitors
block insulin- but not LPA induced GSK-3 phosphorylation
Hermanto et al., Mol Cell Biol 2002
:
While
IGF-I induced activation of IRS-1, Shc,
PI3K , and MAPK pathways was unaffected, IGF-I-inducible beta1 integrin associated kinase activity and association of Crk with p130 ( CAS ) were significantly inhibited by RACK1 overexpression
Amyere et al., Int J Med Microbiol 2002
:
v-Src and K-Ras
activate PI3K and PLC, as demonstrated by in situ production of the corresponding lipid products ... v-Src and
K-Ras activate
PI3K and PLC, as demonstrated by in situ production of the corresponding lipid products
Yu et al., J Biol Chem 2002
:
These experiments demonstrate that EGF and HGF mediated
ERK activation
result in divergent effects on
Gab1/PI3K signaling ... These experiments demonstrate that EGF and
HGF mediated ERK activation result in divergent effects on
Gab1/PI3K signaling
Jiang et al., Frontiers in bioscience : a journal and virtual library 2002
(Diabetes Mellitus, Type 2) :
In the current review, we will discuss the role of these molecules in
insulin mediated
activation of
PI3K , the rational for targeting these molecules for diabetes treatment, and some critical issues in terms of drug development
Miggin et al., Mol Pharmacol 2002
:
Additionally,
PKB/Akt was activated through TPalpha and TPbeta in a
PI3K dependent manner ... Additionally,
PKB/Akt was activated through TPalpha and TPbeta in a
PI3K dependent manner
Qiao et al., Hepatology 2002
:
Activation of
MAPK was partially blocked by inhibitors of
PI3K
Yart et al., J Biol Chem 2002
:
Indeed, both membrane redistribution and phosphorylation of
Gab1 were reduced in the
presence of
PI3K inhibitors or dominant negative p110beta
Liu et al., J Biol Chem 2002
:
EtOH also activated p44/42
mitogen activated protein kinase in a
PI3K dependent manner
Orr et al., J Biol Chem 2002
:
Hep I stimulates a transient increase in ERK activation, which is abrogated by both PTX and
PI3K inhibitors
Reyes-Reyes et al., Biochem J 2002
:
However,
PI-3K was
required for beta1 integrin-, but not beta2 integrin-, mediated
NF-kappaB activation
Gahr et al., J Mol Endocrinol 2002
:
PI3'K activation was
necessary for
HGF- and glucose stimulated INS-1 cell proliferation
Chinni et al., Clin Cancer Res 2002
:
This was also accompanied by the inhibition of
EGF induced phosphorylation of
PI3K by I3C treatment
Standaert et al., Endocrinology 2002
:
The thiazolidenedione, rosiglitazone, increases basal and/or insulin stimulated glucose transport in various cell types by diverse but uncertain mechanisms that may involve
insulin receptor substrate (IRS)-1 dependent
PI3K ... The thiazolidenedione, rosiglitazone, increases basal and/or insulin stimulated glucose transport in various cell types by diverse but uncertain mechanisms that may involve insulin receptor substrate
(IRS)-1 dependent
PI3K ... Presently, in 3T3/L1 adipocytes, rosiglitazone induced sizable increases in basal glucose transport that were : dependent on PI3K, 3-phosphoinositide dependent protein kinase-1 ( PDK-1 ), and PKC-lambda ; accompanied by increases in tyrosine phosphorylation of Cbl and Cbl dependent increases in PI3K and PKC-lambda activity ; but not accompanied by increases in
IRS-1/2 dependent
PI3K or protein kinase B activity ... Presently, in 3T3/L1 adipocytes, rosiglitazone induced sizable increases in basal glucose transport that were : dependent on PI3K, 3-phosphoinositide dependent protein kinase-1 ( PDK-1 ), and PKC-lambda ; accompanied by increases in tyrosine phosphorylation of Cbl and Cbl dependent increases in PI3K and PKC-lambda activity ; but not accompanied by increases in
IRS-1/2 dependent
PI3K or protein kinase B activity ... Additionally, rosiglitazone increased IRS-1 and IRS-2 levels, thereby enhancing insulin effects on IRS-1- and
IRS-2 dependent
PI3K and downstream signaling factors PKC-lambda and protein kinase B ... Additionally, rosiglitazone increased IRS-1 and IRS-2 levels, thereby enhancing
insulin effects on IRS-1- and IRS-2 dependent
PI3K and downstream signaling factors PKC-lambda and protein kinase B
Kuo et al., Oncogene 2002
(Carcinoma, Hepatocellular) :
Transient transfection assays demonstrated that constitutively activated
PI3K and Rac1
enhanced the activation of the
MDR1 promoter by 2-AAF
Ueda et al., Blood 2002
(Calcium Signaling) :
In Y719F, the binding of phosphatidylinositol 3'-kinase (PI3K) to
KIT was lost and KIT mediated cell migration and Ca ( 2+ ) mobilization were
suppressed by PI3K chemical inhibitors or dominant negative
PI3K , suggesting the involvement of Y719 mediated PI3K pathway in cell migration ... In Y719F, the binding of
phosphatidylinositol 3'-kinase (PI3K) to KIT was lost and KIT mediated cell migration and Ca ( 2+ ) mobilization were
suppressed by PI3K chemical inhibitors or dominant negative
PI3K , suggesting the involvement of Y719 mediated PI3K pathway in cell migration
Woulfe et al., J Biol Chem 2002
:
Finally, using human platelets treated with selective inhibitors of phosphatidylinositol 3-kinase (PI3K) and mouse platelets selectively lacking the G ( beta ) ( gamma ) -activated form of his enzyme ( PI3Kgamma ), we show that G ( i ) -mediated
Rap1 activation is
PI3K dependent
Chiarugi et al., J Cell Sci 2002
:
In fact, inhibition of
PTP upon PDGF stimulation
results in upregulation of receptor phosphorylation level, of
PI3K recruitment and activation and of cell cycle rate
Corbetta et al., J Clin Endocrinol Metab 2002
(Adenoma...) :
PI3K blockade by wortmannin, known to prevent G protein betagamma subunit effect on ERK1 and -2,
induced a 30 % reduction of the Ca ( o ) ( 2+ ) -stimulated
ERK1 and -2 activity
Linnemann et al., Virology 2002
:
Moreover,
PI3K was
required to activate the Nef associated
p21 activated kinase (PAK) ... Finally, inhibition of
PI3K blocked the activation of
PAK and decreased the production of viral particles to levels observed with the Nef deleted provirus
Khan et al., Endocrinology 2002
:
IGF-I- and FSH dependent AKT phosphorylation was inhibited by LY29400 ( 10 microM ), a
PI3K inhibitor , and by IGF binding
protein 3 , but not by a PKA inhibitor ( H89 ) ... IGF-I- and FSH dependent AKT phosphorylation was inhibited by LY29400 ( 10 microM ), a
PI3K inhibitor , and by
IGF binding protein 3 , but not by a PKA inhibitor ( H89 ) ... Furthermore, FSH amplifies
IGF-I mediated
PI3K/AKT signaling in Sertoli cells
Iijima et al., Circulation 2002
:
To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of
PI3K and the phosphorylation of MAPK pathways in PDGF-BB stimulated SMCs. RWPs
inhibited the PI3K activity and
p38 ( MAPK ) phosphorylation, but not ERK1/2 phosphorylation, in a concentration dependent manner ... To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of
PI3K and the phosphorylation of MAPK pathways in PDGF-BB stimulated SMCs. RWPs
inhibited the PI3K activity and p38 (
MAPK ) phosphorylation, but not ERK1/2 phosphorylation, in a concentration dependent manner ... To elucidate the signaling mechanism underlying the RWP effects, we investigated the effects of RWPs on the activity of
PI3K and the phosphorylation of MAPK pathways in PDGF-BB stimulated SMCs. RWPs
inhibited the PI3K activity and p38 ( MAPK ) phosphorylation, but not
ERK1/2 phosphorylation, in a concentration dependent manner
Zhang et al., Mol Cell Biol 2002
:
Our results suggest that, in addition to its role as a positive component of the Ras-Erk pathway, Shp2 negatively regulates
EGF dependent
PI3K activation by dephosphorylating Gab1 p85 binding sites, thereby terminating a previously proposed Gab1-PI3K positive feedback loop ... Our results suggest that, in addition to its role as a positive component of the Ras-Erk pathway,
Shp2 negatively
regulates EGF dependent
PI3K activation by dephosphorylating Gab1 p85 binding sites, thereby terminating a previously proposed Gab1-PI3K positive feedback loop
Silfani et al., Arch Biochem Biophys 2002
:
However, it is not known whether
PI3K is
involved in the Ang II-induced activation of
cPLA(2) or if this mechanism is associated with the Ang II-mediated growth of VSMC ... Therefore, we used cultured rat VSMC to examine the
role of
PI3K in the Ang II-dependent phosphorylation of
cPLA(2) , release of AA, and growth induced by Ang II
Duan et al., Biochem Biophys Res Commun 2002
(Breast Neoplasms) :
E2 activates constructs containing multiple copies of the SRF ( pSRF ) and a GAL4-SRF fusion protein ; these responses are accompanied by
PI3-K dependent phosphorylation of
Akt and inhibited by wortmannin/LY294002, the antiestrogen ICI 182780, but not by the mitogen activated protein kinase kinase ( MAPKK ) inhibitor PD98059
Dai et al., Biochem Biophys Res Commun 2002
:
SGKL is activated via its lipid binding domain ( phox homology domain ) in
response to
PI3K signaling
Tsang et al., Biochem Biophys Res Commun 2002
(MAP Kinase Signaling System) :
PD098059 and U0126, two
MAPK kinase inhibitors, and LY294002, a
PI3K inhibitor , significantly blocked thrombin induced [ ( 3 ) H ] thymidine incorporation and cyclin D(1) expression in ASM cells
Lindvall et al., Biochem Biophys Res Commun 2002
:
In addition, we have investigated the
involvement of
PI 3-K in the MAPKs and ERK and JNK phosphorylation, in the presence or absence of
Btk ... In addition, we have investigated the
involvement of
PI 3-K in the MAPKs and
ERK and JNK phosphorylation, in the presence or absence of Btk
Bilderback et al., Am J Physiol Cell Physiol 2002
:
We found that
phosphatidylinositol 3-kinase (PI3K) is activated in OSE cells in
response to elevated extracellular calcium, and the
PI3K inhibitors wortmannin and LY-294002 inhibited extracellular signal regulated kinase ( ERK ) activation by approximately 75 %, similar to effects of the mitogen activated protein kinase/ERK kinase inhibitor PD-98059
Sharma et al., J Biol Chem 2002
(Prostatic Neoplasms) :
Phosphatidylinositol 3-kinase/Akt stimulates androgen pathway through GSK3beta inhibition and nuclear
beta-catenin accumulation
Shah et al., J Gastrointest Surg 2001
(Adenocarcinoma...) :
NF-kappaB dependent gene expression, however, was ultimately suppressed by Ly294002, suggesting that
PI3k dependent activation of
NF-kappaB is IkappaBalpha independent
Kettritz et al., J Am Soc Nephrol 2002
:
PI3-K inhibition by LY294002
blocked both
Akt phosphorylation and superoxide generation
Marshall et al., Mol Cell Biol 2002
(Lymphoma, B-Cell) :
Blockade of phosphatidylinositol 3-kinase (PI3K) activity completely abolished BCR induced recruitment of TAPP1 and TAPP2, while expression of active
PI3K is
sufficient to drive constitutive membrane localization of
TAPP1 and TAPP2 ... Blockade of phosphatidylinositol 3-kinase (PI3K) activity completely abolished BCR induced recruitment of TAPP1 and TAPP2, while expression of active
PI3K is
sufficient to drive constitutive membrane localization of TAPP1 and
TAPP2
Goncharova et al., Am J Physiol Lung Cell Mol Physiol 2002
:
In parallel experiments, stimulation of human PVSM cells with PDGF induced
PI3K dependent activation of Akt, p70 S6 kinase, and
ribosomal protein S6 but not mitogen activated protein kinase ... In parallel experiments, stimulation of human PVSM cells with PDGF induced
PI3K dependent
activation of
Akt , p70 S6 kinase, and ribosomal protein S6 but not mitogen activated protein kinase
Sun et al., J Cell Physiol 2002
(Breast Neoplasms) :
The activation of both ERK and
PI3-K was
essential for
HRG regulation of COXII, i.e., blockage of either pathway eliminated HRG mediated alteration
Pinzani et al., Frontiers in bioscience : a journal and virtual library 2002
:
In addition, PI 3-K is involved in the activation of the Ras-ERK pathway in human HSC, although it is not strictly necessary, since established
PI 3-K inhibitors
inhibit ERK activation only by 40-50 %
Nusser et al., J Biol Chem 2002
:
Furthermore, inhibition of
PI3K significantly
reduced NGF- mediated
Rac1 activation, whereas dominant negative Rac1 abolished the inhibitory signaling to RhoA ... Taken together, these data indicate that
NGF mediated activation of TrkA receptor
stimulates PI3K , which in turn increases Rac1 activity to induce transient RhoA inactivation during the initial phase of neurite outgrowth ... Taken together, these data indicate that NGF mediated activation of
TrkA receptor
stimulates PI3K , which in turn increases Rac1 activity to induce transient RhoA inactivation during the initial phase of neurite outgrowth
Lewandowski et al., Br J Haematol 2002
(Cell Transformation, Neoplastic) :
Interestingly,
PI3-K activity was also
necessary for CD38 expression on normal marrow CD34+ cells and for the ATRA induced upregulation of
CD157 , a CD38 related antigen ... Interestingly,
PI3-K activity was also
necessary for
CD38 expression on normal marrow CD34+ cells and for the ATRA induced upregulation of CD157, a CD38 related antigen ... In conclusion,
PI3-K activity
plays an essential role in the regulation of
CD38 expression on human haematopoietic cells, and might constitute an interesting therapeutic target in haematological disorders involving CD38 overexpression
Forti et al., Biochemistry 2002
(Adrenal Cortex Neoplasms) :
Inhibitors of
PI3K lead to rapid dephosphorylation of Akt/PKB and
block phosphorylation of
Akt/PKB promoted by FGF2 ... Inhibitors of
PI3K lead to rapid dephosphorylation of Akt/PKB and
block phosphorylation of
Akt/PKB promoted by FGF2
Chakravarti et al., Cancer Res 2002
(Brain Neoplasms...) :
It was found that BCNU inhibited radiation induced apoptosis through
EGFR mediated
activation of
PI3-K/AKT via RAS
Kaluz et al., Cancer Res 2002
(Fibrosarcoma) :
The
PI3K inhibitors LY294002 and wortmannin
inhibited CAIX expression in dense cultures in a dose dependent manner, specifically targeting the CA9 promoter ( -173/+31 region ) that was transactivated by constitutively active p110 PI3K subunit
Fukao et al., Nat Immunol 2002
:
PI3K mediated negative feedback regulation of
IL-12 production in DCs
Naga Prasad et al., J Cell Biol 2002
:
Overexpression of the PIK domain displaces endogenous PI3K from betaARK1 and prevents
betaARK1 mediated translocation of
PI3K to activated beta2ARs ... Furthermore, disruption of the
betaARK1/PI3K interaction
inhibits agonist stimulated
AP-2 adaptor protein recruitment to the beta2AR and receptor endocytosis without affecting the internalization of other clathrin dependent processes such as internalization of the transferrin receptor
Lucas et al., Int J Oncol 2002
(Cell Transformation, Neoplastic) :
Modulation of
phospholipase D by Ras proteins
mediated by its effectors Ral-GDS,
PI3K and Raf-1
Rani et al., J Biol Chem 2002
(Fibrosarcoma) :
Studies with PTEN mutants suggested that the lipid kinase activity of
PI3K was
essential for IFN-beta induced transcription of
beta-R1
Meroni et al., J Endocrinol 2002
:
Taken together, these results indicate that FSH increases
P-PKB levels in a
PI3K dependent and PKA independent manner in rat Sertoli cells
Zawalich et al., J Endocrinol 2002
(Obesity) :
They also suggest that, as insulin resistance develops in peripheral tissues, a potential result of impaired
PI3K activation, the same biochemical anomaly in beta-cells
promotes a linked increase in
insulin secretion to maintain glucose homeostasis
Baudhuin et al., Mol Pharmacol 2002
:
LPA/S1P induced Akt activation may be involved in cell survival, because LPA and S1P treatment in HEY ovarian cancer cells results in a decrease in paclitaxel induced
caspase-3 activity in a
PI3-K/MEK/p38 dependent manner
He et al., J Virol 2002
:
The downstream effects of the NS5A-p85 PI3K interaction included increased tyrosine phosphorylation of p85
PI3K in
response to
EGF
Cui et al., Mol Endocrinol 2002
:
We demonstrated that insulin mediated insulin receptor substrate (IRS)-2 associated
PI3K activity was
inhibited by
AT2 receptor stimulation, whereas IRS-1 associated PI3K activity was not significantly influenced ... We demonstrated that
insulin mediated insulin receptor substrate (IRS)-2 associated
PI3K activity was inhibited by AT2 receptor stimulation, whereas IRS-1 associated PI3K activity was not significantly influenced ... Overexpression of a catalytically inactive dominant negative SHP-1 markedly attenuated the AT2 receptor- mediated inhibition of IRS-2 associated
PI3K activity, Akt phosphorylation, and antiapoptotic effect
induced by
insulin
Kandasamy et al., Cancer Res 2002
(Carcinoma, Non-Small-Cell Lung...) :
Furthermore, the loss of PTEN activity or overexpression of
PI3-K dependent
Akt/protein kinase B activity promotes the survival of NSCLC cells ... Furthermore, the loss of PTEN activity or overexpression of
PI3-K dependent
Akt/protein kinase B activity promotes the survival of NSCLC cells
Gentili et al., J Cell Biochem 2002
(MAP Kinase Signaling System) :
PTH dose- and time-dependently
increased PI3K activity with a peak occurring at 2 min ... We report here that
PI3K is also
required for PTH activation of the mitogen activated protein kinases
ERK1 and ERK2 ... We report here that
PI3K is also
required for
PTH activation of the mitogen activated protein kinases ERK1 and ERK2 ... Taken together, the present study demonstrate, for the first time, that PTH rapidly and transiently stimulates PI3K activity and its down effector Akt/PKB in rat enterocytes playing c-Src kinase a central role in
PTH dependent
PI3K activation and that PI3K signaling pathway contributes to PTH mediated MAPK activation
Piccolo et al., Oncogene 2002
(Breast Neoplasms) :
In an effort to understand the signalling pathway that involves PI 3-K regulation of PLCgamma, we found that EGF induces a
PI 3-K dependent translocation of
PLCgamma1 at the leading edge of migrating cells in a wound healing assay
Condorelli et al., Proc Natl Acad Sci U S A 2002
(Cardiomyopathy, Hypertrophic) :
In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through
PI3K dependent
Akt activation
Timms et al., Oncogene 2002
(Breast Neoplasms...) :
PI3K signalling also participated in cell cycle progression, since
PI3K and MAPK coordinately
regulated changes in
cyclin D1 and cdk6 expression
Pene et al., Oncogene 2002
(Multiple Myeloma) :
PI 3-K dependent
GSK-3alpha/beta constitutive phosphorylation was also detected in OPM2 cells that may contribute to high cyclin D1 expression
van den Heuvel et al., J Cell Sci 2002
:
PI3K activation generates 3'-phosphorylated phosphatidylinositol lipids ( PtdIns3P ) and
PKB activation
requires PtdIns3P dependent membrane translocation and phosphorylation by upstream kinases
Woods et al., Neuro Oncol 2002
(Astrocytoma...) :
Phosphatidylinositol 3'-kinase and MAPK/ERK kinase 1/2 differentially
regulate expression of
vascular endothelial growth factor in human malignant astrocytoma cells
Halvorsen et al., Brain Res 2002
(MAP Kinase Signaling System...) :
Survival promoting MEK-ERK and PI3K pathways contribute to viability during MPP ( + ) exposure, both are
activated by
NGF , and loss of
PI3K mediated signaling and NF-kappa B-mediated transcription may commit cells irreversibly to apoptosis in this model
Taher et al., Biochem Biophys Res Commun 2002
(Arteriosclerosis...) :
Stimulation with HGF led to activation of
Met as well as to
activation of
PI3-K , PKB/Akt, MEK, and the MAP kinases Erk1 and -2 ... Stimulation with
HGF led to activation of Met as well as to activation of
PI3-K , PKB/Akt, MEK, and the MAP kinases Erk1 and -2
Boo et al., Am J Physiol Heart Circ Physiol 2002
:
These results suggest that shear stress stimulates
eNOS by two different mechanisms : 1 ) PKA- and
PI3K dependent and 2 ) PKA dependent but PI3K independent pathways
Kang et al., Mol Pharmacol 2002
:
Phosphatidylinositol 3-kinase regulates nuclear translocation of
NF-E2 related factor 2 through actin rearrangement in response to oxidative stress
Hetman et al., J Biol Chem 2002
:
Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and
PI3K were
required for
brain derived neurotrophic factor (BDNF) suppression of GSK3beta activity ... Here, we report that inhibition of
ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and
PI3K were
required for brain derived neurotrophic factor (BDNF) suppression of GSK3beta activity ... Here, we report that inhibition of ERK1/2 increased the basal activity of GSK3beta in cortical neurons and that both ERK1/2 and
PI3K were
required for brain derived neurotrophic factor (BDNF) suppression of
GSK3beta activity ... Activation of both endogenous ERK1/2 and
PI3K signaling pathways was
required for
BDNF to block apoptosis induced by expression of recombinant GSK3beta ... Although both
PI3K and ERK1/2
inhibited GSK3beta activity, neither had an effect on GSK3beta phosphorylation at Tyr-216 ... Interestingly,
PI3K ( but not ERK1/2 )
induced the inhibitory phosphorylation of
GSK3beta at Ser-9
Kang et al., Dev Dyn 2002
:
Phosphatidylinositol-3 (PI-3) kinase regulates cytoskeleton reorganization, cell migration, and
transforming growth factor ( TGF ) beta regulated EMT
Hallmann et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
Although,
IGF-1 stimulated
PI3K activity associated with insulin receptor substrates was unaltered in all cell lines, p85alpha-null ES cells showed diminished protein kinase B activation despite increased PI3K activity associated with the p85beta subunit
Galve-Roperh et al., Mol Pharmacol 2002
(Astrocytoma) :
In conclusion, CB(1) induced
ERK activation was
mediated by
PI3K ( IB ) and this effect may have important consequences in the control of cell death/survival decision
Miyake et al., J Clin Invest 2002
(Glucose Intolerance...) :
Systemic infusion of an adenovirus encoding a dominant negative mutant of PI 3-K ( ( Delta ) p85 ) resulted in liver-specific expression of this protein and in inhibition of the
insulin induced activation of
PI 3-K in the liver within 3 days, without affecting insulin signaling in skeletal muscle ... The mice also exhibited marked decreases in the serum concentrations of FFAs and triglyceride and suppression of
insulin induced
PI 3-K activation in adipose tissue, probably due to the associated hyperinsulinemia
Desbois-Mouthon et al., Hepatology 2002
(Carcinoma, Hepatocellular...) :
By using LY294002 and ML-9, which act as phosphatidylinositol 3-kinase (PI3-K) and Akt inhibitors, respectively, we showed that
GSK-3beta phosphorylation
required PI3-K activation in both cell lines whereas downstream Akt activation was required only in Mahlavu cells
Ruscher et al., J Neurosci 2002
(Hypoxia-Ischemia, Brain) :
EPO activates the neuronal EPO receptor and, subsequently, JAK-2 and thereby
PI3K
Granboulan et al., J Biol Chem 2003
:
Strikingly, we found using fluorescent probes binding specifically to PI3K products that
BCR and Igbeta but not Igalpha
induce PI3K activation in endocytic compartments wherein antigen is transported ... Strikingly, we found using fluorescent probes binding specifically to PI3K products that BCR and Igbeta but not
Igalpha induce
PI3K activation in endocytic compartments wherein antigen is transported ... Strikingly, we found using fluorescent probes binding specifically to PI3K products that BCR and
Igbeta but not Igalpha
induce PI3K activation in endocytic compartments wherein antigen is transported
Clark et al., Mol Cancer Ther 2002
(Breast Neoplasms) :
Akt promoted breast cancer cell survival because a
PI3K inhibitor, LY294002, or transient transfection of a dominant negative Akt mutant
inhibited Akt activity and increased apoptosis
Krystal et al., Mol Cancer Ther 2002
(Carcinoma, Small Cell...) :
Both stem cell factor (SCF) and insulin-like growth factor
(IGF)-I , components of prominent small cell lung cancer ( SCLC ) autocrine loops, as well as FCS, can potently
activate phosphatidylinositol 3-kinase
(PI3K)-Akt signaling, albeit with different kinetics ... Both stem cell factor (SCF) and
insulin-like growth factor (IGF)-I , components of prominent small cell lung cancer ( SCLC ) autocrine loops, as well as FCS, can potently
activate phosphatidylinositol 3-kinase
(PI3K)-Akt signaling, albeit with different kinetics ... Both
stem cell factor (SCF) and insulin-like growth factor (IGF)-I, components of prominent small cell lung cancer ( SCLC ) autocrine loops, as well as FCS, can potently
activate phosphatidylinositol 3-kinase
(PI3K)-Akt signaling, albeit with different kinetics ...
SCF induced
PI3K-Akt activation occurs rapidly but fades within 60 min ; IGF-I and FCS induced activation persists for at least 6 h. SCF and IGF-I mediated growth was potently inhibited by LY294002 in proportion to its ability to inhibit phosphatidylinositol 3-kinase (PI3K)-Akt signaling
Kim et al., J Korean Med Sci 2002
(MAP Kinase Signaling System) :
These results suggest that the IL-1beta mediated MUC2 gene expression and mucin secretion in NCI-H292 cells are regulated through activation of the PKC-MEK/ERK pathway, and that
PI3K is also
involved in the IL-1beta mediated
MUC2 gene expression and mucin secretion ... These results suggest that the IL-1beta mediated MUC2 gene expression and
mucin secretion in NCI-H292 cells are regulated through activation of the PKC-MEK/ERK pathway, and that
PI3K is also
involved in the IL-1beta mediated MUC2 gene expression and mucin secretion
Rizzoli et al., J Neurosci 2002
:
Because LY has been shown recently to potently inhibit casein kinase 2 as well as PI3K, we hypothesize that casein kinase 2 inhibition is responsible for the enhancement of spontaneous release, whereas
PI3K inhibition
induces the block of vesicle
cycling
Patel et al., Diabetes 2003
:
None of the inhibitors significantly inhibited protein content over 20 days, but lipid content and lipogenic activity were inhibited by p70 ( S6 ) kinase and p38
MAPK inhibition but not by p42/44 MAPK or
PI3K inhibition ... None of the inhibitors significantly inhibited protein content over 20 days, but lipid content and lipogenic activity were inhibited by p70 ( S6 ) kinase and
p38 MAPK
inhibition but not by p42/44 MAPK or
PI3K inhibition ... None of the inhibitors significantly inhibited protein content over 20 days, but lipid content and lipogenic activity were inhibited by
p70 ( S6 ) kinase and p38 MAPK inhibition but not by p42/44 MAPK or
PI3K inhibition
Arboleda et al., Cancer Res 2003
(Breast Neoplasms...) :
Furthermore, expression of kinase dead AKT2 ( 181 amino acid methionine [ M ] ), and not kinase dead AKT1 ( 179M ) or AKT3 ( 177M ), was capable of blocking invasion induced by either human
epidermal growth factor receptor-2 ( HER-2 ) overexpression or by
activation of
PI3-K
Pore et al., Cancer Res 2003
(Glioblastoma) :
In the current study we investigated the effect of
PTEN , a negative
regulator of
PI3K signaling commonly mutated in glioblastoma cells, on VEGF expression
Squires et al., Biochem Pharmacol 2003
:
The
PI3K inhibitor LY294002 ( 50 microM )
inhibited PKB phosphorylation in both cells lines, but only induced apoptosis in the MDA-MB-468 line
Bonaccorsi et al., Int J Androl 2003
(Neoplasm Invasiveness...) :
PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells in
response to
EGF and further reduced by treatment with R1881
Farrow et al., Biochem Biophys Res Commun 2003
(Pancreatic Neoplasms) :
The purpose of this study was to examine whether activation of
PPARgamma can increase the expression of the tumor suppressor PTEN and
inhibit PI3K activity ... The purpose of this study was to examine whether activation of PPARgamma can increase the expression of the tumor suppressor
PTEN and
inhibit PI3K activity ... Taken together, our results suggest that activation of PPARgamma may represent a novel approach for the treatment of pancreatic cancer by increasing
PTEN levels and
inhibiting PI3K activity
Niswender et al., Diabetes 2003
(Anorexia...) :
To test the hypothesis that hypothalamic insulin action involves intracellular PI3K signaling, we used histochemical and biochemical methods to determine the
effect of
insulin on hypothalamic
IRS-PI3K activity ... These findings support the hypothesis that the IRS-PI3K pathway is a mediator of insulin action in the arcuate nucleus and, combined with recent evidence that
leptin activates
PI3K signaling in the hypothalamus, provide a plausible mechanism for neuronal cross-talk between insulin and leptin signaling
Chandrasekar et al., Oncogene 2003
(Central Nervous System Neoplasms...) :
Downregulation of
uPA inhibits migration and
PI3k/Akt signaling in glioblastoma cells
Stoica et al., Mol Endocrinol 2003
(Breast Neoplasms) :
Treatment of cells with estradiol resulted in phosphorylation of Akt and a 9-fold increase in Akt activity in 10 min.
Akt activation was blocked by wortmannin and LY 294,002, two inhibitors of
PI 3-K ; by genistein, a protein tyrosine kinase inhibitor and an ER agonist ; by AG825, a selective ErbB2 inhibitor ; and by the antiestrogens ICI 182,780 and 4-hydroxy-tamoxifen ; but not by rapamycin, an inhibitor of the ribosomal protein kinase p70S6K ; nor by AG30, a selective epidermal growth factor receptor inhibitor
Le et al., Oncogene 2003
:
Inhibitors of mTOR,
PI3K , and Ca ( ++ )
impair p70S6K activity, whereas inhibitors of JNK and PKC stimulate p70S6K activity
Lee et al., Experimental biology and medicine (Maywood, N.J.) 2003
:
Additionally, the possible
role for
PI 3-K and PDE in leptin induced control of acetylcholine induced
insulin secretion was examined ...
Leptin may
stimulate PI 3-K to constrain PLC-PKC induced insulin secretion from islets of Lep ( ob ) /Lep ( ob ) mice
Fujino et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
Furthermore, this activation of
PI3K/ERK signaling by the EP ( 4 ) receptors
induces the functional expression of
early growth response factor-1 (EGR-1)
Ruiter et al., Anticancer Drugs 2003
(Neoplasms, Glandular and Epithelial) :
We found that growth factor induced
Akt/PKB activation in these cells is
dependent on
PI3K and that all three ALPs inhibited this pathway in a dose dependent manner ... We found that growth factor induced
Akt/PKB activation in these cells is
dependent on
PI3K and that all three ALPs inhibited this pathway in a dose dependent manner
Park et al., J Immunol 2003
:
Upon treating with group IIA PLA(2),
Akt is phosphorylated in a
PI3K dependent manner ... Pretreatment with LY294002, a PI3K inhibitor, strongly suppressed group IIA
PLA(2) induced iNOS expression and
PI3K/Akt activation
Salinas et al., J Biol Chem 2003
:
In this study, we demonstrate that nerve growth factor (NGF) prevents the accumulation of ROS in dopaminergic PC12 cells challenged with the Parkinson 's disease related neurotoxin 6-hydroxydopamine ( 6-OHDA ) by a mechanism that involves
PI3K/Akt dependent
induction of the stress response protein
heme oxygenase-1 (HO-1) ... Inhibition of
PI3K prevented
NGF induction of HO-1 mRNA and protein and partially reversed its protective effect against 6-OHDA induced ROS release
Gentili et al., Biochim Biophys Acta 2003
:
Intracellular Ca ( 2+ ) chelation ( BAPTA-AM, 5 microM ) affected the tyrosine phosphorylation of
p85alpha and
inhibited PTH dependent
PI3K activation by 75 % in young rats and completely abolished the enzyme activity in aged animals, demonstrating that Ca ( 2+ ) is required for full activation of PI3K in enterocytes stimulated with PTH ... Intracellular Ca ( 2+ ) chelation ( BAPTA-AM, 5 microM ) affected the tyrosine phosphorylation of p85alpha and inhibited
PTH dependent
PI3K activation by 75 % in young rats and completely abolished the enzyme activity in aged animals, demonstrating that Ca ( 2+ ) is required for full activation of PI3K in enterocytes stimulated with PTH ... The data also indicates a positive role for intracellular calcium in one of the early signals of PTH in rat enterocytes, the activation of
PI3K , and that hormone regulation of PI3K activity and
Akt/PKB phosphorylation on Thr ( 308 ) is
impaired with ageing
El-Kholy et al., FASEB J 2003
:
Western blotting confirmed the specific inhibitory effects of LY294002 and wortmannin on
insulin stimulated
PI3K activity
Simoncini et al., Arterioscler Thromb Vasc Biol 2003
:
By using cultured human saphenous vain endothelial cells, we found that cell membrane bound
ERalpha colocalizes with PI3K and may be
responsible for
PI3K activation ... Furthermore, we characterized the subsequent steps in the activation of the PI3K/Akt signaling cascade, comparing the molecular events that follow
insulin or estradiol
activation of
PI3K
Niswender et al., J Histochem Cytochem 2003
:
We conclude that immunocytochemical PIP3 staining can detect changes in
PI3K activation
induced by
insulin and leptin in cell culture and intact liver ... We conclude that immunocytochemical PIP3 staining can detect changes in
PI3K activation
induced by insulin and
leptin in cell culture and intact liver
Albanese et al., Mol Biol Cell 2003
:
Mitogenic induction of G ( 1 ) -S phase progression and
cyclin D1 expression was
PI3K dependent , and cyclin D1 ( -/- ) cells showed reduced PI3K dependent S-phase entry ...
PI3K dependent
induction of
cyclin D1 was blocked by inhibitors of PI3K/Akt/IkappaB/IKKalpha or beta-catenin signaling
Kanda et al., Biochem Biophys Res Commun 2003
:
These results implicate CrkL in
PI3K dependent activation of
Rac by outside-in signaling from alpha4beta1 and suggest that adhesion through alpha4beta1 further activates cytokine receptor associated Jak2 to induce phosphorylation of these receptors
Schwindt et al., Biochemistry 2003
(Adrenal Cortex Neoplasms) :
PKC inhibitor Go6983 and
PI3K inhibitors wortmannin and LY294002 all
inhibit ERK1/2 activation by AVP, but not by FGF2
Pirola et al., J Biol Chem 2003
(MAP Kinase Signaling System) :
PDK1, mTOR, and MAPK inhibitors did not block insulin induced reduction of IRS-1, suggesting that the
PI3K serine-kinase activity
causes IRS-1 serine phosphorylation and its commitment to proteasomal degradation ... Conversely, adenoviral-driven expression of constitutively active
PI3K induced an insulin independent reduction in
IRS-1/2 protein levels ... Conversely, adenoviral-driven expression of constitutively active
PI3K induced an insulin independent reduction in
IRS-1/2 protein levels
Nguyen et al., Mol Endocrinol 2003
:
In addition,
relaxin increased
PI3K activity in THP-1 cells
Kong et al., Mol Endocrinol 2003
:
In these cells, three major p85 containing complexes were formed after EGF treatment : ErbB3-p85, Shc-p85, and a multimeric Gab2-Grb2-SHP2-p85, which accounted for more than 80 % of total
EGF induced
PI3K activity ( Kong, M., C. Mounier, J. Wu, and B. I. Posner, J Biol Chem, 2000, 275 : 36035-36042 ) ... Overexpression of the PH domain of Gab2 did not affect
EGF induced Gab2 phosphorylation,
PI3K activation , and DNA synthesis ... Our data demonstrate that
Gab2 mediates EGF induced
PI3K activation and DNA synthesis in a PH domain independent manner ... Our data demonstrate that Gab2 mediates
EGF induced
PI3K activation and DNA synthesis in a PH domain independent manner
Ma et al., J Neurosci 2003
(Ion Channel Gating...) :
Additionally, muscarinic receptors in PFC slices activated PKC and the focal adhesion kinase
Pyk2 ( a potential molecular link between PKC and Src ) in a
PI3K dependent manner
Dupont et al., Biol Reprod 2003
:
Using specific inhibitors, we demonstrated that the
activation of
Smad-2 was partially blocked by the inhibition of
PI3K but not by the inhibition of ERK1/2 or p38, suggesting a cross-talk between the Smad and PI3K/Akt pathways
Reséndiz et al., Mol Pharmacol 2003
:
These results indicate that shear induced
VWF binding to platelet GpIb-IX-V
stimulates functionally important
PI3-K activity
Mizuno et al., Mol Psychiatry 2003
:
Our findings suggested that
activation of
TrkB/PI3-K and protein synthesis signaling pathway by
BDNF in the hippocampus is important for spatial memory
Maulik et al., J Cell Mol Med 2002
(Carcinoma, Small Cell...) :
We show that association of c-Met with
PI3K and GAB2 is
diminished by inhibiting
c-Met
Burroughs et al., Mol Cancer Res 2003
(MAP Kinase Signaling System) :
Mutation of the hypoxia response element ( HRE ), which mediates hypoxic stimulation of VEGF transcription, did not inhibit the effect of IGF-I on the VEGF promoter, despite the fact that this mutation inhibited
PI3-K stimulated
VEGF promoter activity in prostate cancer cells ... These data indicate that
PI3-K signaling does not
increase VEGF transcription through transactivation by HIF-1 at the HRE in normal PrEC
Wu et al., Genes Cells 2003
:
Phosphatidylinositol 3-kinase signalling may be
involved in
MMP-12 transcriptional activation through AP-1 binding activity
Andresen et al., Hypertension 2003
(MAP Kinase Signaling System) :
We hypothesized that phosphoinositide-3-kinase (PI3K) can also act to recruit Raf to membranes ; therefore, inhibition of
PI3K should
inhibit EGF signaling to ERK
Qin et al., Biochemistry 2003
:
The activation of
Akt , as monitored by its ability to phosphorylate GSK-3alpha/beta and by its S473 phosphorylation, was strictly
dependent on
PI3K activity ... Under our conditions, hydrogen peroxide induced
PI3K and Akt activation was
independent of Lyn,
Syk , Cbl, BCAP, or Ras when each was eliminated individually either by mutation or by a specific inhibitor ... Under our conditions, hydrogen peroxide induced
PI3K and Akt activation was
independent of Lyn, Syk,
Cbl , BCAP, or Ras when each was eliminated individually either by mutation or by a specific inhibitor ... Under our conditions, hydrogen peroxide induced
PI3K and Akt activation was
independent of Lyn, Syk, Cbl,
BCAP , or Ras when each was eliminated individually either by mutation or by a specific inhibitor ... Under our conditions, hydrogen peroxide induced
PI3K and Akt activation was
independent of
Lyn , Syk, Cbl, BCAP, or Ras when each was eliminated individually either by mutation or by a specific inhibitor
Imai et al., Life Sci 2003
(Calcium Signaling) :
SGK1 is one of the protein-serine/threonine kinases that is activated by
insulin in a
PI3K dependent manner
Vieira et al., Mol Cell Biol 2003
:
Moreover, in the
presence of
PI3K inhibitors
Rab5 was found to be active, as deduced from measurements of early endosome antigen 1 binding and by photobleaching recovery determinations
Kawanabe et al., Mol Pharmacol 2003
:
These results indicate that 1 ) Ca ( 2+ ) influx through NSCC-1, NSCC-2, and SOCC plays essential roles in ET-1 induced PYK2 phosphorylation, 2 ) NSCC-2 and SOCC are stimulated by ET-1 via a PI3K dependent cascade, whereas NSCC-1 is stimulated via a PI3K independent cascade, and 3 )
PI3K is
involved in the
PYK2 phosphorylation that depends on Ca ( 2+ ) influx through SOCC and NSCC-2
Li et al., Brain Res Mol Brain Res 2003
(Amyotrophic Lateral Sclerosis...) :
VEGF activated both
PI3-K and MAPK activities in mouse NSC34 motor neuron-like cells
Zipper et al., Toxicological sciences : an official journal of the Society of Toxicology 2003
(Translocation, Genetic) :
Pyrrolidine dithiocarbamate ( PDTC ) induction of the human glutamate cysteine ligase modulatory (
GCLM ) gene is dependent on activation of the mitogen activated protein kinases ( MAPKs ) extracellular regulated kinase (Erk) and p38, and is not
affected by protein kinase C ( PKC ) or
PI3K inhibitors
Lin et al., J Biol Chem 2003
:
Phosphatidylinositol 3-kinase , protein kinase C, and
MEK1/2 kinase
regulation of dopamine transporters (DAT) require N-terminal DAT phosphoacceptor sites
Ghosh-Choudhury et al., J Biol Chem 2003
:
Phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2 (BMP-2) induced myocyte enhancer factor 2A-dependent transcription of
BMP-2 gene in cardiomyocyte precursor cells ...
Phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2 (BMP-2) induced
myocyte enhancer factor 2A-dependent transcription of BMP-2 gene in cardiomyocyte precursor cells
Suh et al., J Biol Chem 2003
:
The TSH induced
S6K1 phosphorylation was
inhibited by a dominant negative p85alpha regulatory subunit or by the
PI3K inhibitors wortmannin and LY294002 ... These findings suggest an interaction between TSHR and
PI3K , which is stimulated by TSH and cAMP and might
involve the downstream
S6K1 but not Akt/protein kinase B ... These findings suggest an interaction between TSHR and
PI3K , which is stimulated by TSH and cAMP and might
involve the downstream S6K1 but not
Akt/protein kinase B ... These findings suggest an interaction between TSHR and
PI3K , which is stimulated by TSH and cAMP and might
involve the downstream S6K1 but not
Akt/protein kinase B
Sade et al., Eur J Immunol 2003
:
The protective effect was attenuated by pharmacological inhibitors of phosphatidylinositol-3 kinase (PI3K) with one exception : inhibition of
PI3K did not abrogate Bcl-x ( L ) expression in the
presence of
IL-7 ... Thus, IL-7 regulates
IAP-2 expression and
inhibits dexamethasone induced apoptosis by activating Akt via
PI3K dependent signaling, but regulates Bcl-x ( L ) expression via a PI3K independent pathway in mature T cells ... Thus, IL-7 regulates IAP-2 expression and
inhibits dexamethasone induced apoptosis by activating Akt via
PI3K dependent signaling, but regulates
Bcl-x ( L ) expression via a PI3K independent pathway in mature T cells
Fung et al., Cell Signal 2003
:
IL-2 activation of a
PI3K dependent
STAT3 serine phosphorylation pathway in primary human T cells ... However, the coupling of
STAT3 serine phosphorylation to
PI3K in
response to IL-2 has yet to be shown in either T cell lines or primary human T cells
Gingery et al., J Cell Biochem 2003
(MAP Kinase Signaling System) :
PI3K inhibition also
blocked MEK1/2,
ERK1/2 , and AKT phosphorylation and NFkappaB activation in purified osteoclasts ...
PI3K inhibition also
blocked MEK1/2, ERK1/2, and
AKT phosphorylation and NFkappaB activation in purified osteoclasts ...
PI3K inhibition also
blocked MEK1/2 , ERK1/2, and AKT phosphorylation and NFkappaB activation in purified osteoclasts ...
PI3K inhibition also
blocked MEK1/2,
ERK1/2 , and AKT phosphorylation and NFkappaB activation in purified osteoclasts ...
PI3K inhibition also
blocked MEK1/2, ERK1/2, and AKT phosphorylation and
NFkappaB activation in purified osteoclasts
Glassford et al., Oncogene 2003
(Calcium Signaling...) :
These findings are further confirmed by studies showing that specific pharmacological inhibitors of Btk ( LFM-A13 ),
PI3-K ( LY294002 and Wortmannin ) and PLCgamma ( U73122 ) also
block cyclin D2 expression and S phase entry following BCR stimulation, as well as triggering apoptosis
Isenovic et al., Metabolism 2003
:
Exposure to IGF-1 for 30 minutes or E2 for 20 minutes increased insulin receptor substrate-1 (IRS-1) association with the regulatory (
p85 ) subunit of PI3K, enhanced tyrosine phosphorylation of p85, and
increased PI3K activity
Le Pabic et al., Hepatology 2003
(Colorectal Neoplasms...) :
The
PI3K inhibitor LY294002 and the mitogen activated protein kinase kinase ( MEK ) inhibitor UO126
prevented ADAM12 induction by TGF-beta, suggesting the involvement of PI3K and MEK activities
Kiian et al., Thromb Haemost 2003
:
Downstream of RhoA, phosphorylation of
myosin light chain ( MLC ) was dramatically upregulated by uPA in a Rho kinase- and
PI3-K dependent manner
Neudauer et al., Exp Cell Res 2003
(MAP Kinase Signaling System...) :
In contrast, similar concentrations of either wortmannin or LY294002 were required to inhibit both
IGF-I induced
PI3K activation and migration
Tang et al., Biochem J 2003
(Astrocytoma...) :
This response was blocked by rapamycin, but was not markedly affected by 100 nM wortmannin, implying separate
roles for mTOR and
PI3K in
S6K1 activation
Utsugi et al., Am J Respir Cell Mol Biol 2003
:
PI3K inhibitors dose-dependently
suppressed TGF-beta1 induced JNK, but not
p38 MAP kinase activation
Koyama et al., Dev Dyn 2003
:
PLCgamma1 directly activates protein kinase C ( PKC ) isozymes ;
PI3K stimulates
protein kinase B ( PKB, also known as Akt ), which ultimately activates PKCs and other proteins ... Both PLCgamma1 and
PI3K are phosphorylated in
response to
EGF
Haga et al., J Vasc Surg 2003
(Disease Models, Animal...) :
Both
PI3K inhibitors specifically
inhibited the increase in Akt phosphorylation in
SMC exposed to oscillatory SS ... Both
PI3K inhibitors specifically
inhibited the increase in
Akt phosphorylation in SMC exposed to oscillatory SS
Hsu et al., Br J Pharmacol 2003
:
5 Results with specific kinase inhibitors indicate that phagocytic action of PS-G was reduced by the presence of wortmannin (
Phosphatidylinositol 3-kinase ,
PI3K inhibitor ), pyrazolpyrimidine 2 ( Src-family tyrosine kinase inhibitor ), Ro318220 ( PKC inhibitor ), and SB203580 ( p38 MAPK inhibitor ), but not by PD98059 ( mitogen activated protein/ERK kinase inhibitor )
Miyashita et al., FEBS Lett 2003
:
The findings suggest that AM plays significant roles in vascular regeneration, associated with PKA- and
PI3K dependent
activation of
Akt in endothelial cells, and possesses therapeutic potential for vascular injury and tissue ischemia
Cozzolino et al., Mol Biol Cell 2003
:
The deleted mutant also inhibits the
PI3K dependent
RhoA activation ensuing receptor activation
Kristof et al., J Biol Chem 2003
(Inflammation) :
The
role of mTOR and
PI3K in the activation of human inducible nitric oxide synthase transcription by cytokines and
lipopolysaccharide (LPS) was investigated in lung epithelial adenocarcinoma ( A549 ) cells ... The
role of mTOR and
PI3K in the activation of human inducible
nitric oxide synthase transcription by cytokines and lipopolysaccharide (LPS) was investigated in lung epithelial adenocarcinoma ( A549 ) cells
Chien et al., J Lipid Res 2003
:
Phosphorylation of
Akt stimulated by OxLDL and epidermal growth factor (EGF) was
attenuated by inhibitors of
PI3-K ( wortmannin and LY294002 ) and intracellular Ca2+ chelator ( BAPTA/AM ) plus EDTA
Parry et al., J Immunol 2003
:
ICOS costimulation
led to greatly augmented levels of
PI3K activity compared with CD28 costimulation, whereas only CD28 costimulation activated c-jun N-terminal kinase
Garami et al., Mol Cell 2003
:
Here we provide evidence that TSC1/2 is a GAP for the small GTPase Rheb and that insulin mediated
Rheb activation is
PI3K dependent ... Here we provide evidence that
TSC1/2 is a GAP for the small GTPase Rheb and that insulin mediated Rheb activation is
PI3K dependent
Krasilnikov et al., Oncogene 2003
(Melanoma) :
ERK and
PI3K negatively
regulate STAT-transcriptional activities in human melanoma cells : implications towards sensitization to apoptosis ... Tyrosine phosphorylation of STAT3/5 and of JAK2 also increased upon treatment of LU1205 cells with either PD or LY, suggesting that constitutive active MAPK and
PI3K signals
inhibit tyrosine phosphorylation of
JAK/STATs
Acconcia et al., IUBMB Life 2003
:
At the present meagre information is available for the role played by the rapid hormone action mechanism ( s ) ( i.e.,
activation of
ERK ,
PI(3)K , PKC-alpha ) in modulating E2-induced gene promoter activity
Welch et al., FEBS Lett 2003
(Second Messenger Systems) :
Vice versa,
Rac can also
stimulate the activation of
PI3K , although the mechanism for this is unclear
Liu et al., J Virol 2003
(Cell Transformation, Viral) :
Furthermore, the
PI3K-specific inhibitor LY294002 could
inhibit Akt activation and cell transformation in all cases, indicating that Akt activation and transformation is PI3K dependent
Ciprés et al., J Biol Chem 2003
:
Our results demonstrate that, in vivo, the increase in cellular levels of
PI3K products is
sufficient to induce
DAGK alpha activation, allowing DAGK alpha relocation to the intact lymphocyte plasma membrane ... These studies are the first to describe a pathway in which, in the absence of receptor regulated calcium increase,
DAGK alpha activation and membrane localization is a direct
consequence of
PI3K activation
Huber et al., Mol Cell Biol 2003
:
We demonstrate that both nephrin and CD2AP interact with the p85 regulatory subunit of phosphoinositide 3-OH kinase (PI3K) in vivo, recruit PI3K to the plasma membrane, and, together with podocin, stimulate
PI3K dependent
AKT signaling in podocytes
Lizcano et al., Biochem J 2003
:
In mammalian cells,
insulin induced
PI3K ( phosphoinositide 3-kinase ) activation, generates the lipid second messenger PtdIns ( 3,4,5 ) P ( 3 ), which is thought to play a key role in triggering the activation of S6K
Redondo et al., Mol Cell Endocrinol 2003
:
GLP-1 , like insulin,
activates PI3K/PKB , p70s6k, p44 and p42 MAP-kinase
Oh et al., J Biol Chem 2003
:
PI3K activation is
required for the activation of protein kinase C (PKC)-alpha and p38 kinase and inhibition of
ERK1/2 ...
PI3K activation is
required for the activation of
protein kinase C (PKC)-alpha and p38 kinase and inhibition of ERK1/2 ...
Stimulation of
PI3K by
IGF-1 resulted in blockage of NO-induced activation of p38 kinase and ERK1/2 and inhibition of PKCalpha and PKCzeta, which in turn suppressed dedifferentiation and apoptosis
Xu et al., J Biol Chem 2003
(Diabetic Nephropathies) :
Surprisingly, inhibition of
PI3K blocks both
ERK and Ki-Ras activation ... Surprisingly, inhibition of
PI3K blocks both ERK and
Ki-Ras activation
Kim et al., Diabetes 2003
(Diabetes Mellitus...) :
Insulin stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and
PI3K activity are impaired 40-50 % in diabetic subjects compared with lean or obese subjects
Bock et al., J Biol Chem 2003
:
Phosphatidylinositol 3-kinase interacts with the adaptor protein Dab1 in
response to
Reelin signaling and is required for normal cortical lamination ... Here we demonstrate that
PI3K activation by Reelin
requires Src family kinase activity and depends on the Reelin triggered interaction of Dab1 with the PI3K regulatory subunit p85alpha ... Here we demonstrate that
PI3K activation by
Reelin requires Src family kinase activity and depends on the Reelin triggered interaction of Dab1 with the PI3K regulatory subunit p85alpha
Heijink et al., Eur J Immunol 2003
:
Together, our results indicate that increased IL-2 dependent
PI3-K signaling
leads to impaired negative feedback control of the production of Th2-type cytokine
IL-5 by the cAMP dependent pathway ... Together, our results indicate that increased
IL-2 dependent
PI3-K signaling leads to impaired negative feedback control of the production of Th2-type cytokine IL-5 by the cAMP dependent pathway
Carricaburu et al., Proc Natl Acad Sci U S A 2003
:
PIP4K II beta expression did not
impair insulin dependent association of
PI3K with insulin receptor substrate 1 (IRS1) but abbreviated Akt activation, indicating that PIP4K II regulates PI-3,4,5-P3 degradation rather than synthesis ... PIP4K II beta expression did not impair insulin dependent association of
PI3K with insulin receptor substrate 1 (IRS1) but abbreviated
Akt activation , indicating that PIP4K II regulates PI-3,4,5-P3 degradation rather than synthesis ... PIP4K II beta expression did not impair
insulin dependent association of
PI3K with insulin receptor substrate 1 (IRS1) but abbreviated Akt activation, indicating that PIP4K II regulates PI-3,4,5-P3 degradation rather than synthesis
Nakayama et al., Biochem Biophys Res Commun 2003
(MAP Kinase Signaling System) :
We also demonstrated that
Raf1 is phosphorylated and
involved in the production of TNF-alpha and tyrosine phosphorylation of
PI3-K via ERK
Pola et al., J Biol Chem 2003
(MAP Kinase Signaling System...) :
Although
somatostatin does not
affect PI3-K , it inhibits ERK 1/2 and the small G-protein Rac activation and ruffle formation induced by PDGF
Mhashilkar et al., Mol Ther 2003
(Breast Neoplasms...) :
Expression of the PI3K pathway members ( p85
PI3K , FAK, ILK-1, Akt, and PLC-gamma ) was downregulated and expression of the PI3K antagonist
PTEN was
increased
Acosta et al., Mol Endocrinol 2003
:
Moreover, we show that both
c-Src/PI3K and c-Src/Fak/Erk1/2 pathways are
involved in the up-regulation of c-myc and
cyclin d1 expression mediated by PRL
Wang et al., Traffic 2003
:
We provided original evidence demonstrating that : ( i ) endogenous
phospholipase C-gamma1 , similar to YFP tagged phospholipase C-gamma1, translocated to endosomes following its initial translocation from cytosol to the plasma membrane in response to epidermal growth factor ; ( ii ) phospholipase C-gamma1 remained phosphorylated in endosomes, but phospholipase C-gamma1 activity is not required for its translocation, which suggests a signaling role for phospholipase C-gamma1 in endosomes ; ( iii ) the PH domain was not required for the initial translocation of phospholipase C-gamma1 from cytosol to the plasma membrane, but it stabilizes phospholipase C-gamma1 in the membrane at a later time ; ( iv ) the function of the phospholipase C-gamma1 PH domain in stabilizing phospholipase C-gamma1 membrane association is very important in maintaining the activity of phospholipase C-gamma1 ; and ( v ) the role of the PH domain in phospholipase C-gamma1 membrane association and activation is
dependent on
PI3K activity
Alahari et al., Exp Cell Res 2003
:
Furthermore, Nischarin does not affect
Rac mediated JNK and
PI3K activities ... Furthermore,
Nischarin does not
affect Rac mediated JNK and
PI3K activities
Santoro et al., Dev Cell 2003
:
We show that growth factor macrophage stimulating protein (MSP)- and its receptor Ron mediated
PI3K activation in keratinocytes
induces phosphorylation of both Ron and
alpha6beta4 integrin at specific 14-3-3 binding sites
Etgen et al., Endocrinology 2003
:
These data suggest that
activation of both
PI3K and MAPK by E ( 2 ) and
IGF-I mediates hormonal facilitation of lordosis behavior
Sundgren et al., Am J Physiol Regul Integr Comp Physiol 2003
(Cardiomegaly...) :
We conclude that 1 ) IGF-1 through IGF1R stimulates cardiomyocyte division in vivo ; hyperplastic growth is the most likely explanation of IGF-1 stimulated heart growth in vivo ; 2 ) IGF-1 through IGF1R does not stimulate binucleation in vitro or in vivo ; 3 ) IGF-1 through IGF1R does not stimulate hypertrophy either in vivo or in vitro ; and 4 )
IGF-1 through IGF1R
requires both ERK and
PI3K signaling for proliferation of near-term fetal sheep cardiomyocytes in vitro
Qi et al., Eur J Biochem 2003
(Carcinoma, Hepatocellular...) :
The upregulation of cell surface SLe ( x ) and
alpha-1,3-fucosyltransferase-VII ( alpha-1,3 Fuc T-VII, enzyme for SLe ( x ) synthesis ) was also
mediated by
PI3K and PKB, since LY294002 and AS-PKB also reduced the expressions of SLe ( x ) and alpha-1,3 FucT-VII, and attenuated the response to insulin
Sukumaran et al., J Biol Chem 2003
:
Taken together, these results suggest that E. coli infection of HBMEC induces
PLC-gamma1 activation in a
PI3K dependent manner to increase Ca2+ levels in HBMEC
Zhou et al., Arterioscler Thromb Vasc Biol 2003
:
LY294002, a
PI3K inhibitor, and N-acetylcysteine, a scavenger of reactive oxygen species,
inhibited the stretch activation of
Akt
Sheng et al., Gut 2003
(Colonic Neoplasms) :
Epidermal growth factor and
transforming growth factor alpha stimulated
PI3K activation which was required for growth factor induced expression of cyclin D1
Miele et al., J Biol Chem 2003
:
In contrast, insulin dependent IRS-1 and IRS-2 tyrosine phosphorylation was severely reduced in cells preincubated with HGA for 24 h.
Insulin stimulated association of
PI3K with IRS-1 and IRS-2, and PI3K activity were reduced by HGA in parallel with the changes in IRS tyrosine phosphorylation, while Grb2-IRS association was unchanged
Carter et al., Leukemia 2003
(Blast Crisis...) :
Neither these nor Akt inhibitor treated OCI-AML3 cells showed changes in XIAP levels, suggesting that
XIAP expression is
regulated by
PI3K downstream effectors other than Akt
Matsumoto et al., J Clin Invest 2003
:
Induction of the hepatic expression of
Srebp1c and of its target genes involved in fatty acid/triglyceride synthesis by fasting and refeeding or by hepatic expression of an active form of
PI3K was inhibited in L-lambdaKO mice compared with that in control animals ... Expression of
Srebp1c induced by insulin or by active
PI3K in primary cultured rat hepatocytes was inhibited by a dominant negative form of PKClambda and was mimicked by overexpression of WT PKClambda
Haga et al., Endothelium : journal of endothelial cell research 2003
:
Phosphorylation of Akt in EC exposed to SS or CS was time dependent but with maximal stimulation at 30 min ( SS ) or 5 min ( CS ) ; SS- or CS-induced
Akt phosphorylation was inhibited in the
presence of
PI3K inhibition
Shenoy et al., J Immunol 2003
:
Inhibition of
PI3K activity
blocked MBP stimulated O ( 2 ) ( - ) production, but not degranulation or
IL-8 production ... Measurement of Akt phosphorylation at Ser ( 473 ) and Thr ( 308 ) confirmed that
MBP stimulated
PI3K activity and also demonstrated indirectly activation of phosphoinositide dependent kinase-1 by MBP ... The time courses for phosphorylation and translocation of the p85 subunit of class I ( A )
PI3K ,
activation of
Akt , and activation of PKCzeta were similar ... We conclude that MBP stimulates a
Src kinase dependent
activation of class I ( A )
PI3K and, in turn, activation of PKCzeta in neutrophils, which contributes to the activation of NADPH oxidase and the resultant O ( 2 ) ( - ) production in response to MBP stimulation ... We conclude that
MBP stimulates a Src kinase dependent activation of class I ( A )
PI3K and, in turn, activation of PKCzeta in neutrophils, which contributes to the activation of NADPH oxidase and the resultant O ( 2 ) ( - ) production in response to MBP stimulation
Lin et al., Mol Pharmacol 2003
:
PTX blocks Akt but not phosphatidylinositol 3-kinase (PI3K) activation in response to PDGF and abrogates
cyclin D1 induction by
PI3K , suggesting an effect of PTX on Akt itself
Singh et al., Metabolism 2003
(Insulin Resistance) :
In EXP-2, the high-fat diet reduced insulin stimulated glucose transport, in part, by impairing
insulin stimulated
PI3-K activation and glucose transporter translocation
Borradaile et al., Diabetes 2003
(Carcinoma, Hepatocellular...) :
Insulin and naringenin induced
PI3K dependent increases in cytosolic and nuclear
SREBP-1 and LDLr expression ... Insulin and naringenin induced
PI3K dependent increases in cytosolic and nuclear SREBP-1 and
LDLr expression ... Similar
PI3K mediated increases in
SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c ...
Insulin and naringenin
increased HepG2 cell
PI3K activity and decreased insulin receptor substrate (IRS)-2 levels ... We conclude that naringenin increases LDLr expression in HepG2 cells via
PI3K mediated upregulation of
SREBP-1 , independent of IRS-1 phosphorylation
Tai et al., Cancer Res 2003
(Multiple Myeloma) :
IGF-I induces a 1.7-2.2 ( MM.1S ) and 2-2.5-fold ( OPM6 ) increase in migration, whereas blocking anti-IGF-I and anti-beta1 integrin monoclonal antibodies,
PI3-K inhibitors, as well as cytochalasin D abrogate IGF-I induced MM cell transmigration
Myou et al., J Immunol 2003
(MAP Kinase Signaling System) :
TAT-Deltap85 and LY294002, a
PI3K inhibitor , blocked the phosphorylation of gIV-PLA(2) at Ser ( 505 ) caused by fMLP, thus inhibiting gIV-PLA(2) hydrolysis and production of AA and LTC ( 4 ) in eosinophils ... We find that
PI3K is
required for
gIV-PLA(2) activation and hydrolytic production of AA in activated eosinophils ... We find that
PI3K is
required for
gIV-PLA(2) activation and hydrolytic production of AA in activated eosinophils ... Our data suggest that this essential
PI3K independently
activates gIV-PLA(2) through a pathway that does not involve MAPK ... Our data suggest that this essential
PI3K independently
activates gIV-PLA(2) through a pathway that does not involve MAPK
Zhang et al., J Biol Chem 2003
:
Phosphorylation of VEGFR2 at Tyr-801 and Tyr-1175, the critical sites for
VEGF induced
PI3K-Akt signaling, was not involved in TNF mediated Akt activation ... Taken together, our data demonstrated that TNF induces transactivation between Etk and VEGFR2, and
Etk directly
activates PI3K-Akt angiogenic signaling independent of VEGF induced VEGFR2-PI3K-Akt signaling pathway ... Taken together, our data demonstrated that TNF induces transactivation between Etk and VEGFR2, and Etk directly activates
PI3K-Akt angiogenic signaling independent of
VEGF induced VEGFR2-PI3K-Akt signaling pathway
She et al., Clin Cancer Res 2003
(Breast Neoplasms) :
We show here that pharmacologic down-regulation of constitutive
PI3K/Akt pathway signaling using the PI3K inhibitor LY294002 similarly
restores EGFR stimulated
Akt signaling and sensitizes MDA-468 cells to ZD1839
Liu et al., Circulation 2003
(MAP Kinase Signaling System) :
In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K) dependent increase in nitric oxide synthase activity as well as
PI3K dependent activation of
extracellular signal regulated kinase 1/2 and p70 S6 kinase ... In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K) dependent increase in
nitric oxide synthase activity as well as
PI3K dependent
activation of extracellular signal regulated kinase 1/2 and p70 S6 kinase
Andersson et al., Cell Signal 2003
:
In Xenopus aggregation, we suggest that melatonin stimulation of the
Mel1c receptor via G ( beta gamma )
activates PI3-K that, directly or indirectly via MAPK, activates PDE
Morrison et al., J Virol 2003
:
LMP2A activated Akt in a
PI3K dependent manner, and the downstream Akt targets glycogen synthase kinase 3beta ( GSK3beta ) and the Forkhead transcription factor
FKHR were phosphorylated and inactivated in LMP2A expressing HFK cells ... LMP2A activated
Akt in a
PI3K dependent manner, and the downstream Akt targets glycogen synthase kinase 3beta ( GSK3beta ) and the Forkhead transcription factor FKHR were phosphorylated and inactivated in LMP2A expressing HFK cells ...
LMP2A activated Akt in a
PI3K dependent manner, and the downstream Akt targets glycogen synthase kinase 3beta ( GSK3beta ) and the Forkhead transcription factor FKHR were phosphorylated and inactivated in LMP2A expressing HFK cells ... The cytoplasmic accumulation of
beta-catenin downstream of LMP2A was
independent of
PI3K signaling, whereas its nuclear translocation was dependent on PI3K signaling
Kobayashi et al., J Biol Chem 2004
(Neoplasm Invasiveness...) :
Here, we show that 1 ) TGF-beta1 induced a rapid increase of the PI3K activity that was accompanied by increased expression ( 5-fold ) of the uPA mRNA ; 2 ) pharmacological inhibition of
PI3K or AS-PI3K ODN transfection
inhibited TGF-beta1 stimulated
Akt phosphorylation ; 3 ) both PI3K pharmacological inhibitors and forced expression of AS-PI3K ODN reduced TGF-beta1 stimulated uPA mRNA and protein expression by approximately 70 % compared with controls ; 4 ) concentrations of PI3K inhibitors, sufficient to inhibit uPA up-regulation, inhibited TGF-beta1 dependent HRA cell invasion ; 5 ) the AS-PI3K ODN cells had a decreased ability to invade the extracellular matrix layer as compared with controls ; and 6 ) when the AS-PI3K ODN cells were injected intraperitoneally into nude mice, the mice developed smaller intraperitoneal tumors and showed longer survival
Amin et al., Int J Oncol 2003
:
Similarly, inhibition of
PI3K activation by its specific inhibitor LY294002
suppressed Akt phosphorylation
Steinle et al., Auton Neurosci 2003
:
NGF increased choroidal endothelial cell migration by 50 % over control and this was inhibited by pretreatment with LY294002 (
PI3K inhibitor ),
Akt inhibitor, and MMP2/9 inhibitor ... NGF increased choroidal endothelial cell migration by 50 % over control and this was inhibited by pretreatment with LY294002 (
PI3K inhibitor ), Akt inhibitor, and
MMP2/9 inhibitor
Théberge et al., Arch Biochem Biophys 2003
:
These data indicate that prolongation of
insulin stimulated ERK 1/2 and
PI3-K activation by VS is due to a more stable complex formation of IRS-1 with the p ( 85 alpha ) subunit which may, in turn, be responsible for its ability to enhance and extend the biological effects of insulin
Yue et al., J Steroid Biochem Mol Biol 2003
(Breast Neoplasms...) :
In aromatase over expressing MCF-7 cells,
aromatase activity was
reduced by inhibitors of MAPK and
PI3K suggesting the involvement of protein phosphorylation in the regulation of aromatase activity
Kim et al., J Biol Chem 2004
:
Down-regulation of PTEN by NIK/NF-kappaB results in activation of the PI3K/Akt pathway and augmentation of
TNF-alpha induced
PI3K/Akt stimulation
Yamagishi et al., Brain Res Mol Brain Res 2003
(Potassium Deficiency) :
Here we found that
IGF-1 had a greater survival promoting effect than BDNF, and
activated PI3-K to a higher level and maintained the level for a longer time
Zhuang et al., Photochem Photobiol 2003
:
Thus, activation of
Akt by 1O2 is
mediated by
PI3-K and contributes to a survival response that counteracts cell death after 1O2 induced injury
Isenovic et al., Endocrinology 2004
(MAP Kinase Signaling System) :
To more specifically determine the
role of
PI3K in
Ang II-regulation of alpha ( 1 ) -and beta ( 1 ) -gene transcription, cells were cotransfected with a dominant negative p85 construct
Yamada et al., Biochem J 2004
:
The
PI3K inhibitor LY294002
inhibited the ActD induced activation of
Akt and p70S6K, and completely abolished the effects of PLD1 or PLD2, whereas inhibition of ERK activity by the MEK inhibitor U0126 had a milder effect ... The
PI3K inhibitor LY294002
inhibited the ActD induced activation of Akt and
p70S6K , and completely abolished the effects of PLD1 or PLD2, whereas inhibition of ERK activity by the MEK inhibitor U0126 had a milder effect
Chakraborty et al., Neuroscience 2003
:
Activation of
PI3K by
IL-2 was also blocked by tyrphostin A25, a selective inhibitor of PTK, suggesting activation of the latter by IL-2 is upstream to PI3K activation
Tfelt-Hansen et al., Endocrinology 2004
(Hypercalcemia...) :
Taken together, our data show that
activation of
PI3K and p38 MAPK but not of MEK1/ERK by the
CaR promotes proliferation of H-500 cells as well as affords protection against apoptosis
Pardo et al., Int Immunol 2003
:
Altogether, the results suggest that TCR/CD3 induced
FasL gene transcription is
controlled by
PI3K and PKCtheta activation, while this signaling pathway is not implicated in CTL degranulation, which is rather dependent on the activation of classical PKC isoforms
Knobbe et al., Brain Pathol 2003
(Brain Neoplasms...) :
In contrast, we did not find any aberrations in the inositol polyphosphate phosphatase like-1 gene ( INPPL1 ), whose gene product may also counteract
Pi3k dependent
Akt activation
Senbonmatsu et al., EMBO J 2003
(Cardiomegaly) :
AT(2) enhances expression of p85 alpha
PI3K followed by enhanced p70 ( S6 ) kinase, essential to protein synthesis
Marcinkowska et al., Anticancer Res 2003
:
Phosphatidylinositol-3 kinase dependent activation of
Akt does not correlate with either high mitogenicity or cell migration induced by FGF-1
Lee et al., J Biol Chem 2004
:
Expression of the monocyte differentiation marker
CD11b was also induced by D ( 3 ) in a
PI3K dependent manner and gene silencing using shRNA showed that p110alpha was also required for this effect
Tanaka et al., J Biol Chem 2004
(MAP Kinase Signaling System...) :
Here, we show that 1 ) nontoxic concentrations of TGF-beta1 activated Src kinase ; 2 ) TGF-beta1 rapidly phosphorylates ERK1/2 and Akt, but not p38 ; 3 ) pharmacological Src inhibitor PP2 or antisense ( AS ) c-Src oligodeoxynucleotide ( ODN ) treatment reduced TGF-beta1 induced phosphorylation of ERK1/2 and Akt by 85-90 % compared with controls ; 4 ) pharmacological inhibition of MAPK by PD98059 abrogated TGF-beta1 mediated Akt stimulation, whereas TGF-beta1 induced
ERK1/2 stimulation was not
inhibited by
PI3K inhibitor LY294002 or AS-PI3K ODN transfection ; 5 ) up-regulation of uPA mRNA in response to TGF-beta1 was almost totally blocked by PP2 and PD98059 and partially ( approximately 55 % ) by LY294002 ; 6 ) TGF-beta1 induced uPA mRNA up-regulation was inhibited by treatment with AS ODNs to c-Src or PI3K by 90 or 60 %, respectively, compared with control ODN treatment ; and 7 ) blockade of the release of the transcription factor NF-kappaB by pyrrolidinedithiocarbamate reduced the TGF-beta1 induced activation of the uPA gene by approximately 65 %
Martin et al., J Biol Chem 2004
:
Inhibition of
PI3K reduced the increase in Nrf2 protein levels and activation of the
ho1 promoter
Williams et al., J Immunol 2004
(Disease Susceptibility...) :
Inhibition of
PI3K resulted in increased serum levels of IL1-beta, IL-2, IL-6, IL-10, IL-12, and
TNF-alpha in septic mice ... Inhibition of
PI3K resulted in increased serum levels of IL1-beta, IL-2, IL-6,
IL-10 , IL-12, and TNF-alpha in septic mice ... Inhibition of
PI3K resulted in increased serum levels of IL1-beta, IL-2, IL-6, IL-10,
IL-12 , and TNF-alpha in septic mice ... Inhibition of
PI3K resulted in increased serum levels of
IL1-beta , IL-2, IL-6, IL-10, IL-12, and TNF-alpha in septic mice ... Inhibition of
PI3K resulted in increased serum levels of IL1-beta,
IL-2 , IL-6, IL-10, IL-12, and TNF-alpha in septic mice ... Inhibition of
PI3K resulted in increased serum levels of IL1-beta, IL-2,
IL-6 , IL-10, IL-12, and TNF-alpha in septic mice
El Mabrouk et al., Am J Physiol Heart Circ Physiol 2004
(Hypertension) :
Our data demonstrate that
PI3K and SAM68 are
involved in
ANG II signaling and that SAM68 is differentially regulated in VSMCs from SHR
Lu et al., Biochem Biophys Res Commun 2004
(Breast Neoplasms...) :
They are consistent with the view that the IGF-IR mediated attenuation of trastuzumab induced growth inhibition we recently described is dependent on
IGF-I induced
PI3K signaling rather than IGF-I induced MAPK signaling
Li et al., Gastroenterology 2004
:
EGF increased
PI 3-K and active Akt2 in ileal BBM at the same time that it increased PI 3-K dependent trafficking of NHE3 to BBM and stimulation of Na absorption
Arimura et al., J Biol Chem 2004
:
Both CD28 and its relative, inducible costimulator (ICOS), have a binding motif for phosphatidylinositol 3-kinase (PI3K) in their cytoplasmic tail, and the binding of
PI3K leads to activation of a
serine/threonine kinase , Akt
Bertagnolo et al., Cell Signal 2004
:
The
Vav/p85 interaction is
essential for the ATRA induced
PI 3-K activity and for association of PI 3-K with actin, particularly in the nucleus ... The
Vav/p85 interaction is
essential for the ATRA induced
PI 3-K activity and for association of PI 3-K with actin, particularly in the nucleus
Street et al., J Biol Chem 2004
(Carcinoma, Hepatocellular...) :
NS5A mediated activation of
PI3K resulted in increased phosphorylation and activity of
Akt/protein kinase B and concomitantly provided protection against the induction of apoptosis in both replicon harboring cells and cells stably expressing NS5A alone ... NS5A mediated activation of
PI3K resulted in increased phosphorylation and activity of
Akt/protein kinase B and concomitantly provided protection against the induction of apoptosis in both replicon harboring cells and cells stably expressing NS5A alone
Fiory et al., J Biol Chem 2004
:
PI3K inhibition also
reduced insulin degradation and intact
insulin release by 50 and 75 %, respectively
Choi et al., Oncogene 2004
:
The specific
PI3K inhibitor LY294002
inhibits PI3K/Akt signaling and potentiates the radiation induced apoptosis, suggesting that activation of the PI3K/Akt signaling pathway is involved in the increased radio-resistance in cells overexpressing 12V-Ha-Ras ... Taken together, these findings explain the opposite effects of Ha-Ras and Ki-Ras on modulation of radiosensitivity, and suggest that differential
activation of
PI3K/Akt and Rac/p38 MAPK signaling by
Ha-Ras and Ki-Ras may account for the opposing response to the ionizing radiation ... Taken together, these findings explain the opposite effects of Ha-Ras and Ki-Ras on modulation of radiosensitivity, and suggest that differential
activation of
PI3K/Akt and Rac/p38 MAPK signaling by Ha-Ras and
Ki-Ras may account for the opposing response to the ionizing radiation
Levinthal et al., J Biol Chem 2004
:
Furthermore, we show that transient
PI3K inhibition
prevents the delayed activation of
MEK-1 , a direct activator of ERK, during oxidative stress
Shao et al., Cancer Res 2004
(Cell Transformation, Neoplastic...) :
Induction of
K-Ras activated
PI3K and mTOR in IECs
Safi et al., Mol Cell Biol 2004
:
Activation of
PI3-K by insulin or expression of an active form of PI3-K p110
induces a rapid translocation of
CKIP-1 to the plasma membrane ...
Activation of
PI3-K by
insulin or expression of an active form of PI3-K p110 induces a rapid translocation of CKIP-1 to the plasma membrane
Giuliani et al., Leukemia 2004
(Multiple Myeloma...) :
Moreover, we also found that the
PI3K kinase inhibitors, but not p38 MAPK inhibitors,
reduced VEGF secretion by myeloma cells and increase the inhibitory effect of MEK1 inhibitors
Yaspelkis et al., Life Sci 2004
:
Leptin appeared to mediate these effects by normalizing
insulin stimulated
PI3-K activation and GLUT4 protein concentration in the RG
Papapetropoulos et al., Mol Pharmacol 2004
:
In addition, wortmannin, a
PI3-K inhibitor,
blocked both the vanadate induced phosphorylation of
eNOS and the increase in cGMP accumulation
Pfeil et al., Prostate 2004
(Prostatic Neoplasms) :
IGF-1,
EGF , and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of Akt in DU145 cells and activation was completely
blocked by the
PI3K inhibitor LY294002 ... IGF-1, EGF, and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of
Akt in DU145 cells and activation was completely
blocked by the
PI3K inhibitor LY294002 ...
IGF-1 , EGF, and heregulin but not PDGF or activators of protein kinase A induced phosphorylation of Akt in DU145 cells and activation was completely
blocked by the
PI3K inhibitor LY294002
Sandra et al., Oral Oncol 2004
(Ameloblastoma...) :
MK could induce phosphorylation of p44/42
MAPK ( Thr202/Tyr204 ) and Akt ( Ser473 and Thr308 ), and by pretreatment of PD98059, MEK1 inhibitor, or LY294002,
PI3K inhibitor, MK-stimulated-phosphorylation of MAPK and Akt and MK-stimulated growth of AM-1 cells were
inhibited ... MK could induce phosphorylation of p44/42 MAPK ( Thr202/Tyr204 ) and
Akt ( Ser473 and Thr308 ), and by pretreatment of PD98059, MEK1 inhibitor, or LY294002,
PI3K inhibitor, MK-stimulated-phosphorylation of MAPK and Akt and MK-stimulated growth of AM-1 cells were
inhibited
Newton et al., Expert Rev Anticancer Ther 2004
(Brain Neoplasms...) :
Loss of function of the tumor suppressor gene
PTEN also frequently
contributes to upregulation of
PI3K/Akt
Pozo-Guisado et al., Int J Cancer 2004
(Breast Neoplasms) :
Stimulation of
PI3K activity by RES was
ERalpha dependent since it could be blocked by the antiestrogen ICI 182,780
Zhu et al., Neuroscience 2004
(MAP Kinase Signaling System) :
Of note, wortmannin and U0126, as well as kappabeta-decoy DNA, abolished the anti-apoptotic effect of TGF-beta1, corroborating the notion that both
PI3k/Akt and MAPK/Erk1,2 pathways, and NF-kappabeta activity are
necessary for the anti-apoptotic activity of
TGF-beta1
Asilmaz et al., J Clin Invest 2004
(Disease Models, Animal...) :
Leptin treatment at this dose improved
insulin stimulated insulin receptor and insulin receptor substrate 2 (IRS-2) phosphorylation, IRS-2 associated
PI3K activity, and Akt activity in liver
Ruiz-León et al., J Neurochem 2004
(Neuroblastoma) :
In agreement with a participation of both Ras/MAPK- and PI3K/Akt mediated mechanisms, transient expression of constitutive active forms of Ras,
PI3K and other components of both signalling pathways
led to a significant increase of
APP promoter activity ... Taken together, our results suggest that simultaneous activation of at least two signalling pathways, Ras/MAPK and
PI3K/Akt , is
necessary to mediate a full activation of the APP promoter by
BDNF ... Taken together, our results suggest that simultaneous activation of at least two signalling pathways, Ras/MAPK and
PI3K/Akt , is
necessary to mediate a full activation of the
APP promoter by BDNF
Tejedo et al., Endocrinology 2004
:
In addition, we found that NO produces
c-Src/PI3K- and PKG dependent
activation of
ERK 1/2 ... In addition, we found that NO produces
c-Src/PI3K- and PKG dependent
activation of
ERK 1/2
Meroni et al., J Endocrinol 2004
(MAP Kinase Signaling System) :
At the same time, it was proposed that in 8-day-old Sertoli cells the effects of FSH on phosphorylated PKB ( P-PKB ) levels can be explained by a combination of increased secretion of endogenous IGF-I, decreased IGF binding protein-3 (IGFBP-3) production, and a synergistic action of FSH on
IGF-I dependent
PI3K activation ... At the same time, it was proposed that in 8-day-old Sertoli cells the effects of FSH on phosphorylated PKB ( P-PKB ) levels can be explained by a combination of increased secretion of endogenous IGF-I, decreased
IGF binding protein-3 (IGFBP-3) production, and a synergistic
action of FSH on IGF-I dependent
PI3K activation
Sánchez-Martín et al., J Biol Chem 2004
:
We have identified Vav, a guanine nucleotide exchange factor for Rac-1, and PI3K/Akt, as regulators of the activation and inactivation phases of the activity of Rac-1, respectively, in the context of LFA-1 signaling based on the following experimental evidence : ( i ) LFA-1 induced activation of Vav and
PI3K/Akt with kinetics consistent with a regulatory role for these molecules on Rac-1, ( ii ) overexpression of a constitutively active Vav mutant induces activation of Rac independently of LFA-1 stimulation whereas overexpression of a dominant negative Vav mutant
blocks LFA-1 mediated
Rac activation, ( iii ) pharmacological inhibition of PI3K/Akt prevented the fall in the activity of Rac-1 after its initial activation but had no effect on Vav activity, and ( iv ) overexpression of a dominant negative or a constitutively active Akt-1 induced or inhibited, respectively, Rac-1 activity
Bailey et al., Mol Endocrinol 2004
:
PI3K activates a downstream
serine/threonine kinase , Akt ; therefore, we investigated the role of Akt in the interaction between PRL and TGF-beta signaling
Laprise et al., J Cell Physiol 2004
:
Akt, MEK, and ERK activation levels return to control levels 60 min after calcium restoration ; ( 2 ) the use of E-cadherin blocking antibodies efficiently prevents Akt phosphorylation and MEK-ERK inhibition after 70 min of calcium restoration ; ( 3 ) using the PI3K inhibitor LY294002 ( 15 microM ) in calcium switch experiments, we demonstrate that the assembly of adherens junctions activates Akt activity and triggers the inhibition of ERK1/2 activities in a PI3K dependent manner ; ( 4 ) adenoviral infection of confluent Caco-2/15 cells with a constitutively active mutant of Akt1 strongly represses ERK1/2 activities ; ( 5 ) inhibition of
PI3K abolishes Akt activity but
leads to a rapid and sustained activation of the
MEK-ERK1/2 in confluent differentiating Caco-2/15 cells, but not in undifferentiated growing Caco-2/15 cells
Viswambharan et al., Circ Res 2004
:
In conclusion, rHDL inhibits thrombin induced human endothelial TF expression through inhibition of
RhoA and
activation of
PI3K but not Akt/eNOS
Slomiany et al., IUBMB Life 2004
(Gastritis...) :
Our findings suggest that PAF, through the interference with
PI3K dependent
cNOS activation, plays a critical role in influencing the extent of pathological consequences of H. pylori infection on the synthesis of gastric mucin
Mourani et al., Circulation 2004
(Carotid Artery Injuries) :
Finally, decreased activity of
PTEN , an endogenous negative
regulator of
PI3K signaling, was associated with high in vivo SMC growth rates, and morpholino mediated loss of endogenous PTEN induced a serum independent growth phenotype in cultured serum dependent SMCs
Schulze-Bergkamen et al., Hepatology 2004
:
PI3K/Akt activation by
HGF results in the induction of antiapoptotic proteins such as Mcl-1
Acitores et al., J Endocrinol 2004
:
We first explored the
effect of
GLP-1 , compared with that of insulin, on the activation of
PI3K , PKB, p70s6 kinase (p70s6k) and p44/42 mitogen activated protein kinases ( MAPKs ) and the action of specific inhibitors of these kinases on the insulin- and GLP-1 induced increment in glycogen synthase a activity ... The study showed that
GLP-1 , like insulin,
activated PI3K/PKB , p70s6k and p44/42
St-Germain et al., Molecular cancer 2004
(Endometrial Neoplasms) :
Inhibition of
PI 3-K with Wortmannin and LY294002 blocked IkappaB phosphorylation,
reduced NF-kappaB nuclear activity, reduced COX-2 expression and induced apoptosis ... Inhibition of
PI 3-K with Wortmannin and LY294002 blocked IkappaB phosphorylation, reduced NF-kappaB nuclear activity,
reduced COX-2 expression and induced apoptosis
Jang et al., Biochem Biophys Res Commun 2004
:
Catalase also
induced activation of NF-kappaB,
PI3K , ERKs, p38s, or JNKs. Catalase induced COX-2 expression was abrogated by treatment of MG-132 ( a NF-kappaB inhibitor ) or LY294002 ( a PI3K inhibitor ), but not by treatment of PD98059 ( an ERK inhibitor ), SB203580 ( a p38 inhibitor ), or SP600125 ( a JNK inhibitor ) ... Moreover, inhibition of
PI3K by LY294002
caused partial decrease of catalase induced COX-2 transcription and steady-state
COX-2 transcript levels, but not COX-2 mRNA stability
López-Pedrera et al., Haematologica 2004
(Leukemia, Promyelocytic, Acute...) :
Yet,
PI3K inhibitor LY294002 significantly
reduced AM80 elicted
ERK-1/-2 activity ... Yet,
PI3K inhibitor LY294002 significantly
reduced AM80 elicted
ERK-1/-2 activity
Gao et al., Am J Physiol Cell Physiol 2004
(Ovarian Neoplasms) :
Expression of the cyclin kinase inhibitor
p16(INK4a) was
induced by the
PI3K inhibitor, whereas steady-state levels of p21 ( CIP1/WAF1 ) were decreased in the same experiment ... Expression of the cyclin kinase inhibitor p16(INK4a) was
induced by the
PI3K inhibitor, whereas steady-state levels of
p21 ( CIP1/WAF1 ) were decreased in the same experiment ... The inhibition of
PI3K activity also
inhibited the phosphorylation of AKT and
p70S6K1 , but not extracellular regulated kinase 1/2 ... The inhibition of
PI3K activity also
inhibited the phosphorylation of
AKT and p70S6K1, but not extracellular regulated kinase 1/2
Huang et al., J Neurochem 2004
(Synaptic Transmission) :
These results suggest that a
PI3K/PKC dependent
insulin signaling, which controls postsynaptic surface AMPA receptor numbers through PP-independent endocytosis, may be a major expression mechanism of insulin-LTD in hippocampal CA1 neurons
Yamamori et al., Biochem Biophys Res Commun 2004
:
The aim of this study was to examine the mechanism underlying the
PI3K regulation of
p47(phox) phosphorylation ... Pharmacological inhibition of
PI3K attenuated both fMLP stimulated p47(phox) phosphorylation and
NADPH oxidase activity in HL-60 cells differentiated to a neutrophil-like phenotype ... Pharmacological inhibition of
PI3K attenuated both fMLP stimulated
p47(phox) phosphorylation and NADPH oxidase activity in HL-60 cells differentiated to a neutrophil-like phenotype ... Furthermore,
PI3K inhibitors
reduced the activation of
phospholipase Cgamma2 without affecting tyrosine phosphorylation on it ... These results suggest that
PI3K regulates the phosphorylation of NADPH oxidase component
p47(phox) by controlling diacylglycerol dependent PKCs but not Akt ... These results suggest that
PI3K regulates the phosphorylation of NADPH oxidase component p47(phox) by controlling diacylglycerol dependent PKCs but not
Akt
Ivins Zito et al., J Cell Physiol 2004
:
Here, we show that overexpression of a catalytically inactive mutant of SHP-2 inhibited
insulin-like growth factor-1 (IGF-1) dependent
PI3K and Akt activation
Huang et al., World J Gastroenterol 2004
(Carcinoma, Hepatocellular...) :
Effects of
PI3K and p42/p44 MAPK on overexpression of
vascular endothelial growth factor in hepatocellular carcinoma
Lee et al., Biochem Biophys Res Commun 2004
:
TGFbeta mediated phosphorylation of
Akt at Ser-473 was
inhibited by dominant negative ILK and
PI3K inhibitors, LY294002 and wortmannin ... In addition,
PI3K inhibitor, dominant negative Akt, and dominant negative ILK could not
block TGFbeta mediated C-terminal phosphorylation of
Smad2
Zhan et al., Biochem Biophys Res Commun 2004
(Leukemia, Megakaryoblastic, Acute) :
Phosphorylation of
Akt at serine 473 and its downstream molecular Bad at serine 136 was induced by HAPO, but was
blocked by two
PI3K inhibitors, LY294002 and wortmannin
St-Germain et al., Int J Oncol 2004
(Endometrial Neoplasms) :
Inhibition of
PI 3-K with Wortmannin and LY294002
blocked Akt phosphorylation and inhibited expression of COX-2 in mutated-PTEN cells ... Inhibition of
PI 3-K with Wortmannin and LY294002 blocked Akt phosphorylation and
inhibited expression of
COX-2 in mutated-PTEN cells
Philpott et al., Proc Natl Acad Sci U S A 2004
:
We propose that integrin mediated
PI3K induction of
NF-kappaB activates an autocrine TNF-alpha pathway required for DC maturation in response to Ad
Hirai et al., Brain Res Mol Brain Res 2004
(Anoxia) :
PI3K inhibition in neonatal rat brain slices during and after hypoxia
reduces phospho-Akt and increases cytosolic cytochrome c and apoptosis
Ortiz et al., American journal of physiology. Renal physiology 2004
:
In other cells,
eNOS activation by shear stress is
mediated by
phosphatidylinositol 3-OH kinase (PI3)-kinase
Chandramohan et al., J Immunol 2004
:
We demonstrate that pharmacologic inhibitors of
PI3K or BCR engagement lead to decreased inactive cytoplasmic levels and
increased active functional nuclear
FOXO3a
Strassheim et al., J Immunol 2004
(Inflammation) :
PI3-K blockade did not
inhibit nuclear translocation of
NF-kappa B , but did prevent Ser ( 536 ) phosphorylation of the p65 subunit of NF-kappa B, an event required for maximal transcriptional activity of NF-kappa B ... Inhibition of
PI3-K also
prevented activation of
p38 mitogen activated protein kinase and extracellular receptor activated kinase 1/2 in TLR2 stimulated neutrophils
Wang et al., Genes Dev 2004
(Carcinoma, Hepatocellular...) :
Liver tumors escape negative control of proliferation via
PI3K/Akt mediated block of
C/EBP alpha growth inhibitory activity
Pierchala et al., J Biol Chem 2004
:
Inhibition of both
PI3K and PKCs
promoted the expression and phosphorylation of the proapoptotic transcription factor
c-Jun , indicating that these pathways inhibit programmed cell death at the stage of proapoptotic gene expression
Li et al., J Appl Physiol 2004
(Anoxia) :
ANG II-induced PN expression was
blocked by the AT(1)-receptor antagonist losartan and by inhibitors of
PI3K and MEK1/2 ... In contrast, FGF-1 induced
OPN expression was
blocked by inhibitors of JNK or MEK1/2 but not of
PI3K , p70S6K, or p38MAPK
Saleem et al., Oncogene 2004
(Edema...) :
We found that Lupeol treatment to mouse skin resulted in the inhibition of TPA induced ( i )
activation of
PI3K , ( ii ) phosphorylation of Akt at Thr ( 308 ), ( iii ) activation of NF-kappaB and IKKalpha, and ( iv ) degradation and phosphorylation of
IkappaBalpha
Xie et al., Prostate 2004
(Disease Progression...) :
Regulation of
interleukin-6 mediated
PI3K activation and neuroendocrine differentiation by androgen signaling in prostate cancer LNCaP cells ... Addition of androgen blocks
IL-6 mediated
PI3K activation and NE differentiation in LNCaP cells ... In addition, androgen treatment enhances the interaction between AR and gp130, interrupts the
IL-6 induced gp130 mediated
PI3K activation, which may lead to inhibition of IL-6 mediated NE differentiation in LNCaP cells
Ma et al., Biochem Pharmacol 2004
:
Furthermore, DEP promoted phosphorylation of
Akt , a substrate of phosphatidylinositol 3-kinase (PI3K), on Ser-473 and Thr-308 in a
PI3K dependent manner, and enhanced phosphorylation of down-stream p70/p85 S6 kinases ( p70/p85S6K ) as well as glycogen synthase kinase-3beta ( GSK-3beta ) ... Furthermore, DEP promoted phosphorylation of Akt, a substrate of phosphatidylinositol 3-kinase (PI3K), on Ser-473 and Thr-308 in a
PI3K dependent manner, and enhanced phosphorylation of down-stream p70/p85 S6 kinases ( p70/p85S6K ) as well as
glycogen synthase kinase-3beta ( GSK-3beta )
Chen et al., J Biol Chem 2004
(Cryptosporidiosis) :
The cellular expression of either a dominant negative mutant of
PI3K ( PI3K-Deltap85 ) or functionally deficient mutants of frabin
inhibited C. parvum induced
Cdc42 accumulation at the host cell-parasite interface
Rajala et al., Biochemistry 2004
:
These results suggest that multiple signaling pathways could regulate the
PI3K activity and subsequent
activation of
Akt in the retina
Galmozzi et al., J Cell Physiol 2004
(Carcinoma...) :
Both the increase in
c-Myc protein levels and P2L enhanced translational activity were
inhibited by the
PI3K inhibitor wortmannin
Isenovic et al., Int J Mol Med 2004
:
IGF-1 increased the association between IRS-1 and p85, and
Ang II as well as
PI3K inhibition decreased this IGF-1 effect
Schmidt et al., BMC biology 2004
(MAP Kinase Signaling System) :
Surprisingly, three structurally different
PI3K inhibitors
block Ras, MEK and
Erk activation in PEPs by Epo
Kim et al., J Immunol 2004
:
Like TGF-beta1, the
PI3K inhibitor LY294002
blocked iNOS expression and death in cultured microglial cells ... TGF-beta1 was further found to decrease
LPS induced
activation of
PI3K and Akt
Bian et al., Invest Ophthalmol Vis Sci 2004
:
PI3K dependent induction of hRPE c-fos and
AP-1 nuclear translocation may be a target for therapies aimed at modulating MCP-1 in retinal diseases
Jiang et al., Mol Cell Biol 2004
(Cell Transformation, Neoplastic...) :
Ectopic expression of RhoB, but not the close relative
RhoA ,
inhibits Ras,
PI3K , and Akt induction of transformation, migration, and invasion and induces apoptosis and anoikis ... Ectopic expression of
RhoB , but not the close relative RhoA,
inhibits Ras,
PI3K , and Akt induction of transformation, migration, and invasion and induces apoptosis and anoikis
Sliva et al., Curr Cancer Drug Targets 2004
(Neoplasm Invasiveness...) :
The inhibition of PKC and
PI3K signaling ( through NF-kappaB and AP-1 )
suppressed the secretion of
uPA , resulting in the inhibition of motility of highly invasive breast cancer cells
Flaxenburg et al., J Immunol 2004
:
Also, wortmanin and a dominant-inhibitory mutant of
PI3K inhibited CD40 induced overexpression of
VEGF
Baki et al., EMBO J 2004
(Alzheimer Disease...) :
PS1 activates
PI3K thus inhibiting GSK-3 activity and tau overphosphorylation : effects of FAD mutations ... Furthermore, conditions that inhibit this association prevent the
PS1 induced
PI3K/Akt activation , indicating that PS1 stimulates PI3K/Akt signaling by promoting cadherin/PI3K association ... PS1 FAD mutations inhibit the
PS1 dependent
PI3K/Akt activation, thus promoting GSK-3 activity and tau overphosphorylation at AD-related residues
Halevy et al., Exp Cell Res 2004
(MAP Kinase Signaling System) :
UO126, a specific MAPK pathway inhibitor, had no effect on PI3K activity or Akt phosphorylation, implying that at least in muscle cells, the MAPK/ERK pathway is not required for
HGF induced
PI3K activation ... Moreover, the finding that
PI3K activity is
required for HGF induced
MAPK activation suggests its additional role in proliferation, rather than exclusively in the differentiation of adult myoblasts
Debiais et al., Exp Cell Res 2004
:
FGF-2 increased
PI3K activity but did not
induce phosphorylation of
Akt or the downstream effector p70 S6 kinase ...
FGF-2 increased
PI3K activity but did not induce phosphorylation of Akt or the downstream effector p70 S6 kinase ... The results indicate that the immediate protective
effect of
FGF-2 on human osteoblastic cell apoptosis involves
PI3K and inhibition of downstream caspases, independently of GSK-3 and beta-catenin-Lef/Tcf mediated transcription
O-charoenrat et al., Int J Cancer 2004
(Carcinoma, Squamous Cell...) :
Selective inhibition of ERK/MAPK ( by PD98059 or U0126 ) and
PI3K ( by LY294002 or wortmannin )
led to marked reduction of both basal and BTC induced
MMP-9 activity and invasive ability of HNSCC cells ... Taken together, our data show that
BTC induces MMP-9 production and invasion primarily through activation of EGFR, MAPK and
PI3K/Akt in HNSCC cells ... Taken together, our data show that BTC
induces MMP-9 production and invasion primarily through activation of EGFR, MAPK and
PI3K/Akt in HNSCC cells
Elad-Sfadia et al., J Biol Chem 2004
:
Co-transfectants of K-Ras/galectin-3, but not of H-Ras/galectin-3, exhibited enhanced and prolonged
epidermal growth factor stimulated increases in Ras-GTP, Raf-1 activity, and
PI3-K activity ... Thus, unlike galectin-1, which prolongs Ras activation of
ERK and
inhibits PI3-K , K-Ras-GTP/galectin-3 interactions promote, in addition to PI3-K and Raf-1 activation, a third inhibitory signal that attenuates active ERK
Gerling et al., Neurochem Int 2004
:
Accordingly, inhibition of
PI3-K by wortmannin and
MAPK-kinase ( MEK )
inhibition by UO126 abolished the neuroprotective effects
Teusch et al., J Immunol 2004
:
In contrast to previous studies, identifying Rac1-PI3K as an upstream element in TLR2 initiated response to NF-kappaB,
PI3K signaling was not
required for
RhoA or PKCzeta activity
Zhuang et al., American journal of physiology. Renal physiology 2004
:
Inhibition of
PI3K with LY-294002
blocked Akt phosphorylation and proliferation, whereas U-0126 blocked
ERK1/2 phosphorylation but had no effect on proliferation ... Inhibition of
PI3K with LY-294002
blocked Akt phosphorylation and proliferation, whereas U-0126 blocked ERK1/2 phosphorylation but had no effect on proliferation ... These results show that
EGFR activation is required for RPTC proliferation and migration and that proliferation is
mediated by
PI3K , whereas migration is mediated by p38
Schiffer et al., J Biol Chem 2004
:
CD2AP was not
required for
PI3K/AKT activation by insulin and epidermal growth factor, indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling ... CD2AP was not required for
PI3K/AKT activation by insulin and
epidermal growth factor , indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling ... CD2AP was not required for
PI3K/AKT activation by
insulin and epidermal growth factor, indicating that CD2AP is a selective mediator of anti-apoptotic TGF-beta signaling
Bełtowski et al., J Physiol Pharmacol 2004
:
inhibition of medullary Na ( + ), K ( + )
-ATPase by leptin is
mediated by
PI3K and requires integrity of actin cytoskeleton
Jia et al., J Biol Chem 2004
:
VEGF-D induced strong but more transient phosphatidylinositol 3-kinase (PI3K) mediated Akt activation and increased
PI3K dependent endothelial
nitric-oxide synthase phosphorylation and cell survival more weakly
Liu et al., J Surg Res 2004
:
In this study, we investigate the
role of PLC and
PI3-K in platelet derived growth factor ( PDGF ) and
extracellular matrix protein ( ECM ) induced SMC proliferation and migration
Qiu et al., Mol Hum Reprod 2004
:
In the
presence of
PI3K inhibitors ( Wortmannin ), EGF stimulated trophoblast migration and phosphorylation of
AKT and P70S6K ( Thr ( 389 ) and Thr ( 421 ) /Ser ( 424 ) ) were decreased, while EGF induced ERK phosphorylation was not affected ... mTOR/p70S6K is important in
PI3K- but not MAPK mediated trophoblast migration in
response to
EGF
Jang et al., Biochem Biophys Res Commun 2004
(Adenocarcinoma) :
Specifically, IL-1beta induced nuclear translocation of NF-kappaB was in part attenuated by LY294002, but not by GF109203X, SB203580, and SP600125, suggesting
PI3K dependent nuclear translocation of
NF-kappaB in response to IL-1beta
Le Blanc et al., Circ Res 2004
(Ion Channel Gating) :
Mutants of PI3K transfected into vascular myocytes also revealed the essential role of the lipid-kinase activity of
PI3K in Ang II-induced
Ca2+ responses
Campbell et al., Circ Res 2004
(MAP Kinase Signaling System) :
ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors ; when
PI3K was inhibited,
ERK phosphorylation could be
induced by microinjected activated Akt, indicating important cross-talk between the PI3K and ERK1/2 pathways ... ERK1/2 phosphorylation was reduced not only by MAPK pathway inhibitors but also by PI3K and mTOR inhibitors ; when
PI3K was inhibited, ERK phosphorylation could be
induced by microinjected activated
Akt , indicating important cross-talk between the PI3K and ERK1/2 pathways
Aikin et al., Endocrinology 2004
:
In addition,
IGF-I suppressed cytokine mediated JNK activation in a
PI3K dependent manner ... In addition,
IGF-I suppressed cytokine mediated JNK activation in a
PI3K dependent manner
Hou et al., J Neurosci 2004
:
Two structurally unrelated
PI3K inhibitors, LY294002 and wortmannin,
blocked the DHPG induced increases in phosphorylation of
Akt and mTOR ... Two structurally unrelated
PI3K inhibitors, LY294002 and wortmannin,
blocked the DHPG induced increases in phosphorylation of Akt and
mTOR ... Finally, we observed that both
PI3K inhibitors and rapamycin, an
mTOR inhibitor , prevented mGluR-LTD induced by DHPG
Bonaccorsi et al., J Cancer Res Clin Oncol 2004
(Prostatic Neoplasms) :
In addition, we determined the effect of the compound on
EGF stimulated
PI3 K/AKT pathway activation, in view of the key role exerted by this pathway in carcinoma cell invasion
Duan et al., Exp Cell Res 2004
:
It is suggested that
PI3K and ERK/MAPK
mediated the activation of
SPK and would be involved in the HGF induced migration of endothelial cells
Domínguez-Cáceres et al., Oncogene 2004
:
Activation of the
PI3K by
PRL was necessary for the expression of c-MycmRNA and W53 cell proliferation, as the PI3K inhibitor LY294002 abolished them
Wu et al., J Neurochem 2004
:
AMPA mediated neuroprotection is blocked by
PP1 , an inhibitor of src family kinases, LY294002, a
PI3-K inhibitor , or U0126, a MAPK kinase ( MEK ) inhibitor ... Thus, AMPA receptors protect neurons through a mechanism involving BDNF release, TrkB receptor activation, and a signaling pathway involving a
PI3-K dependent activation of
MAPK that increases BDNF expression
Simoncini et al., Steroids 2004
:
For instance, estrogens and glucocorticoids trigger rapid vasodilatation due to rapid induction of nitric oxide synthesis in endothelial cells via the
estrogen receptor dependent
activation of MAPK and
PI3K , leading to relevant pathophysiological consequences, in vitro and in vivo
Bonaccorsi et al., Steroids 2004
(Neoplasm Invasiveness...) :
In addition,
EGF stimulated
PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR
Sajan et al., J Clin Endocrinol Metab 2004
(Obesity) :
Relative to adipocytes of lean women,
insulin stimulated [ ( 3 ) H ] 2-deoxyglucose uptake and activation of insulin receptor
substrate-1/PI3K and aPKCs, but not PKB, were diminished in adipocytes of obese women
Krugmann et al., Curr Biol 2004
:
We found no evidence for direct regulation of ARAP3 's Rho GAP activity by PtdIns ( 3,4,5 ) P ( 3 ) in vitro, but
PI3K activity was
required for activation by
Rap in a cellular context, suggesting that PtdIns ( 3,4,5 ) P ( 3 ) -dependent translocation of ARAP3 to the plasma membrane may be required for further activation by Rap
Chaudhary et al., Toxicology 2004
:
Pharmacological inhibition of phosphatidylinositol 3' kinase (PI3'K) by wortmannin and p38 mitogen activated protein kinase ( MAPK ) by SB203580 reveal that
PI3'K mediates Be-specific
p45 phosphorylation and IL6 release, whereas p38 MAPK regulates the release of IL6 and IL10 and the phosphorylation of p45 independent of metal-salt treatment ... Pharmacological inhibition of phosphatidylinositol 3' kinase (PI3'K) by wortmannin and p38 mitogen activated protein kinase ( MAPK ) by SB203580 reveal that
PI3'K mediates Be-specific p45 phosphorylation and
IL6 release, whereas p38 MAPK regulates the release of IL6 and IL10 and the phosphorylation of p45 independent of metal-salt treatment
Hwang et al., Carcinogenesis 2004
(Prostatic Neoplasms) :
Phosphatidylinositol-3 kinase/Akt/mammalian target of rapamycin signaling was also
involved in vanadate induced
HIF-1alpha expression, but it was independent of AMPK signaling pathway
Ma et al., Endocrinology 2004
(Acute Disease...) :
In contrast,
insulin induced tyrosine phosphorylation of IRS-1/2 and association between IRS-1/2 and
PI3K were dramatically reduced after hemorrhage
Stevens et al., Journal of thrombosis and haemostasis : JTH 2004
:
Furthermore,
ILK activity is dually
regulated by
PI3K and PKC in thrombin stimulated platelets and regulated by PI3K in collagen stimulated cells
Qiao et al., J Biol Chem 2004
:
The phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, reduced both basal and IGF-1 stimulated RUNX2 DNA binding activity in the absence of changes in RUNX2 protein as did the overexpression of the phosphatidylinositol 3-phosphate phosphatase, confirming that
PI3K signaling
mediates RUNX2 activation
Bonaccorsi et al., Int J Cancer 2004
(Neoplasm Invasiveness...) :
EGF stimulated
PI3K activity, a key signaling pathway for invasion of these cells, and EGF-PI3K interaction are also decreased in PC3-AR cells and further reduced by treatment with androgen
Velling et al., EMBO Rep 2004
:
Here we show that
PI3K dependent phosphorylation of
Akt in response to ligation of beta1-integrins occurs efficiently in the absence of FAK tyrosine phosphorylation
Viard et al., Nat Neurosci 2004
:
We show that the effect of
PI3K is
mediated by
Akt/PKB and specifically requires Ca(v)beta ( 2 ) subunits ... We show that the effect of
PI3K is
mediated by
Akt/PKB and specifically requires Ca(v)beta ( 2 ) subunits
Vigorito et al., J Immunol 2004
:
By contrast, Vav function is essential for
PI3K activation following membrane Ig
(mIg)/CD19 coligation ... By contrast, Vav function is essential for
PI3K activation following
membrane Ig (mIg)/CD19 coligation
Chang et al., Mol Pharmacol 2004
:
In this study, we explore the
role of Ras,
phosphoinositide-3-OH-kinase (PI3K) , Akt, and transcription factor nuclear factor-kappaB (NF-kappaB) in YC-1 induced
COX-2 expression in A549 cells ... A Ras inhibitor ( manumycin A ), a
PI3K inhibitor ( wortmannin ), an Akt inhibitor ( 1l-6-Hydroxymethyl-chiro-inositol2- [ ( R ) -2-O-methyl-3-O-octadecylcarbonate ] ), and an NF-kappaB inhibitor [ pyrrolidine dithiocarbamate ( PDTC ) ] all
reduced YC-1 induced
COX-2 expression ... Taken together, these results indicate that YC-1 might activate the sGC/cGMP/PKG pathway to induce Ras and
PI3K/Akt activation, which in turn initiates IKKalpha/beta and NF-kappaB activation and finally
induces COX-2 expression in A549 cells
Rangarajan et al., Cancer Cell 2004
(Cell Transformation, Neoplastic) :
Cell type-specific differences also exist in the requirements for tumorigenic transformation : immortalized human fibroblasts require the activation of Raf and Ral-GEFs, human embryonic kidney cells require the activation of
PI3K and Ral-GEFs, and human mammary epithelial cells
require the activation of Raf, PI3K, and
Ral-GEFs
Paling et al., J Biol Chem 2004
:
Treatment with the reversible
PI3K inhibitor, LY294002, or more specific
inhibition of class I (
A ) PI3K via regulated expression of dominant negative Deltap85, led to a reduction in the ability of LIF to maintain self-renewal, with cells concomitantly adopting a differentiated morphology
Qiu et al., Reproduction 2004
(MAP Kinase Signaling System) :
We showed for the first time that
EGF activated both
PI3K/Akt and MAPK/extracellular-signal regulated kinase ( ERK ) signalling in HTR8/SVneo, and increased both MMP-9 and TIMP-1 mRNAs and protein concentrations ... Our results suggest that the activation of both
PI3K and MAPK pathways in extravillous trophoblasts is
necessary for the up-regulation of MMP-9 and
TIMP-1 expression by EGF ... Our results suggest that the activation of both
PI3K and MAPK pathways in extravillous trophoblasts is
necessary for the up-regulation of
MMP-9 and TIMP-1 expression by EGF
Kim et al., Cell Signal 2004
:
We have characterized the
role of Drosophila
PI3K and AKT in
ERK pathway activation involving insulin induced proliferation using Drosophila Schneider cells
Skinner et al., J Biol Chem 2004
(Ovarian Neoplasms) :
The inhibition of
PI3K by LY294002
inhibited p70S6K1 and HDM2 activity in the cells ... The inhibition of
PI3K by LY294002
inhibited p70S6K1 and HDM2 activity in the cells ... The inhibition of
PI3K by LY294002
inhibited p70S6K1 and
HDM2 activity in the cells
Tian et al., Acta Pharmacol Sin 2004
(Cardiomegaly) :
CT-1 simultaneously
activated phosphorylation of STAT3, ERK1/2, and
PI3-K in rat cardiomyocytes ... The hypertrophic effect of CT-1 was essentially
mediated by
STAT3 , independent of
PI3-K , and negatively regulated by ERK1/2 via inhibiting the phosphorylation of STAT3
Zhang et al., Cancer Res 2004
(Rhabdomyosarcoma...) :
Inhibition of either pathway reduced expression of cyclins D1, D2, and D3 in RMS lines, whereas only
PI3K inhibitors
blocked cyclin D1 , D2, and D3 expression in ET lines
Lei et al., J Biol Chem 2004
:
PP1 or
PP2 blocked T3-stimulated PKB/Akt phosphorylation at serine 473 and
PI3K activity that was activated by an active mutant of Src ; however, wortmannin did not inhibit the T3-stimulated Src kinase activity ...
PP1 or PP2
blocked T3-stimulated PKB/Akt phosphorylation at serine 473 and
PI3K activity that was activated by an active mutant of Src ; however, wortmannin did not inhibit the T3-stimulated Src kinase activity
Choi et al., J Recept Signal Transduct Res 2004
:
To study the
role of
PI3K in insulin stimulation of
ERK , we employed PI3K inhibitor LY294002 and mouse embryonic R- fibroblasts lacking IGF-1 receptors ... To study the
role of
PI3K in
insulin stimulation of ERK, we employed PI3K inhibitor LY294002 and mouse embryonic R- fibroblasts lacking IGF-1 receptors ... In these R- cells,
PI3K inhibition by LY294002 enhanced insulin stimulation of
ERK phosphorylation whereas LY294002 inhibited insulin stimulation of Akt phosphorylation ... In these R- cells,
PI3K inhibition by LY294002 enhanced insulin stimulation of ERK phosphorylation whereas LY294002
inhibited insulin stimulation of
Akt phosphorylation ... In these R- cells,
PI3K inhibition by LY294002 enhanced insulin stimulation of ERK phosphorylation whereas LY294002
inhibited insulin stimulation of Akt phosphorylation ...
PI3K inhibition
increased IRS-1-Grb2 complex formation and ras activity following insulin treatment of cells ...
PI3K inhibition
increased IRS-1-Grb2 complex formation and ras activity following insulin treatment of cells ... Increased insulin
stimulation of
ERK by
PI3K inhibition was mediated by the MEK/ERK pathway, but did not involve inhibitory Ser259 phosphorylation of raf that was reported to be mediated by Akt ... Increased
insulin stimulation of ERK by
PI3K inhibition was mediated by the MEK/ERK pathway, but did not involve inhibitory Ser259 phosphorylation of raf that was reported to be mediated by Akt ... In summary,
PI3K inhibition in R- cells
enhanced insulin stimulation of
ERK phosphorylation by mechanisms involving enhancement of IRS-1 tyrosine phosphorylation, IRS-1-Grb2 complex formation and the ras/MEK/ERK pathway ... In summary,
PI3K inhibition in R- cells
enhanced insulin stimulation of ERK phosphorylation by mechanisms involving enhancement of IRS-1 tyrosine phosphorylation, IRS-1-Grb2 complex formation and the ras/MEK/ERK pathway
Bao et al., Am J Physiol Lung Cell Mol Physiol 2005
:
We found that KGF induces a dose- and time dependent increase in Akt kinase activity and that, as expected, activation of
Akt via KGF is
PI3K dependent
Gagnon et al., Gynecol Oncol 2004
(Uterine Neoplasms) :
KLE cells remained resistant to PI 3-K inhibitor, indicating that
Akt phosphorylation might be, in part,
independent of
PI 3-K in this cell line
Maeda et al., Biochem Biophys Res Commun 2004
:
Expression of Gab1
PI3K-m in SK-N-MC human primitive neuroectodermal tumor cells expressing wild-type RET markedly
impaired Akt phosphorylation, Rac1 activation, and lamellipodia formation that were induced by GDNF whereas expression of Gab1 SHP2-m partially impaired Erk activation ... Expression of Gab1
PI3K-m in SK-N-MC human primitive neuroectodermal tumor cells expressing wild-type RET markedly
impaired Akt phosphorylation,
Rac1 activation, and lamellipodia formation that were induced by GDNF whereas expression of Gab1 SHP2-m partially impaired Erk activation
Barata et al., J Exp Med 2004
(Precursor Cell Lymphoblastic Leukemia-Lymphoma) :
IL-7 induced
PI3K dependent phosphorylation of
Akt and its downstream targets GSK-3, FOXO1, and FOXO3a ...
PI3K signaling was also
required for cell size increase, up-regulation of CD71, expression of the glucose transporter
Glut1 , uptake of glucose, and maintenance of mitochondrial integrity ...
PI3K signaling was also
required for cell size increase, up-regulation of
CD71 , expression of the glucose transporter Glut1, uptake of glucose, and maintenance of mitochondrial integrity
McCubrey et al., Oncogene 2004
(Cell Transformation, Neoplastic...) :
MEK or
PI3K inhibitors
suppressed ERK or Akt activation, respectively, and induced apoptosis in the v-ErbB : ER-responsive cells ... MEK or
PI3K inhibitors
suppressed ERK or
Akt activation, respectively, and induced apoptosis in the v-ErbB : ER-responsive cells
Carini et al., Gastroenterology 2004
(Reperfusion Injury) :
PI3K activation in preconditioned hepatocytes
required the stimulation of
adenosine A 2A receptors and was mimicked by adenosine A 2A receptors agonist CGS21680 ... In the cells treated with CGS21680,
PI3K activation was
prevented either by inhibiting
adenylate cyclase and PKA with, respectively, 2,5-dideoxyadenosine and H89 or by blocking Galphai-protein and Src tyrosine kinase with, respectively, pertussis toxin and PP2 ... In the cells treated with CGS21680,
PI3K activation was
prevented either by inhibiting adenylate cyclase and
PKA with, respectively, 2,5-dideoxyadenosine and H89 or by blocking Galphai-protein and Src tyrosine kinase with, respectively, pertussis toxin and PP2 ... This suggested that PKA phosphorylated
adenosine A 2A receptors may
activate PI3K by coupling it with Galphai-protein through Src ...
PI3K is
activated following hepatocyte hypoxic preconditioning by the combined stimulation of adenosine A 2A receptors, PKA, Galphai protein, and
Src ...
PI3K is
activated following hepatocyte hypoxic preconditioning by the combined stimulation of
adenosine A 2A receptors, PKA, Galphai protein, and Src ...
PI3K is
activated following hepatocyte hypoxic preconditioning by the combined stimulation of adenosine A 2A receptors,
PKA , Galphai protein, and Src
Tybulewicz et al., Eur J Immunol 2004
(Second Messenger Systems) :
Unexpectedly, they show that while the BCR induced phosphorylation of the
PI3K dependent kinase
Akt is reduced in p85alpha-deficient cells, the phosphorylation of two downstream targets of Akt -- FOXO1 and ribosomal protein S6 -- is largely unaffected
Scholz et al., J Invest Surg 2004
:
We further showed that
CD29/TNF-alpha mediated
effects involved
PI3K and tyrosine kinase dependent signaling via MAPK but were independent of nuclear transcription factor (NF)-kappaB activity ... We further showed that
CD29/TNF-alpha mediated
effects involved
PI3K and tyrosine kinase dependent signaling via MAPK but were independent of nuclear transcription factor (NF)-kappaB activity
Zhuang et al., J Neurosci 2004
(Hyperalgesia...) :
Capsaicin and NGF induce phosphorylation of the PI3K downstream target
AKT ( protein kinase B ), which is
blocked by the
PI3K inhibitors LY294002 and wortmannin, indicative of the activation of PI3K by both agents ...
ERK activation by capsaicin and NGF was also blocked by
PI3K inhibitors ... ERK
activation by capsaicin and
NGF was also blocked by
PI3K inhibitors ... In acutely dissociated DRG neurons, the capsaicin induced
TRPV1 current was strikingly potentiated by NGF, and this potentiation was completely
blocked by
PI3K inhibitors and primarily suppressed by MEK inhibitors ... Therefore,
PI3K induces heat hyperalgesia, possibly by regulating TRPV1 activity, in an
ERK dependent manner
Ahn et al., EMBO J 2004
:
Here we show that nuclear
PI3K and its upstream regulator PIKE
mediate the antiapoptotic activity of
nerve growth factor (NGF) in the isolated nuclei
Zhou et al., Am J Physiol Cell Physiol 2005
:
Although
IL-13 induced activation of
PI3K-Akt , the activation did not contribute to the synergy observed with TGF-beta1 plus IL-13 in TIMP-1 expression and in fact may dampen it
Descamps et al., J Immunol 2004
(Multiple Myeloma) :
Altogether, these results suggest that CD45 negatively regulates
IGF-1 dependent activation of
PI3K ... Altogether, these results suggest that
CD45 negatively
regulates IGF-1 dependent activation of
PI3K
Saito et al., Stroke 2004
(Brain Ischemia) :
We administered the PI3-K inhibitor, LY294002, into mouse brains after tFCI and examined the
role of
PI3-K in the ILK pathway and expression of the
ILK/Akt complex by immunohistochemistry, Western blot analysis, and coimmunoprecipitation ... We administered the PI3-K inhibitor, LY294002, into mouse brains after tFCI and examined the
role of
PI3-K in the ILK pathway and expression of the
ILK/Akt complex by immunohistochemistry, Western blot analysis, and coimmunoprecipitation
Akiba et al., Biochem Pharmacol 2004
:
Although caffeine did not alter
insulin induced activation of
PI3K and protein kinase C-zeta (PKCzeta), an isoform of atypical PKC, which is reported to have an important role in insulin induced GLUT4 translocation, we found that insulin induced phosphorylation and activation of Akt were blocked by pre-treatment with caffeine
Everly et al., J Virol 2004
:
Activation of
PI3K can
affect the activity of
beta-catenin , the target of the wnt signaling pathway ... Neither the cytoplasmic accumulation of
beta-catenin nor the nuclear inactivation of GSK3beta was
affected by the inhibition of
PI3K signaling
Bertrand et al., Leukemia 2005
:
However, only inhibition of both
PI3K and MEK or both mTOR and MEK
resulted in a dramatic increase in the number of
annexinV ( + ) /PI ( + ) apoptotic events within a 24 h period
Gerasimovskaya et al., J Appl Physiol 2005
:
However, activation of
PI3K was not
required for activation of
ERK1/2 , implying a parallel involvement of these pathways in the proliferative response of fibroblasts to hypoxia
Chae et al., J Neurophysiol 2005
:
NRG1- and TGF(beta)1 evoked stimulation of K ( Ca ) is
blocked by inhibitors of
PI3K by overexpression of a dominant negative form of Akt, by overexpression of CTMP, an endogenous negative regulator of Akt, and by application of the Akt inhibitor 1L-6-hydroxymethyl-chiro-inositol 2- ( R ) -2-O-methyl-3-O-octadecylcarbonate ( HIMO )
Gálvez et al., J Biol Chem 2005
:
Inhibition of
PI3K or actin polymerization
impaired CCL2 induced
MT1-MMP activity
Gupta et al., Lung 2004
(Carcinoma, Non-Small-Cell Lung...) :
Pharmacologically inhibiting
PI3K led to decreased
Akt phosphorylation and radio sensitization of all three cell lines
Parikh et al., J Immunol 2004
:
Because inhibition of
PI3K or its target Akt also
triggers mitochondrial translocation of
Bax in T cells and apoptosis in Bax transfected cell lines, we generated Bax deletion mutants to identify the region ( s ) that confers sensitivity to regulation by MEK1 and Akt
Smith et al., J Biol Chem 2005
:
Furthermore, DEX mediated inhibition of
LEF/TCF transcriptional activity was attenuated in the
presence of dominant negative forms of either
PI3K or protein kinase B/Akt
Melikova et al., Exp Hematol 2004
:
Activation of
PI3K following beta1-integrin engagement on human CD34+ cells
results in subsequent phosphorylation of
PYK2 , and is required for the recruitment of the PI3K/PYK2 complex to beta1-integrins at the cell surface
Leblais et al., Circ Res 2004
(Calcium Signaling...) :
These results suggest that beta1-AR stimulation activates PI3K via a PKA dependent mechanism, and that G ( betagamma ) and the subsequent activation of
betaARK1 are critically
involved in the PKA induced
PI3K signaling which, in turn, negates cAMP induced positive inotropic effect via inhibiting sarcolemmal Ca2+ influx and the subsequent increase in intracellular Ca2+ transients, without altering the receptor mediated phospholamban phosphorylation, in intact cardiomyocytes ... These results suggest that beta1-AR stimulation activates PI3K via a PKA dependent mechanism, and that G ( betagamma ) and the subsequent activation of betaARK1 are critically involved in the
PKA induced
PI3K signaling which, in turn, negates cAMP induced positive inotropic effect via inhibiting sarcolemmal Ca2+ influx and the subsequent increase in intracellular Ca2+ transients, without altering the receptor mediated phospholamban phosphorylation, in intact cardiomyocytes
Kihara et al., Biochem Biophys Res Commun 2004
:
Galantamine
induced phosphorylation of
Akt , an effector of phosphatidylinositol 3-kinase (PI3K), while
PI3K inhibitors blocked the protective effect and Akt phosphorylation
Solinas et al., FEBS Lett 2004
:
Our results suggest that the direct effect of leptin in stimulating thermogenesis in skeletal muscle is mediated by substrate
cycling between de novo lipogenesis and lipid oxidation, and that this cycle
requires both
PI3K and AMPK signaling ... Our results suggest that the direct effect of
leptin in stimulating thermogenesis in skeletal muscle is mediated by substrate cycling between de novo lipogenesis and lipid oxidation, and that this cycle
requires both
PI3K and AMPK signaling
Krepinsky et al., Cell Signal 2005
:
Although phosphatidylinositol-3-kinase (PI3-K) may mediate Raf-1 activation,
PI3-K inhibition with wortmannin or LY294002
had no effect on stretch induced
Raf-1 activation
Venugopal et al., Proc Natl Acad Sci U S A 2004
(Insulin Resistance) :
Insulin induced
PAI-1 gene expression is
up-regulated by a specific inhibitor of
PI3K
Li et al., Frontiers in bioscience : a journal and virtual library 2005
(Prostatic Neoplasms) :
DIM also inhibited EGFR expression, PI3K kinase activity, and Akt activation, and abrogated the
EGF induced activation of
PI3K in prostate cancer cells
Miura et al., Biochemistry 2004
:
Although
insulin receptor substrate-1 (IRS-1) and IRS-2, among other factors,
activate PI3K , there is little information on the relative roles of IRS-1and IRS-2 during aPKC activation by insulin action in specific cell types ... Although insulin receptor substrate-1 (IRS-1) and
IRS-2 , among other factors,
activate PI3K , there is little information on the relative roles of IRS-1and IRS-2 during aPKC activation by insulin action in specific cell types ... These findings provide evidence that directly links both IRS-1 and IRS-2 to aPKC activation in immortalized brown adipocytes, and further suggest that
IRS-1 and IRS-2 are
required for the activation of
Cbl/PI3K during insulin action in these cells ... These findings provide evidence that directly links both IRS-1 and IRS-2 to aPKC activation in immortalized brown adipocytes, and further suggest that IRS-1 and
IRS-2 are
required for the activation of
Cbl/PI3K during insulin action in these cells
Morisco et al., Circ Res 2005
(Insulin Resistance) :
Short-term stimulation induces an additive effect on insulin induced glucose uptake, and this effect is mediated by phosphorylation of Akt in threonine 308 through PKA/Ca2+ dependent and PI3K independent pathway, whereas insulin evoked threonine phosphorylation of
Akt is exclusively
PI3K dependent
Huang et al., Mol Cell Neurosci 2005
:
Insulin also induced rapid and long-term ( 30 h )
PI 3-K dependent phosphorylation of Akt and cAMP response element binding protein (
CREB ) ... Insulin also induced rapid and long-term ( 30 h )
PI 3-K dependent phosphorylation of
Akt and cAMP response element binding protein ( CREB )
Farias et al., Oncogene 2005
(Breast Neoplasms...) :
Cellular
retinol binding protein-I inhibits
PI3K/Akt signaling through a retinoic acid receptor dependent mechanism that regulates p85-p110 heterodimerization
Yanagawa et al., Endocr Relat Cancer 2004
(Ascites...) :
The anti-apoptotic effect of AMF has been described by other authors who have shown that the AMF over expressing cells were resistant to mitomycin-C induced apoptosis showing regression of Apaf-1 and
caspase-9 dependent on
PI3K and MAP kinase
Larizza et al., Leukemia & lymphoma 2005
(Acute Disease...) :
PI3K dependent activation of AKT and
STAT activation was observed in Kasumi-1 cells ...
PI3K dependent activation of
AKT and STAT activation was observed in Kasumi-1 cells
Schnitzer et al., FEBS Lett 2005
:
We investigated how
PI3K/Akt and glycogen synthase kinase 3beta ( GSK3beta )
affect HIF-1alpha in human RKO cells under prolonged periods of severe hypoxia/anoxia
Kamata et al., Int J Hematol 2004
:
The results also showed that activation of extracellular signal regulated kinase, but not
p38 mitogen activated protein kinase, induced by these cytokines is partly
mediated by
PI3K activation
Weber et al., Biol Reprod 2005
:
Our data suggest that gap junctions and
PI 3-K activity are
necessary for GtH and
IGF-I to induce and maintain OMC in white bass
Merck et al., Blood 2005
:
A
PI3K dependent up-regulation of
IL-10 release is observed with all the TLR ligands used, whereas regulation of IL-12 production is variable depending on the TLR stimulated
Bonaccorsi et al., Ann N Y Acad Sci 2004
(Neoplasm Invasiveness...) :
In addition,
EGF stimulated
PI3K activity, a key signaling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881, indicating decreased functionality of EGFR
Angelillo-Scherrer et al., J Clin Invest 2005
(Thrombosis) :
Gas6 , through its receptors,
activates PI3K and Akt and stimulates tyrosine phosphorylation of the beta3 integrin, thereby amplifying outside-in signaling via alphaIIbbeta3
Duca et al., Mol Pharmacol 2005
:
The simultaneous inhibition of PKA and
PI3K , by N- ( 2- ( p-bromocinnamylamino ) ethyl ) -5-isoquinolinesulfonamide ( H89 ) and 2- ( 4-morpholynil ) -8-phenyl-4H-1-bemzopyran-4-one ( LY294002 ), respectively,
blocked MEK1/2 and
ERK1/2 phosphorylation, as did lactose, an EBP antagonist ... The simultaneous inhibition of PKA and
PI3K , by N- ( 2- ( p-bromocinnamylamino ) ethyl ) -5-isoquinolinesulfonamide ( H89 ) and 2- ( 4-morpholynil ) -8-phenyl-4H-1-bemzopyran-4-one ( LY294002 ), respectively,
blocked MEK1/2 and ERK1/2 phosphorylation, as did lactose, an EBP antagonist ... kappaE induced
Raf-1 phosphorylation and activation in a
PI3K dependent manner
Koma et al., Lab Invest 2005
:
KIT-Y719F does not
activate PI3-K , whereas KIT-Y821F does
González et al., Regul Pept 2005
:
In rat hepatocytes, activation of
PI3K/PKB , PKC and PP-1
mediates the GLP-1 induced stimulation of
glycogen synthase ... In conclusion,
GLP-1 , like insulin, stimulates glucose uptake, and this
involves activation of
PI3K/PKB , p44/42 MAPKs, partially p70s6k, and possibly PKC ; Ex-4 and Ex-9 both have GLP-1-like effect upon glucose transport, in which both share with GLP-1 an activation of PI3K/PKB -- partially in the case of Ex-4 -- and p44/42 MAPKs but not p70s6k ... In conclusion,
GLP-1 , like insulin, stimulates glucose uptake, and this
involves activation of
PI3K/PKB , p44/42 MAPKs, partially p70s6k, and possibly PKC ; Ex-4 and Ex-9 both have GLP-1-like effect upon glucose transport, in which both share with GLP-1 an activation of PI3K/PKB -- partially in the case of Ex-4 -- and p44/42 MAPKs but not p70s6k
Ahn et al., Cell Physiol Biochem 2005
:
Wortmannin inhibited NF-kappaB binding and transcriptional activity without inhibiting NF-kappaB translocation to the nucleus, indicating that
PI3K/Akt signaling
activates NF-kappaB transcriptional activity directly
Hellwig-Bürgel et al., Cell Physiol Biochem 2005
:
The study shows that
PI3K but not MAPKK-1 inhibition
resulted in the loss of hypoxic and IL-1beta induced
HIF-1alpha accumulation, whereas VEGF synthesis was reduced by either intervention ... Thus,
PI3K signaling is
required for HIF-1alpha accumulation and
VEGF synthesis, whereas MAPKK-1 signaling is required for VEGF synthesis only ... Thus,
PI3K signaling is
required for
HIF-1alpha accumulation and VEGF synthesis, whereas MAPKK-1 signaling is required for VEGF synthesis only
Huang et al., FEMS Microbiol Lett 2005
(Inflammation) :
We show here that inhibition of
PI3K in T84 intestinal epithelial cells
results in augmentation of Salmonella induced
interleukin-8 (IL-8) production at the level of both protein and mRNA
Felekkis et al., Mol Cancer Res 2005
(Breast Neoplasms) :
Inhibition of
PI3K with LY294002 or a dominant negative p85 construct
blocked AND-34 mediated Rac and
Akt activation ... Inhibition of
PI3K with LY294002 or a dominant negative p85 construct
blocked AND-34 mediated
Rac and Akt activation ... Although
R-Ras can
activate PI3K , transfection with constitutively active R-Ras failed to induce Rac activation and AND-34 overexpression failed to induce R-Ras activation ... Our studies suggest that AND-34 mediated
PI3K activation
induces Rac activation and anti-estrogen resistance in human breast cancer cell lines
Jang et al., Cell Signal 2005
:
Interestingly, there was
PI3K dependent
activation of
AKT , p70S6K, JNKs, and NF-kappaB in response to catalase ... Interestingly, there was
PI3K dependent
activation of AKT,
p70S6K , JNKs, and NF-kappaB in response to catalase ... Interestingly, there was
PI3K dependent
activation of AKT, p70S6K, JNKs, and
NF-kappaB in response to catalase
Lelievre et al., Blood 2005
:
Deficiency in the p110alpha subunit of
PI3K results in diminished
Tie2 expression and Tie2 ( -/- ) -like vascular defects in mice
Martinez-deMena et al., J Mol Endocrinol 2005
:
PI3K is
stimulated by
insulin and serum, and NE increases the effect of insulin
Banno et al., J Biol Chem 2005
:
Furthermore, the
PI3K/Akt activation in response to H ( 2 ) O ( 2 ) was
reduced by transfection of either PLD2KR or the dominant negative
Pyk2DN ... Furthermore, the
PI3K/Akt activation in response to H ( 2 ) O ( 2 ) was
reduced by transfection of either
PLD2KR or the dominant negative Pyk2DN
Kodani et al., Oncol Rep 2005
(Adenocarcinoma...) :
The combination of FK228 with
UCN-01 , another
PI3K/Akt pathway
inhibitor , also exerted a synergistic effect
Koh et al., Brain Res Mol Brain Res 2005
:
To evaluate the protective effects of low concentration of DADS on oxidative stress injured nPC12 cells, the viability of the cells ( pretreated with DADS for 2 h vs. not pretreated ) was evaluated 24 h after exposure to 100 microM H2O2 for 30 min. Compared to the cells treated with 100 microM H2O2 only, pretreatment of the cells with 20 microM DADS before exposure to 100 microM H2O2 increased the viability and induced activation of
PI3K and Akt, inactivation of GSK-3, and inhibition of cytochrome c release,
caspase-3 activation , and PARP cleavage ... These results indicate that low concentration of DADS has neuroprotective effects by activating
PI3K/Akt and by
inhibiting GSK-3 activation, cytochrome c release,
caspase-3 activation, and PARP cleavage, whereas high concentration is rather cytotoxic
Hers et al., Biochem J 2005
:
The effect of
insulin on phosphorylation of both these sites
required the activation of
PI3K and the MAPKs ( mitogen activated protein kinases ) ERK1/2 ( extracellular-signal regulated kinase 1 and 2 ), but not the activation of mTOR ( mammalian target of rapamycin ) /p70S6 kinase, JNK ( c-Jun N-terminal kinase ) or p38MAPK ... The differential effect of inhibition of ERK1/2 on insulin stimulated IRS-1 phosphorylation of Ser312/Ser616 and tyrosine indicates that these events are independent of each other and that phosphorylation of Ser312/Ser616 is not responsible for the negative regulation of
IRS-1 tyrosine phosphorylation
mediated by
PI3K in primary adipocytes
Carón et al., Mol Cancer Ther 2005
(Carcinoma...) :
In HCT116 cells expressing H-RAS V12, PI3K dependent radioresistance is mediated by both H-RAS dependent translocation of PI3K into the plasma membrane and heregulin induced
activation of membrane localized
PI3K via
ERBB3 ... In HCT116 cells expressing H-RAS V12, PI3K dependent radioresistance is mediated by both
H-RAS dependent translocation of
PI3K into the plasma membrane and heregulin induced activation of membrane localized PI3K via ERBB3
Carón et al., Mol Cancer Ther 2005
(Carcinoma...) :
Activated forms of
H-RAS and K-RAS differentially
regulate membrane association of
PI3K , PDK-1, and AKT and the effect of therapeutic kinase inhibitors on cell survival ... Activated forms of H-RAS and
K-RAS differentially
regulate membrane association of
PI3K , PDK-1, and AKT and the effect of therapeutic kinase inhibitors on cell survival
Benomar et al., Biochem J 2005
:
Furthermore,
leptin or insulin pre-treatment
increased basal
PI3K activity and IRS-1 or IRS-2 association with p85 and abolished acute insulin or leptin effect, in addition to the down-regulation of IRS-1 and IRS-2
Lee et al., Leuk Res 2005
:
The upregulation of
PTEN by DMSO
lead to the decrease of Akt phosphorylation, a downstream of
PI3K
Molnarfi et al., J Immunol 2005
:
The use of cycloheximide and actinomycin D shows that sIL-1Ra was an immediate early gene
induced by
IFN-beta and that
PI3K was controlling sIL-1Ra gene transcription ... Although both inhibitors of
PI3K and MEK1
diminished the Ser ( 727 ) phosphorylation of
STAT1 induced by IFN-beta, only Ly294002 inhibited sIL-1Ra production
Sedding et al., Circ Res 2005
:
Furthermore,
caveolin-1 is
essential for the integrin mediated activation of
PI3-K/Akt
Yau et al., Cancer Res 2005
(Neovascularization, Pathologic...) :
Inhibition of
integrin linked kinase by a selective small molecule inhibitor, QLT0254,
inhibits the
PI3K/PKB/mTOR , Stat3, and FKHR pathways and tumor growth, and enhances gemcitabine induced apoptosis in human orthotopic primary pancreatic cancer xenografts
Xu et al., J Clin Invest 2005
(Synaptic Transmission) :
We developed mice in which a fluorescent reporter for PI3K activity is targeted to either Agrp or POMC neurons and used 2-photon microscopy to measure dynamic
regulation of
PI3K by
insulin and leptin in brain slices ... We developed mice in which a fluorescent reporter for PI3K activity is targeted to either Agrp or POMC neurons and used 2-photon microscopy to measure dynamic
regulation of
PI3K by insulin and
leptin in brain slices
Mahon et al., Cell Signal 2005
:
Thus,
A-Raf can regulate PLCgamma1 signalling via a PDGFR dependent mechanism and may also
regulate PI3K signalling via a PDGFR independent mechanism ... Thus, A-Raf can regulate PLCgamma1 signalling via a
PDGFR dependent mechanism and may also regulate
PI3K signalling via a PDGFR independent mechanism
Nagel et al., Leukemia 2005
(Hodgkin Disease) :
HLXB9 activates
IL6 in Hodgkin lymphoma cell lines and is
regulated by
PI3K signalling involving E2F3 ...
HLXB9 activates IL6 in Hodgkin lymphoma cell lines and is
regulated by
PI3K signalling involving E2F3
Merighi et al., J Biol Chem 2005
(MAP Kinase Signaling System...) :
Here, we show that the A ( 3 ) adenosine receptor agonist Cl-IB-MECA stimulates
PI3K dependent phosphorylation of
Akt leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation ... Using A375 cells, we show that A ( 3 ) adenosine receptor stimulation results in
PI3K dependent phosphorylation of
Akt , leading to the reduction of basal levels of ERK1/2 phosphorylation, which in turn inhibits cell proliferation
Riol-Blanco et al., J Immunol 2005
(MAP Kinase Signaling System) :
CCR7 induced activation of
PI3K/Akt ; however, these enzymes did not regulate either chemotaxis or the speed of DCs
Farese et al., Biochem Soc Trans 2005
(Diabetes Mellitus...) :
These defects in muscle aPKC activation are due to both impaired activation of
insulin receptor substrate-1 dependent
PI3K ( phosphoinositide 3-kinase ) and the direct activation of aPKCs by the lipid product of PI3K, PI-3,4,5- ( PO4 ) 3
Abell et al., Nat Cell Biol 2005
:
Here we show that expression of the
PI(3)K regulatory subunits p55alpha and p50alpha is
induced by
Stat3 during involution ... We propose a novel mechanism in which
Stat3 regulates apoptosis by inducing expression of distinct
PI(3)K regulatory subunits to downregulate PI(3)K-Akt mediated survival signalling
Carpentier et al., Rev Neurol (Paris) 2005
(Brain Neoplasms...) :
High expression of the EGF receptor by tumor cells,
activation of the
PI3K/Akt and the
Ras/Raf pathways represent interesting targets for new selective drugs under development
Moissoglu et al., Biochem Biophys Res Commun 2005
(Cell Transformation, Neoplastic) :
Interestingly, FAK was required for full activation of PI3K by PDGF whereas the
activation of
PI3K by
insulin was significantly increased in FAK-/- cells
Nyga et al., Biochem J 2005
:
Taken together, our results indicate that
Gab2 is
required for caSTAT5 induced cell proliferation by regulating both the
PI3K/Akt and the Ras/MAPK pathways
Da Silva et al., Nat Neurosci 2005
:
PMGS induces axon specification by enhancing TrkA activity locally, which triggers phosphatidylinositol-3-kinase
(PI3K)- and Rac1 dependent
inhibition of
RhoA signaling and the consequent actin depolymerization in one neurite only
Chen et al., Pancreas 2005
(Diabetes Mellitus, Type 2) :
The
PI3K inhibitor wortmannin
suppressed pV-induced
insulin release at 3.3 mmol/L but not at 16.7 mmol/L glucose in both GK and Wistar rat islets
Chamaon et al., Biochem Biophys Res Commun 2005
(Astrocytoma) :
This suggest, that
PI3K and MAPK signalling is
involved in
PTTG regulation not only in malignant astrocytomas but also in non-tumorous cells
Pasapera et al., J Steroid Biochem Mol Biol 2005
:
Transactivation of estrogen-sensitive genes by FSH or PKA activators were blocked ( approximately 90 % ) by H89 ( PKA inhibitor ) and LY294002 but not by Wortmannin (
PI3-K inhibitors ), 4-OH-tamoxifen, ICI182,780 or SB203580 ( p38
MAPK inhibitor ) ; PD98059 ( ERK1/2 inhibitor ) partially ( approximately 30 % ) blocked the FSH mediated effect ... Transactivation of estrogen-sensitive genes by FSH or PKA activators were blocked ( approximately 90 % ) by H89 ( PKA inhibitor ) and LY294002 but not by Wortmannin (
PI3-K inhibitors ), 4-OH-tamoxifen, ICI182,780 or SB203580 (
p38 MAPK inhibitor ) ; PD98059 ( ERK1/2 inhibitor ) partially ( approximately 30 % ) blocked the FSH mediated effect
Gradilone et al., Biol Cell 2005
:
Since glucagon is capable of stimulating PI3K activity in hepatocytes and a cross talk between cAMP and PI3K has been suggested, in the present study, we examine whether
PI3K activation is
involved in the glucagon induced translocation of
AQP8
Xie et al., Mol Biol Cell 2005
:
PI3K inhibitors
blocked calcium activation of PLC-gamma1 as well as the induction of keratinocyte differentiation markers
involucrin and transglutaminase ...
PI3K inhibitors
blocked calcium activation of
PLC-gamma1 as well as the induction of keratinocyte differentiation markers involucrin and transglutaminase ... These data indicate that calcium activates PLC-gamma1 via increased
PIP3 formation
mediated by c-src- and fyn activated
PI3K
Nicholl et al., J Vasc Surg 2005
:
uPA activation of
PI3K and MKK3/6 was
EGFR dependent and that of MEK1 was EGFR independent ...
uPA activation of
PI3K and MKK3/6 was EGFR dependent and that of MEK1 was EGFR independent
Bertagnolo et al., Exp Cell Res 2005
(Leukemia, Promyelocytic, Acute) :
We have previously demonstrated that the amount and the tyrosine phosphorylation of Vav are up-regulated in both whole cells and nuclei of tumoral promyelocytes induced to granulocytic maturation by ATRA and that tyrosine phosphorylated
Vav does not display any ATRA induced GEF activity but
contributes to the regulation of
PI 3-K activity
Facchini et al., FEBS Lett 2005
:
In turn Src can activate
PI3K and PKC-delta, and all these signaling proteins are
required for
ODC induction ... In turn
Src can
activate PI3K and PKC-delta, and all these signaling proteins are required for ODC induction
Krötz et al., J Am Coll Cardiol 2005
:
In HUVEC, SHP-1 counteracts basal and stimulated NAD ( P ) H-oxidase activity by negative regulation of
PI3K dependent
Rac1 activation ; SHP-1 thus seems to be an important part of endothelial antioxidative defense controlling the activity of the O2 ( *- ) -producing NAD ( P ) H-oxidase
Staruschenko et al., Biochim Biophys Acta 2005
:
Constitutively active
PI3-K that is incapable of interacting with K-Ras ( K227E p110alpha )
acted as dominant negative with respect to the regulation of ENaC even in the presence of
K-Ras
Sheu et al., Cell Signal 2005
(Inflammation) :
Both NO donor and
LPS/IFN-gamma markedly
activated the
PI3K activity and the phosphorylation of Akt and nuclear factor (NF)-kappaB DNA binding activity in mesangial cells, which could be inhibited by LY294002 and transfection of dominant negative vectors of PI3K/p85 and Akt ... Both NO donor and
LPS/IFN-gamma markedly
activated the
PI3K activity and the phosphorylation of Akt and nuclear factor (NF)-kappaB DNA binding activity in mesangial cells, which could be inhibited by LY294002 and transfection of dominant negative vectors of PI3K/p85 and Akt
Imagawa et al., Arch Biochem Biophys 2005
:
These findings suggest that NADPH oxidase is activated by CD through a PKC independent signaling pathway in PMNs, and this pathway involves the
activation of
PLD through
PI3-K
Suga et al., Arch Biochem Biophys 2005
(MAP Kinase Signaling System) :
Furthermore, LY294002 or
Akt inhibitor did not affect the AVP induced phosphorylation of p38 MAP kinase and SB203580 did not
affect the phosphorylation of
PI3K or Akt ... These results suggest that
PI3K/Akt plays a part in the AVP induced phosphorylation of
HSP27 , maybe independently of p38 MAP kinase, in aortic smooth muscle A10 cells
Arnold et al., J Immunol 2005
:
The virus induced
ICAM-1 up-regulation was
dependent on protein kinase C and A,
PI3K , and p38 MAPK activity
Almeida et al., Cell Death Differ 2005
(MAP Kinase Signaling System) :
The results indicate that the protective effect of
BDNF in hippocampal neurons against glutamate toxicity is
mediated by the
PI3-K and the Ras/MAPK signaling pathways, and involves a long-term change in protein synthesis
Auld et al., Biochem J 2005
:
CRHSP24 became phosphorylated at Ser52 when HEK-293 ( human embryonic kidney ) cells were stimulated with IGF-1 ( insulin-like growth factor-1 ) and this was
prevented by inhibitors of
PI3K ( phosphoinositide 3-kinase ), but not by rapamycin [ an inhibitor of mTOR ( mammalian target of rapamycin ) ] or PD 184352, an inhibitor of the classical MAPK ( mitogen activated protein kinase ) cascade and hence the activation of RSK
Lubin et al., Neuroscience 2005
:
Interestingly, inhibition of ERK but not
PI3K blocked the kainate mediated increase in
phospho-IkappaBalpha
Shah et al., J Cell Physiol 2006
(MAP Kinase Signaling System) :
However, the extent to which
EGF-R transactivation is
essential for GPCR agonist stimulated
PI3K activation is not known ... In C9 hepatocytes, agonist activation of AT1 angiotensin II ( AT1-R ), lysophosphatidic acid (LPA), and EGF receptors caused phosphorylation of Akt through activation of the
EGF-R in a
PI3K dependent manner ... However,
ERK1/2 activation by these agonists in these cells was
independent of
PI3K activation ... However,
ERK1/2 activation by these agonists in these cells was
independent of
PI3K activation ... In contrast, agonist stimulation of HEK 293 cells stably expressing AT1-R caused
ERK1/2 phosphorylation that was independent of EGF-R transactivation but
required PI3K activation
Kristof et al., J Pharmacol Exp Ther 2005
(Prostatic Neoplasms) :
In human lung epithelial adenocarcinoma ( A549 ) cells, LY303511, like rapamycin, inhibited mTOR dependent phosphorylation of S6K, but not
PI3K dependent phosphorylation of
Akt
Li et al., Int J Biochem Cell Biol 2005
(MAP Kinase Signaling System) :
Here we tested the hypothesis that
PI3K/Akt mediated inactivation of GSK-3beta and
activation of
mTOR contribute to the anabolic effects of IGF-I in dexamethasone treated myotubes ... Our results suggest that
PI3K/Akt mediated inactivation of GSK-3beta and
activation of
mTOR contribute to the anabolic effects of IGF-I in dexamethasone treated myotubes
Mawrin et al., Clin Cancer Res 2005
(Meningeal Neoplasms...) :
Atypical and malignant meningiomas showed higher levels of
phospho-Akt compared with benign tumors, and their proliferation could be
inhibited by
PI3K blocking using wortmannin
Wiedmann et al., J Neurosci Res 2005
(Second Messenger Systems) :
However, whether
PI3K/Akt regulates
MEF2 and the role of MEF2 in IGF-1 mediated survival of neurons are unknown
Bar et al., Cell Death Differ 2005
:
The
PI3K inhibitor LY294002
prevents p53 induction by DNA damage and attenuates chemotherapy induced apoptosis ... These findings invoke an unexpected positive
role for
PI3K in
p53 activation by anticancer agents, and suggest that the efficacy of PI3K inhibitors in cancer therapy may be greatly affected by the tumor p53 status
Perrino et al., J Am Coll Cardiol 2005
(Disease Models, Animal...) :
Catalytically inactive
PI3KgammaPI3K overexpression in CSQ mice
inhibited betaARK1 associated
PI3K activity, normalized betaAR levels, and preserved betaAR responsiveness to isoproterenol ( ISO )
Chen et al., Nat Neurosci 2005
:
Inhibitors of
PI3K signaling also
blocked increases in
ERK/MAP kinase activity associated with memory retrieval
Aksoy et al., Eur J Immunol 2005
:
Here, we investigated the consequences of pharmacological inhibition of
PI3K on Toll-IL-1 receptor domain containing adapter inducing IFN-beta ( TRIF ) -dependent signaling, which
induces IFN-beta gene expression downstream of TLR3 and TLR4 ... In the same models of DC activation,
PI3K inhibition
increased DNA binding activity of NF-kappaB, but not
interferon response factor (IRF)-3 , the key transcription factors required for TLR mediated IFN-beta synthesis ... In the same models of DC activation,
PI3K inhibition
increased DNA binding activity of
NF-kappaB , but not interferon response factor (IRF)-3, the key transcription factors required for TLR mediated IFN-beta synthesis ... Experiments carried out in HEK 293T cells stably expressing TLR3 or TLR4 confirmed that inhibition of
PI3K activity
enhances NF-kappaB dependent promoters as well as
IFN-beta promoter activities without interfering with transcription at the positive regulatory domain III-I ... Furthermore, wortmannin
enhanced NF-kappaB activity induced by TRIF overexpression in HEK 293T cells, while overexpression of catalytically active
PI3K selectively attenuated TRIF mediated NF-kappaB transcriptional activity ... We conclude that inhibition of
PI3K activity enhances TRIF dependent NF-kappaB activity, and thereby
increases IFN-beta synthesis elicited by TLR3 or TLR4 ligands ... We conclude that inhibition of
PI3K activity
enhances TRIF dependent
NF-kappaB activity, and thereby increases IFN-beta synthesis elicited by TLR3 or TLR4 ligands
Beurel et al., Int J Oncol 2005
(Carcinoma, Hepatocellular) :
Therefore,
PI3K mediated
GSK-3beta inhibition could be a mechanism by which cancer cells escape from chemotherapy induced apoptosis
Aquila et al., J Clin Endocrinol Metab 2005
:
In uncapacitated sperm, both
insulin and leptin
increased PI3K activity, Akt S473, and glycogen synthase kinase-3 S9 phosphorylation ... In uncapacitated sperm, both insulin and
leptin increased
PI3K activity, Akt S473, and glycogen synthase kinase-3 S9 phosphorylation
Rahimi et al., J Immunol 2005
:
IL-10
induced the phosphorylation of
PI3K and p42/44 ERK
MAPK ...
IL-10 induced the phosphorylation of
PI3K and p42/44 ERK MAPK ... Taken together, these results suggest that IL-10 induced CD14 up-regulation in human monocytic cells may be mediated by
STAT-1 activation through the activation of
PI3K either alone or in concert with the ERK MAPK ... Taken together, these results suggest that IL-10 induced
CD14 up-regulation in human monocytic cells may be
mediated by STAT-1 activation through the activation of
PI3K either alone or in concert with the ERK MAPK
Strassheim et al., J Immunol 2005
:
SHIP ( -/- ) neutrophils demonstrated significantly increased activation of the
PI3K dependent kinase
Akt after exposure to PGN
Bullard et al., Basic Res Cardiol 2005
(Myocardial Infarction...) :
To examine the mechanistic pathways involved in EPO mediated protection, we co-administered the
ERK 1/2 inhibitor, U0126 ( 10 uM ) or the
PI3K inhibitors , wortmannin, ( 100 nM ) and LY294002 ( 15 microM ) at reperfusion ... To examine the mechanistic pathways involved in EPO mediated protection, we co-administered the
ERK 1/2 inhibitor, U0126 ( 10 uM ) or the
PI3K inhibitors , wortmannin, ( 100 nM ) and LY294002 ( 15 microM ) at reperfusion
Kao et al., Immunology 2005
:
Tyrosine kinase inhibitors ( genistein and tyrphostin AG126 ),
PI3K inhibitors ( wortmannin and LY 294002 ), and a p38 MAPK inhibitor ( SB 203580 )
attenuated LTA induced
iNOS expression and NO release in concentration dependent manners
Singh et al., Biochem Biophys Res Commun 2005
:
Two of the key signalling processes known to be involved in the regulation of cytoskeletal remodelling were investigated :
PI(3)K dependent
Akt phosphorylation and intracellular calcium concentration [ Ca ( 2+ ) ] ( i )
Bernardini et al., FASEB J 2005
:
Our observations indicate that chemoattractant receptor engagement induces
Fyn dependent
PI 3K activation in association with LFA-1 and suggests that Fyn is necessary to initiate and/or to regulate chemoattractant mediated LFA-1 activation to promote directional migration
Dessauer et al., Ann N Y Acad Sci 2005
:
We have described a novel bifurcated pathway by which
relaxin stimulates Gs alpha and
PI3K/PKCzeta leading to increased cAMP production and increased VEGF gene expression
Nguyen et al., Ann N Y Acad Sci 2005
:
Relaxin also stimulates
protein kinase C zeta (PKCzeta) translocation to the plasma membrane in a
PI3K dependent manner in THP-1 and MCF-7 cells
Soodvilai et al., American journal of physiology. Renal physiology 2005
:
In the present study, we investigated whether EGF stimulated
OAT3 activity was
dependent on tyrosine kinase and
PI3K ... We showed that
EGF stimulation of OAT3 was
reduced by inhibition of tyrosine kinase or
PI3K , suggesting that they play a role in the stimulatory process ... We showed that EGF stimulation of
OAT3 was
reduced by inhibition of tyrosine kinase or
PI3K , suggesting that they play a role in the stimulatory process ... Inhibitory effects also indicated that tyrosine kinase and PI3K are involved in the MAPK pathway for
EGF stimulation of OAT3 in intact renal proximal tubules, with
PI3K acting upstream and tyrosine kinase acting downstream of mitogen-activated/extracellular signal regulated kinase kinase activation ... Inhibitory effects also indicated that tyrosine kinase and PI3K are involved in the MAPK pathway for EGF
stimulation of
OAT3 in intact renal proximal tubules, with
PI3K acting upstream and tyrosine kinase acting downstream of mitogen-activated/extracellular signal regulated kinase kinase activation
Reistad et al., Toxicological sciences : an official journal of the Society of Toxicology 2005
:
We suggest that tyrosine kinase mediated activation of
PI3K could
result in enhanced activation of calcium dependent PKC by enhanced
PLC activity, followed by intracellular calcium release leading to ROS formation in neutrophil granulocytes
Galaria et al., J Surg Res 2005
:
ATF mediated migration is
PI3-K dependent and activates two separate pathways : ERK1/2 and akt ... ATF induces akt phosphorylation through a PI3K mediated but ras independent mechanism while both ras and
PI3K are
required for
ERK1/2 activation ...
ATF induces akt phosphorylation through a PI3K mediated but ras independent mechanism while both ras and
PI3K are required for ERK1/2 activation
Button et al., Exp Physiol 2005
:
Phosphatidylinositol 3-kinase and ERK1/2 are not
involved in
adenosine A1 , A2A or A3 receptor mediated preconditioning in rat ventricle strips
Varma et al., Am J Physiol Heart Circ Physiol 2005
(Hyperglycemia) :
We conclude that d-glucose regulates
Akt signaling through threonine phosphorylation of Akt and that hyperglycemia impaired
PI3k-Akt signaling may
promote EC proliferative dysfunction in diabetes
Ha et al., Cardiovasc Res 2005
(Cardiomegaly...) :
Our results demonstrate that
TLR4 is a novel receptor contributing to the development of cardiac hypertrophy in vivo and that both the TLR4 mediated pathway and
PI3K/Akt/mTOR signaling are
involved in the development of cardiac hypertrophy in vivo
Di Segni et al., J Mol Neurosci 2005
:
The PI3K signaling pathway might be involved in this effect of NRG as the downstream effector of PI3K, protein kinase B ( PKB/AkT ), is activated by NRG in the presence of Abeta, and
PKB/AkT activation is
inhibited by the
PI3K inhibitor, LY294002 ... The PI3K signaling pathway might be involved in this effect of NRG as the downstream effector of PI3K, protein kinase B ( PKB/AkT ), is activated by NRG in the presence of Abeta, and
PKB/AkT activation is
inhibited by the
PI3K inhibitor, LY294002
Dimova et al., Thromb Haemost 2005
(MAP Kinase Signaling System...) :
Inhibition of either the
PI3K by LY294002 or ERK1/2 by U0126
reduced HIF-1alpha protein levels while both inhibitors together completely abolished the IGF-1 effect on
HIF-1alpha
Badr et al., J Immunol 2005
(HIV Infections) :
Unlike CXCL12,
gp120 did not
induce the activation of phospholipase Cbeta3 and
PI3K downstream from CXCR4, whereas p38 MAPK activation was observed ... Unlike CXCL12, gp120 did not
induce the activation of phospholipase Cbeta3 and
PI3K downstream from CXCR4, whereas
p38 MAPK activation was observed ... Unlike CXCL12, gp120 did not
induce the activation of phospholipase Cbeta3 and
PI3K downstream from CXCR4, whereas p38
MAPK activation was observed
Min et al., J Immunol 2005
:
It also led to the production of reactive oxygen species via PKC- and
PI3K dependent activation of
NADPH oxidase in the endothelial cells, and antioxidants suppressed the responses to TRANCE
Abdelmegeed et al., J Pharmacol Exp Ther 2005
:
Heterogeneous nuclear RNA analysis revealed that AA suppressed
CYP2E1 gene transcription by approximately 50 % and that inhibition of
PI 3-K and PKC
diminished this AA-mediated effect on transcription
Alladina et al., J Vasc Res 2005
:
Inhibition of
PI3K reduces
p-Akt , with concurrent reductions in c-FLIP ( S ) and Bcl-2, and so renders endothelium sensitive to TRAIL induced apoptosis through the extrinsic and intrinsic pathways
Trisciuoglio et al., Mol Biol Cell 2005
(MAP Kinase Signaling System...) :
Involvement of
PI3K and MAPK signaling in bcl-2 induced
vascular endothelial growth factor expression in melanoma cells
Tai et al., Cancer Res 2005
(Multiple Myeloma) :
Immunoblotting analysis specifically showed that
PI3-K/AKT , nuclear factor-kappaB (NF-kappaB), and extracellular signal regulated kinase activation
induced by
CD40L ( 5 mug/mL ) was inhibited by CHIR-12.12 ( 5 mug/mL )
Nagoshi et al., J Clin Invest 2005
(Myocardial Reperfusion Injury) :
Biochemical analyses demonstrated that chronic
Akt activation
induces feedback inhibition of
PI3K activity through both proteasome dependent degradation of insulin receptor substrate-1 (IRS-1) and inhibition of transcription of IRS-1 as well as that of IRS-2
Yang et al., J Biol Chem 2005
:
In contrast,
PI3K does not
mediate IFNalpha/beta induced p100 processing, although
PI3K is involved in the pathway resulting in IkappaB alpha degradation ... In contrast,
PI3K does not
mediate IFNalpha/beta induced
p100 processing, although PI3K is involved in the pathway resulting in IkappaB alpha degradation ... Thus, IFN induces NF-kappaB activation to mediate IFN dependent cell survival signals through a `` canonical '' pathway of
IkappaB alpha proteolysis
mediated by
PI3K/Akt and a `` noncanonical '' pathway of p100 processing mediated by NIK/TRAF
Barata et al., Leukemia & lymphoma 2005
(Leukemia-Lymphoma, Adult T-Cell) :
IL-7 induces the activation of Jak/STAT, MEK/Erk and
PI3K/Akt signaling pathways in T-ALL cells ...
PI3K signaling is
required for the induction of
Bcl-2 , the down-regulation of p27 ( kip1 ) and cell cycle progression ...
PI3K signaling is also
required for the expression of the glucose transporter
Glut1 , uptake of glucose, activation of the metabolic machinery, increase in cell size, and maintenance of mitochondrial integrity
Dackour et al., In Vitro Cell Dev Biol Anim 2005
(Laryngeal Neoplasms...) :
Inhibiting either the enzymatic activity or the synthesis of
PI3K in uninfected laryngeal cells
blocked expression of
keratin-13 (K13) , a protein induced during normal differentiation ... Using ribonucleic acid interference to reduce protein levels of integrin linked kinase 1 or phosphoinositide dependent protein kinase 1, intermediates in the
activation of
Akt by
PI3K , or reducing levels of Akt-1 itself did not inhibit K13 expression by normal laryngeal keratinocytes
Mehta et al., J Immunol 2005
(MAP Kinase Signaling System) :
In this report, we show that in intestinal epithelial cells, HB-EGF triggered
PI3K dependent phosphorylation of
Akt ... This
PI3K effect was
HB-EGF dependent
Wain et al., Cell Signal 2005
:
However, co-ligation of the B cell antigen receptor and FcgammaRIIB inhibits the
PI3K dependent phosphorylation of PKB and
ERK1/2 in response to CXCL12 ... However, co-ligation of the B cell antigen receptor and FcgammaRIIB inhibits the
PI3K dependent phosphorylation of
PKB and ERK1/2 in response to CXCL12
Morrison et al., Am J Physiol Endocrinol Metab 2005
:
Because NPY/AgRP neurons project to the hypothalamic paraventricular nucleus ( PVN ), we next investigated whether
leptin activation of PVN neurons is similarly
PI3K dependent ... We conclude that leptin requires intact
PI3K signaling both to
inhibit hypothalamic Npy and
Agrp gene expression and activate neurons within the PVN ... We conclude that leptin
requires intact
PI3K signaling both to inhibit hypothalamic
Npy and Agrp gene expression and activate neurons within the PVN ... We conclude that
leptin requires intact
PI3K signaling both to inhibit hypothalamic Npy and Agrp gene expression and activate neurons within the PVN
Laurino et al., J Cell Sci 2005
:
PI3K activation by
IGF-1 is essential for the regulation of membrane expansion at the nerve growth cone ... Our results show that IGF-1, but not
BDNF , significantly and rapidly
stimulates IRS/PI3K/Akt and membrane expansion ... Our results show that
IGF-1 , but not BDNF, significantly and rapidly
stimulates IRS/PI3K/Akt and membrane expansion ... Finally, our results show that, upon
stimulation with
IGF-1 , most active
PI3K becomes associated with distal microtubules in the proximal or central domain of the growth cone
Han et al., J Biol Chem 2005
(Carcinoma...) :
Taken together, these findings suggest that activation of
PPARbeta/delta induces PGE2 receptor subtype EP4 expression through
PI3-K signals and increases human lung carcinoma cell proliferation in response to PGE2
El-Assal et al., Gastroenterology 2005
(Colitis, Ischemic...) :
HB-EGF enhances restitution after intestinal ischemia/reperfusion via
PI3K/Akt and
MEK/ERK1/2 activation
Furukawa et al., Cell Metab 2005
:
Inactivation of ROK also reduces
insulin stimulated IRS-1 tyrosine phosphorylation and
PI3K activity
Araki et al., Free Radic Biol Med 2005
:
PLA2,
COX , PKC, NADH dehydrogenase, and XO inhibitors
prevented the CA-induced ROS generation but not ERK 1/2,
PI 3 K , p38 MAPK, and MLCK inhibitors ...
PLA2 , COX, PKC, NADH dehydrogenase, and XO inhibitors
prevented the CA-induced ROS generation but not ERK 1/2,
PI 3 K , p38 MAPK, and MLCK inhibitors
Glassford et al., Eur J Immunol 2005
:
The inhibitors of PI3K activity, LY294002 and Wortmannin, also abrogate cyclin D2 induction by BCR cross linking, confirming that the class IA
PI3K is
necessary for
cyclin D2 induction in response to BCR stimulation ... Furthermore, using both p85alpha-null and p110delta-null B cells and inhibitors of PI3K, this study demonstrates for the first time, that
BCR cross linking induces cyclin D2 mRNA expression via transcriptional activation of the cyclin D2 promoter and that this transcriptional activation of cyclin D2
requires PI3K activity ... Furthermore, using both p85alpha-null and p110delta-null B cells and inhibitors of PI3K, this study demonstrates for the first time, that BCR cross linking induces cyclin D2 mRNA expression via transcriptional activation of the cyclin D2 promoter and that this transcriptional activation of
cyclin D2 requires
PI3K activity
Webb et al., J Immunol 2005
:
This work demonstrates that
PI3K activity is critical for T cell development and
depends on the combined function of p110gamma and
p110delta ... This work demonstrates that
PI3K activity is critical for T cell development and
depends on the combined function of
p110gamma and p110delta
Vilariño et al., J Immunol 2005
:
The kinetics, dose response, and pharmacologic characteristics of the IL-3 priming of stimulus induced Erk phosphorylation support the involvement of a yet unknown mechanism that is independent of
IL-3 induced Erk and
PI3K activation
Slomiany et al., IUBMB Life 2005
:
The impedance by leptin of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an
inhibitor of
PI3K , as well as by
ERK inhibitor, PD98059
Newcomb et al., J Biol Chem 2005
:
Phosphatidylinositol 3-kinase is
required for rhinovirus induced airway epithelial cell
interleukin-8 expression
Catarzi et al., Biochim Biophys Acta 2005
:
Therefore, we suggest a redox circuit whereby, upon PDGF stimulation, PKC,
PI3K and NADPH oxidase activity
contribute to complete
c-Src kinase activation, thus promoting maximal phosphorylation and activation of PDGFr tyrosine phosphorylation
Luo et al., Cell cycle (Georgetown, Tex.) 2005
(Neoplasms) :
Here we discuss some recent studies identifying the mechanisms by which
p85 , the regulatory subunit of PI3K, negatively
regulates PI3K signaling
Schwab et al., Apoptosis 2005
(Neuroblastoma) :
PI3-K inhibitor, LY294002,
reduced IGF-I stimulated phosphorylation of
FKHR , FKHRL1, and Akt, but did not affect Erk phosphorylation ...
PI3-K inhibitor, LY294002,
reduced IGF-I stimulated phosphorylation of FKHR,
FKHRL1 , and Akt, but did not affect Erk phosphorylation ...
PI3-K inhibitor, LY294002,
reduced IGF-I stimulated phosphorylation of FKHR, FKHRL1, and
Akt , but did not affect Erk phosphorylation ...
PI3-K inhibitor, LY294002, reduced IGF-I stimulated phosphorylation of FKHR, FKHRL1, and Akt, but did not
affect Erk phosphorylation
Wang et al., Shock 2005
(Endotoxemia...) :
The enhanced
MMP-9 levels induced by peptidoglycan was
attenuated by inhibitors of p38 mitogen activated protein kinases ( MAPK ), ( SB202190, 25 microM ) and ERK1/2 ( PD98059, 25 microM ) and inhibitors of Src Tyrosine kinase ( PP2, 5 microM ) and
PI3-K ( LY294002, 25 microM )
Kang et al., Stem Cells Dev 2005
:
bFGF did not
induce activation of
PI3K or PKC, but induced activation of ERK ( extracellular signal regulated kinase )
Le Pabic et al., J Hepatol 2005
:
The
involvement of
PI3K in
ADAM12 expression, similar to that previously observed for collagen I and fibronectin, suggests common pathways for gene up-regulation in hepatic stellate cells that occur during liver fibrogenesis and contribute to tumor progression
Vadlamudi et al., Cancer Res 2005
(Breast Neoplasms...) :
The altered localization of
PELP1 was
sufficient to trigger the interaction of PELP1 with the p85 subunit of phosphatidylinositol-3-kinase (PI3K), leading to
PI3K activation
Wlodarski et al., Cancer Res 2005
(Burkitt Lymphoma...) :
Both direct Akt ( Akt inhibitors I-III ) and a
PI3K inhibitor ( wortmannin at 1 nmol/L )
suppressed Akt phosphorylation without significantly affecting mTOR activation
Fukaya et al., Oncol Rep 2005
(Lung Neoplasms...) :
Inhibition of
PI3K-Akt signaling in LM8 by a PI3K inhibitor, LY294002, or by a dominant negative form of Akt,
resulted in suppression of
MMP secretion, in vitro invasiveness, cell locomotion and in vivo pulmonary metastasis
González et al., Int J Mol Med 2005
(Diabetes Mellitus, Type 2) :
Apart from the much higher basal
PI3K activity and impaired
response to
insulin of p44/42 MAP kinases in the diabetic patients, the changes in enzyme activity caused by either hormone or peptide, although not identical, were essentially comparable
Cao et al., Am J Physiol Cell Physiol 2006
:
Thrombin also induced the expression of
FGF-2 in a
PI3K-Akt-Fra-1 dependent and mTOR independent manner, and neutralizing anti-FGF-2 antibodies inhibited thrombin stimulated VSMC DNA synthesis and motility
Jones et al., J Immunol 2005
:
Protein kinase B ( PKBalpha/Akt1 ) a
PI3K dependent
serine-threonine kinase , promotes T cell viability in response to many stimuli and regulates homeostasis and autoimmune disease in vivo
Wong et al., Life Sci 2005
(Enterovirus Infections) :
The activity of
GSK3beta , a downstream target of these pathways, was negatively
regulated by the activation of both MAPK/ERK and
PI3K/Akt
Nur-E-Kamal et al., Stem Cells 2006
:
Inhibitors of
PI3K reduced the expression level of
Nanog in mESCs cultured on 3D nanofibrillar surfaces
Rajala et al., J Virol 2005
:
We demonstrate phosphorylation of GSK-3beta and nuclear translocation of the
p65 subunit of NF-kappaB, both downstream targets of the PI3K/Akt pathway, in adenovirus infected corneal fibroblasts in a
PI3K dependent manner ... We demonstrate phosphorylation of
GSK-3beta and nuclear translocation of the p65 subunit of NF-kappaB, both downstream targets of the PI3K/Akt pathway, in adenovirus infected corneal fibroblasts in a
PI3K dependent manner ... The results presented in this paper provide the first direct evidence that
PI3K mediated
Akt activation in adenovirus infected corneal cells may contribute to viral pathogenesis by the prolongation of cell viability
Jung et al., J Clin Immunol 2005
(MAP Kinase Signaling System...) :
The inhibition of
PI 3-K did not significantly
activate p38
MAPK or ERK 1/2 in PPD stimulated human monocytes ... The inhibition of
PI 3-K did not significantly
activate p38 MAPK or
ERK 1/2 in PPD stimulated human monocytes
Chang et al., J Lipid Res 2005
:
In summary, we conclude that KGF requires both
PI3K and JNK signaling pathways to induce SREBP-1, which in turn
induces SCD-1 and FAS expression in H292 cells ... In summary, we conclude that KGF
requires both
PI3K and JNK signaling pathways to induce
SREBP-1 , which in turn induces SCD-1 and FAS expression in H292 cells ... In summary, we conclude that KGF requires both
PI3K and JNK signaling pathways to induce SREBP-1, which in turn
induces SCD-1 and
FAS expression in H292 cells
Kzhyshkowska et al., Immunobiology 2005
:
Our data indicate that
PI3K activity is
required for the transfer of
stabilin-1 and its ligand acLDL from early to late endosomal compartments
Feliers et al., Kidney Int 2005
(MAP Kinase Signaling System) :
VEGF stimulated
Akt phosphorylation in a
PI3K dependent manner
Unni et al., Breast Cancer Res 2005
(MAP Kinase Signaling System...) :
PI3-K activity was
inhibited by
MSC followed by dephosphorylation of Akt ...
MSC inhibits cell growth by
inhibiting the activity of
PI3-K and its downstream effector molecules in mouse mammary tumor cells in vitro
Maldonado et al., Biochem Biophys Res Commun 2005
(Calcium Signaling) :
IGF-1 induced
CREB phosphorylation was
mediated by MEK1/ERK,
PI3-K , p38-MAPK, as well as Ca ( 2+ ) /calmodulin kinase and calcineurin
Park et al., Toxicol Appl Pharmacol 2006
(Lymphoma) :
In contrast, the enhanced AP-1 DNA binding activities and
p38 MAPK phosphorylation were significantly
suppressed by specific inhibitors for PKC and p38 MAPK, but not by
PI3-K inhibitors ... In contrast, the enhanced AP-1 DNA binding activities and p38
MAPK phosphorylation were significantly
suppressed by specific inhibitors for PKC and p38 MAPK, but not by
PI3-K inhibitors ... In contrast, the enhanced
AP-1 DNA binding activities and p38 MAPK phosphorylation were significantly
suppressed by specific inhibitors for PKC and p38 MAPK, but not by
PI3-K inhibitors
Stanger et al., Cancer Cell 2005
(Cell Transformation, Neoplastic...) :
To determine the role of the phosphatidylinositol 3-kinase (PI3-K) pathway in pancreas development, we generated a pancreas-specific knockout of
Pten , a negative
regulator of
PI3-K signaling
Ihle et al., Mol Cancer Ther 2005
(Carcinoma, Non-Small-Cell Lung...) :
Recent work shows that
phosphatidylinositol-3-kinase (PI3-K) is coupled to the EGFR only in NSCLC cell lines expressing ErbB-3 and that EGFR inhibitors do not
inhibit PI3-K signaling in these cells ... Recent work shows that phosphatidylinositol-3-kinase (PI3-K) is coupled to the EGFR only in NSCLC cell lines expressing ErbB-3 and that
EGFR inhibitors do not
inhibit PI3-K signaling in these cells
DeAngelis et al., Oncogene 2006
(Breast Neoplasms...) :
The importance of
IRS-1 activation of
PI3K in T-antigen transformation is supported by the finding that a constitutively activated p110 subunit of PI3K, a target of IRS-1, overcomes the inability of T antigen to transform MEFs with a serine phosphorylated IRS-1
Huang et al., Acta Pharmacol Sin 2005
(Breast Neoplasms...) :
The
PI3K inhibitors wortmannin and Ly294002, but not rapamycin, completely
inhibited the phosphorylation of
Akt and PRAS40
Cechin et al., Neurochem Res 2005
(Glioma) :
The LPA induced phosphorylation of ERK 1/2 and
CREB was
blocked by inhibition of
PI3K , PKC and MEK, but that of Akt was only inhibited by wortmannin, the PI3K inhibitor ... The LPA induced phosphorylation of
ERK 1/2 and CREB was
blocked by inhibition of
PI3K , PKC and MEK, but that of Akt was only inhibited by wortmannin, the PI3K inhibitor ... The LPA induced phosphorylation of
ERK 1/2 and CREB was
blocked by inhibition of
PI3K , PKC and MEK, but that of Akt was only inhibited by wortmannin, the PI3K inhibitor
Waggoner et al., J Immunol 2005
:
Suppression of
IL-12 did not result from increased IL-10 or TGF-beta, but was
dependent on
PI3K activation
Caldwell et al., Curr Biol 2005
:
Here, we show that the expression of activated Ras,
PI3 kinase (PI3K), or Raf specifically in the PG
reduces body size, whereas activated Ras or
PI3K , but not Raf, increases PG cell size
Chang et al., Microbes Infect 2006
:
Flavivirus induces interferon-beta gene expression through a pathway involving RIG-I dependent IRF-3 and
PI3K dependent
NF-kappaB activation
Tjin et al., Blood 2006
(Lymphoma, B-Cell...) :
In MET positive DLBCL cells, HGF induces MEK dependent activation of ERK and
PI3K dependent phosphorylation of PKB, GSK3, and
FOXO3a ... In MET positive DLBCL cells, HGF induces MEK dependent activation of ERK and
PI3K dependent phosphorylation of
PKB , GSK3, and FOXO3a
Chen et al., Mol Biol Cell 2005
:
MG132 induced DNA binding activity of C/EBPdelta, but not C/EBPbeta was regulated by p38,
PI3K , Src, and protein kinase C. Small interfering RNA of C/EBPdelta
suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription ... MG132 induced DNA binding activity of C/EBPdelta, but not
C/EBPbeta was
regulated by p38,
PI3K , Src, and protein kinase C. Small interfering RNA of C/EBPdelta suppressed COX-2 expression, further strengthening the role of C/EBPdelta in COX-2 gene transcription
Li et al., American journal of physiology. Renal physiology 2006
:
Inhibition of
PI3K with either wortmannin or LY-294002 significantly
increased channel activity in the
CCD from rats on a K-deficient ( KD ) diet or on a normal-K diet ... We conclude that
PI3K is involved in mediating the effect of low K intake on ROMK channel activity in the CCD and that the effect of PI3K on SK channels
requires the involvement of
PTK and the cytoskeleton
Tyner et al., Nat Med 2005
(Respirovirus Infections) :
The protective effect of Ccl5 requires activation of the
Ccr5 chemokine receptor and consequent bilateral
activation of G ( alphai )
-PI3K-AKT and G ( alphai ) -MEK-ERK signaling pathways ... The protective effect of
Ccl5 requires activation of the Ccr5 chemokine receptor and consequent bilateral activation of G ( alphai )
-PI3K-AKT and G ( alphai ) -MEK-ERK signaling pathways
Hashimoto et al., Int J Mol Med 2005
:
This APJ dependent activation of
Akt/PKB was significantly
inhibited by the pretreatment of pertussis toxin ( PTx ) and a
PI3K inhibitor, LY29004 ... This APJ dependent activation of
Akt/PKB was significantly
inhibited by the pretreatment of pertussis toxin ( PTx ) and a
PI3K inhibitor, LY29004
Kondo et al., Oncol Rep 2005
:
We found that both
PI 3-K inhibitors, wortmannin and LY294002, markedly
suppressed phosphorylation of
Akt and Bad in HL-60 cells ... Although
PI 3-K inhibitors did not
affect Fas expression in HL-60 cells, cellular FLICE-inhibitory protein ( c-FLIP ) levels were markedly reduced by PI 3-K inhibitor treatment
Wong et al., Biotechnol Bioeng 2006
:
The phosphoinositide 3-kinase (PI3K) inhibitor, wortmannin, totally blocked the effect of both zinc and insulin on Akt activation, indicating the
involvement of
PI3K in the activation of
Akt by zinc, rather than zinc acting on Akt directly
Shi et al., Mol Cancer Ther 2005
(Multiple Myeloma) :
Rapamycin enhanced basal AKT activity, AKT phosphorylation, and
PI3K activity in multiple myeloma cells and prolonged
activation of
AKT induced by exogenous IGF-I ... Thus,
mTOR inhibitors
activate PI3-K/AKT in multiple myeloma cells ; activation depends on basal IGF-R signaling ; and enhanced IRS-1/IGF-I receptor interactions secondary to inhibited IRS-1 serine phosphorylation may play a role in activation of the cascade
Parry et al., Mol Cell Biol 2005
:
Lastly, PD-1 ligation is more effective in suppressing CD3/CD28 induced changes in the T-cell transcriptional profile, suggesting that differential
regulation of
PI3K activation by
PD-1 and CTLA-4 ligation results in distinct cellular phenotypes ... Lastly, PD-1 ligation is more effective in suppressing CD3/CD28 induced changes in the T-cell transcriptional profile, suggesting that differential
regulation of
PI3K activation by PD-1 and
CTLA-4 ligation results in distinct cellular phenotypes
Chang et al., J Biomed Sci 2005
:
Suppression of
PI3K activity in integrin alpha6beta1 activated platelets induces an
increase in
Cdc42 activity and more filopodium formation
Asano et al., Cancer Res 2005
(Pancreatic Neoplasms) :
Furthermore,
IRS-1 was phosphorylated on a p85 binding site ( Y ( 612 ) ), and IRS-specific small interfering RNA potently
inhibited activation of
PI3K and Akt in transfected cells ... Furthermore,
IRS-1 was phosphorylated on a p85 binding site ( Y ( 612 ) ), and IRS-specific small interfering RNA potently
inhibited activation of
PI3K and Akt in transfected cells
Ahn et al., Blood 2006
:
Reduction of LIME expression by the introduction of siRNA resulted in the disruption of
BCR mediated activation of MAPK, calcium flux, NF-AT,
PI3K , and NF-kappaB
Almeida et al., J Biol Chem 2005
:
Wnt3a induced phosphorylation of
GSK-3beta and downstream activation of beta-catenin mediated transcription
required ERK,
PI3K , and Akt signaling ... Wnt3a induced phosphorylation of GSK-3beta and downstream activation of
beta-catenin mediated transcription
required ERK,
PI3K , and Akt signaling
Sugimori et al., J Bone Miner Metab 2005
:
BMP-2 prevents apoptosis of the N1511 chondrocytic cell line through
PI3K/Akt mediated
NF-kappaB activation ... Akt was rapidly phosphorylated in response to BMP-2 treatment ; however, the inhibition of
PI3K by Wortmannin markedly
reduced the phosphorylation of
Akt by BMP-2 ... Thus, BMP-2 induced
NF-kappaB activation is
mediated by
PI3K/Akt signaling
Romano et al., J Cell Physiol 2006
:
PI3K , ERK, JNK, and p38 kinases, known to mediate PDGF-BB signaling in the canonic dedifferentiative and proliferative response of smooth muscle cells ( SMC ) were rapidly
activated by
PDGF-BB but only p38 remained activated after 2-day stimulation
Wang et al., Cell Death Differ 2006
:
RA/BDNF treatment activates
Cdk5 mediated
PI3K/Akt and ERK pathways ... Inhibition of
Cdk5 inhibits
PI3K/Akt and ERK phosphorylation and Bcl-2 expression, and thus sensitizes the differentiated cells to DNA-damage
Okamura et al., Life Sci 2006
:
These results suggest that the
CKIepsilon induced down-regulation of
PI3K/Akt signaling through PTEN lead to amplified sensitivity to apoptosis
Andò et al., Mol Cell Endocrinol 2005
:
Interestingly, in the presence of a disruptor of
insulin signaling wortmannin, an
inhibitor of
PI3K , the intrinsic activity of G6PDH drops
Qi et al., J Biol Chem 2006
(Carcinoma, Hepatocellular) :
The
PI3K inhibitor, LY294002,
blocked IL-3 stimulated
Akt activity and partially blocked Bim ( EL ) phosphorylation
Hagiwara et al., Nephrol Dial Transplant 2006
(Diabetes Mellitus, Type 2...) :
EPA and specific inhibitors of ERK1/2, JNK and
PI3K decreased levels of MCP-1 in MMCs. EPA
suppressed phosphorylation of ERK1/2 and
p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice ... EPA and specific inhibitors of ERK1/2, JNK and
PI3K decreased levels of MCP-1 in MMCs. EPA
suppressed phosphorylation of
ERK1/2 and p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice
Wilkes et al., Cancer Res 2005
:
PI3K activation occurs in the presence of dominant negative dynamin and is
required for
p21 activated kinase-2 kinase activity and the increased proliferation and morphologic change induced by TGF-beta in vitro ...
PI3K activation occurs in the
presence of dominant negative
dynamin and is required for p21 activated kinase-2 kinase activity and the increased proliferation and morphologic change induced by TGF-beta in vitro
Ko et al., FEBS Lett 2005
:
Furthermore, PAF induced
NF-kappaB activation was blocked by selective inhibitors of Ca ( 2+ ),
PI3K , or extracellular signal regulated kinase ( ERK ) ... Our results suggest that PAF induced
MMP-9 expression, in a NF-kappaB dependent manner, is
regulated by Ca ( 2+ ),
PI3K and ERK signaling pathways ... Our results suggest that PAF induced MMP-9 expression, in a
NF-kappaB dependent manner, is regulated by Ca ( 2+ ),
PI3K and ERK signaling pathways
Bando et al., Exp Eye Res 2006
(MAP Kinase Signaling System...) :
We performed the gel contraction assay to evaluate the effect of PDGF in cultured ARPE-19 cells under the presence or absence of PD98059,
MAPK inhibitor or wortmannin,
PI3K inhibitor
Bonaccorsi et al., Steroids 2006
(Neoplasm Invasiveness...) :
In PC3-AR cells, we demonstrated a disruption of EGFR signalling properties ( reduced EGF induced EGFR autotransphosphorylation, reduced
EGF stimulated
PI3K activity as well as EGFR-PI3K interaction ) contributing to the lower invasive phenotype of these cells
Sun et al., Mol Pharmacol 2006
(Prostatic Neoplasms) :
Together, our results suggest that beta-cat/Tcf-4 signaling transcriptionally activates ET-1 in CaP cells ; meanwhile, ET-1 enhances
beta-cat/Tcf-4 signaling and in turn further increases ET-1 expression in a
PI3K dependent manner
Kim et al., J Pharmacol Exp Ther 2006
:
These results show that
PI3K/Akt/p70S6K signaling is active in the insulin mediated up-regulation of the antioxidant defense system and that low
insulin levels, as encountered in diabetes, potentially
increase the susceptibility of hepatocytes to xenobiotic mediated and/or oxidative stress mediated damage
Kim et al., Carcinogenesis 2006
(Prostatic Neoplasms) :
Importantly, the degree of Akt and
PI3K phosphorylations
induced by
EGF were also significantly suppressed
Pischke et al., Cell Mol Biol Incl Cyto Enzymol 2005
(Inflammation) :
Since activation of heme oxygenase-1 and PI3K/Akt both protect the cellular environment, we postulated that
PI3K/Akt can
regulate the induction of
heme oxygenase-1 by proinflammatory stress
Chen et al., Sci China C Life Sci 2005
:
Results show that both exogenous and endogenous EETs could remarkably enhance eNOS expression and its phosphorylation at Ser1179 and Thr497 residues ;
PI3K inhibitor LY294002 could
inhibit EETs induced increase in
eNOS-Ser ( P ) 1179 but had no effect on the change of eNOS-Thr ( P ) 497, while Akt inhibitor could attenuate the increase in phosphor-eNOS at both residues ; both of the two inhibitors could block EETs enhanced eNOS expression
Amin et al., Blood 2006
:
Antisense oligodeoxynucleotides ( ODNs ) and inhibitors of Src,
PI3K , p38, and NFkappaB significantly
reduced rhMIF induced MN
VCAM-1 and ICAM-1 expression ( P < .05 ) ... Antisense oligodeoxynucleotides ( ODNs ) and inhibitors of Src,
PI3K , p38, and NFkappaB significantly
reduced rhMIF induced MN VCAM-1 and
ICAM-1 expression ( P < .05 )
Festuccia et al., Endocr Relat Cancer 2005
(Prostatic Neoplasms) :
PI3K inhibition, by LY294002 or after PTEN transfection,
restores EGFR stimulated
Akt signalling and sensitizes the cells to pro-apoptotic action of gefitinib
Zhang et al., J Mol Endocrinol 2005
(Breast Neoplasms...) :
Moreover, these same IGF-I induced responses were also inhibited by the antiestrogen ICI 182780 and this was in contrast to a previous report suggesting that ICI 182780 did not affect
IGF-I dependent
activation of
PI3-K or induction of cyclin D1 expression
Lu et al., Int J Oncol 2006
(Prostatic Neoplasms) :
PI3K-Akt signaling is
involved in the regulation of
p21 ( WAF/CIP ) expression and androgen independent growth in prostate cancer cells ... The purpose of this study is to investigate the
role of
PI3K-Akt signaling in prostate cancer cell growth and
androgen receptor (AR) mediated gene expression
Morton et al., Cell Metab 2005
(Body Weight) :
These findings suggest that hypothalamic
leptin signaling is an important determinant of glucose metabolism and that the underlying neuronal mechanism
involves PI3K
Wang et al., Biochem J 2006
:
The dose-response relationships of
PI3K-inhibitor induced inhibition of
Rho , MLC phosphorylation and contraction were similar to that of PI3K-C2alpha inhibition, but not to that of the class I PI3K inhibition
Robertson et al., J Immunol 2005
:
We demonstrate that
PI3K is
required for TCR stimulated
ERK activation in CTL, which we have shown previously to be required for CTL degranulation ... These studies demonstrate that
PI3K regulates
ERK activity leading to CTL degranulation, and identify paxillin as a target of ERK downstream of the TCR
David et al., J Immunol 2005
:
In that pharmacological inhibitors of
PI3K inhibited LPS induced activation of p21Ras, but not activation of
ERK , we concluded that LPS induced activation of ERK occurs through a pathway that is not dependent on the activation of p21Ras ... In that pharmacological inhibitors of
PI3K inhibited LPS induced activation of
p21Ras , but not activation of ERK, we concluded that LPS induced activation of ERK occurs through a pathway that is not dependent on the activation of p21Ras
Yoo et al., J Immunol 2005
:
Instead,
IL-18 activated the
PI3K/Akt and MEK/ERK1/2 pathways
Kumar et al., Mol Cell Biol 2006
(Cell Transformation, Neoplastic) :
In addition, we show that Galpha12QL stimulates the phosphorylation of forkhead transcription factor
FKHRL1 via AKT in a PDGFRalpha- and
PI3K dependent manner ... Since AKT promotes cell growth by blocking the transcription of antiproliferative genes through the inhibitory phosphorylation of forkhead transcription factors, our results describe for the first time a PDGFRalpha dependent signaling pathway involving
PI3K-AKT-FKHRL1 ,
regulated by
Galpha12QL in promoting cell growth
Dai et al., Mol Cell Biol 2006
:
Interestingly, PLCgamma2 deficiency had no effect on
BCR mediated
PI3K activation, whereas PI3K deficiency only partially blocked activation of PLCgamma2 ... Interestingly, PLCgamma2 deficiency had no effect on BCR mediated PI3K activation, whereas
PI3K deficiency only partially
blocked activation of
PLCgamma2
Yang et al., Clin Exp Immunol 2006
(MAP Kinase Signaling System...) :
The
enhancement of
IL-12 levels by inhibition of
PI 3-K and ERK 1/2 was not reversed by neutralization of TNF-alpha or addition of rhTNF-alpha, suggesting that the negative regulation of IL-12 is not mediated by concomitant TNF-alpha suppression
Bonaccorsi et al., Mol Cell Endocrinol 2006
(Neoplasm Invasiveness...) :
EGF stimulated
PI3K activity, a key signalling pathway for invasion of these cells, was decreased in PC3-AR cells and further reduced by treatment with R1881
Vigorito et al., Cell Signal 2006
:
Synergistic activation of PKD by the B cell antigen receptor and
CD19 requires
PI3K , Vav1 and PLCgamma ... Synergistic activation of
PKD by the B cell antigen receptor and CD19
requires PI3K , Vav1 and PLCgamma ... We found that PKD activation upon BCR engagement or coligation of the
BCR with CD19 is entirely
dependent on
PI3K and PLCgamma but differ in the requirement for Vav proteins ... We found that
PKD activation upon BCR engagement or coligation of the BCR with CD19 is entirely
dependent on
PI3K and PLCgamma but differ in the requirement for Vav proteins ... These findings show that Vav proteins and
PI3K regulation of PLCgamma
contributes to the activation of
PKD in response to BCR and or CD19 cross linking ... These findings show that
Vav proteins and
PI3K regulation of PLCgamma contributes to the activation of PKD in response to BCR and or CD19 cross linking
Namkoong et al., Exp Mol Med 2005
:
These results clearly show that PGE2 increased angiogenesis by activating the NO/cGMP signaling pathway through
PKA/PI3K/Akt dependent increase in
eNOS activity
Gelling et al., Cell Metab 2006
(Diabetes Mellitus, Experimental) :
Conversely, increased
PI3K signaling
induced by hypothalamic overexpression of either IRS-2 or
protein kinase B ( PKB, a key downstream mediator of PI3K action ) enhanced the glycemic response to insulin by approximately 2-fold in STZ-DM rats ... Conversely, increased
PI3K signaling
induced by hypothalamic overexpression of either
IRS-2 or protein kinase B ( PKB, a key downstream mediator of PI3K action ) enhanced the glycemic response to insulin by approximately 2-fold in STZ-DM rats
Takasawa et al., FEBS Lett 2006
:
The Reg/ATF-2 induced
cyclin D1 promoter activation was
attenuated by
PI(3)K inhibitors such as LY294002 and wortmannin
Liu et al., Eur J Cell Biol 2006
:
PI3K is
required for insulin stimulated but not EGF stimulated
ERK1/2 activation ... However, the
role of
PI3K in
ERK-1/2 activation induced by tyrosine kinase receptors was not fully understood ... However, the
role of
PI3K in
ERK-1/2 activation induced by tyrosine kinase receptors was not fully understood ... Here, we report that two structurally distinct
PI3K inhibitors, wortmannin and LY294002,
inhibited insulin induced activation of
ERK1/2 but had no effect on EGF induced activation of ERK1/2 in hepatocellular carcinoma BEL-7402 and SMMC-7721 cells, breast cancer MCF-7 cells, and prostate cancer LNCaP cells ... These results indicate that
PI3K plays different roles in the activation of Ras/ERK1/2 signaling by insulin and
EGF , and that insulin stimulated, but not EGF stimulated, ERK1/2 and Akt signalings diverge at PI3K ... These results indicate that
PI3K plays different roles in the activation of
Ras/ERK1/2 signaling by insulin and EGF, and that insulin stimulated, but not EGF stimulated, ERK1/2 and Akt signalings diverge at PI3K ... These results indicate that
PI3K plays different roles in the activation of Ras/ERK1/2 signaling by
insulin and EGF, and that insulin stimulated, but not EGF stimulated, ERK1/2 and Akt signalings diverge at PI3K
Wu et al., Kidney Int 2006
:
P-PI3-K blockade downregulated the
CTGF stimulated expression of
P-PI3-K , P-Akt, and NF-kappaB but not P-p42/44 MAPK, and partially decreased the release of the above chemokines ... LXA ( 4 ) dose-dependently inhibited the
CTGF stimulated mRNA expression and protein release of the above chemokines, and the expression of P-p42/44MAPK,
P-PI3-K , P-Akt, and NF-kappaB
Qiao et al., Cancer Lett 2006
(Neuroblastoma) :
GRP induced activation of
PI3-K , resulting in neuroblastoma cell growth promotion, is
potentiated by down-regulation of
TGF-beta/Smad signaling ...
GRP induced activation of
PI3-K , resulting in neuroblastoma cell growth promotion, is potentiated by down-regulation of TGF-beta/Smad signaling
Nevzorova et al., Br J Pharmacol 2006
:
The
PI3K inhibitor, LY294002 ( 1 microM ),
inhibited insulin- ( 174.9+/-5.9 to 142.7+/-2.7 % ) and zinterol- ( 166.9+/-7.6 to 141.1+/-8.1 % ) but not 8 Br-cAMP stimulated GU
Reagan-Shaw et al., Cancer Res 2006
(Breast Neoplasms...) :
Further, our data showed that
PI3K knockdown
resulted in a significant activation of
FoxO ; interestingly, a simultaneous knockdown of FoxO1a rescued the cells from apoptosis
Wang et al., J Nutr 2006
:
Unlike insulin, the
PI3-K inhibitor wortmannin did not reverse GE antilipolysis, and GE did not
affect phosphorylation of
protein kinase B (PKB)
van Duijn et al., Prostate 2006
(Prostatic Neoplasms) :
PI3K/Akt signaling
regulates p27 ( kip1 ) expression via Skp2 in PC3 and DU145 prostate cancer cells, but is not a major factor in p27 ( kip1 ) regulation in LNCaP and PC346 cells ... We compared the
involvement of
PI3K/PTEN/Akt signaling in the regulation of the cell-cycle regulator
p27 ( kip1 ) and investigated the mechanism of PI3K/PTEN/Akt modulation of p27 ( kip1 ) in the prostate cancer cell lines LNCaP, PC346, PC3, and DU145 ... In PC3 and DU145 cells, Skp2 is the main determinant in the
PI3K/Akt dependent regulation of
p27 ( kip1 )
Brando-Lima et al., Int Immunopharmacol 2006
:
This effect is inhibited by D-galactose and PI3K inhibitors, and is accompanied by an increase in IL-2 receptor expression and by a
PI3K dependent
IL-2 gene expression and IL-2 protein synthesis
Caparrós et al., Blood 2006
(Calcium Signaling...) :
DC-SIGN ligation on dendritic cells
results in ERK and
PI3K activation and modulates cytokine production
Kuo et al., J Cell Physiol 2006
(MAP Kinase Signaling System) :
Our data showed that extracellular signal regulated kinase ( ERK ) pathway inhibitor PD98059, but not the c-Jun N-terminal kinase (JNK) inhibitor SP600125, p38 kinase inhibitor SB203580, and
PI3K inhibitor wortmannin,
attenuated Src induced
MMP-2 promoter activity
Shin et al., EMBO J 2006
:
Inhibition of
PI3K signaling
restored the downregulation of
SRF and Egr-1 expression caused by oncogenic Ras ... Inhibition of
PI3K signaling
restored the downregulation of SRF and
Egr-1 expression caused by oncogenic Ras
Takahashi et al., EMBO J 2006
:
Depletion of
NHERF2 by small interfering RNA similarly
increased PI3K signaling
Yin et al., J Mol Cell Cardiol 2006
:
Isoproterenol induced secretion of
IL-6 was mainly mediated by Gs-AC-cAMP signaling cascade and could be negatively
regulated by Gi and
PI3K
Huang et al., Biochem J 2006
:
Somatostatin acting via G ( i ) 1-coupled sstr3 receptor, DPDPE ( [ D-Pen2,D-Pen5 ] enkephalin ; where Pen is penicillamine ) acting via G ( i ) 2-coupled delta-opioid receptors, and cyclopentyl adenosine acting via G ( i ) 3-coupled
adenosine A1 receptors preferentially
activated PI3K ( phosphoinositide 3-kinase ) and ILK ( integrin linked kinase ), whereas ACh ( acetylcholine ) acting via G ( i ) 3-coupled M2 receptors preferentially activated PI3K, Cdc42 ( cell division cycle 42 ) /Rac1, PAK1 ( p21 activated kinase 1 ) and p38 MAPK ( mitogen activated protein kinase )
Kristensen et al., APMIS 2005
:
In addition,
gp130 activation
leads to both
PI3K and Src activation
Yamaguchi et al., Cancer Res 2006
(Colorectal Neoplasms) :
On the other hand,
ATF3 expression was not
affected by another
PI3K inhibitor, wortmannin, as well as phosphatase and tensin homologue or dominant negative Akt overexpression ... On the other hand,
ATF3 expression was not
affected by another
PI3K inhibitor, wortmannin, as well as phosphatase and tensin homologue or dominant negative Akt overexpression
Zhang et al., J Biol Chem 2006
:
In this study we investigated a potential link between the
PI3K-Akt pathway and the cigarette smoke ( CS ) -stimulated epidermal growth factor receptor mediated
FRA-1 induction in non-oncogenic HBE cells ... In this study we investigated a potential link between the
PI3K-Akt pathway and the cigarette smoke ( CS ) -stimulated
epidermal growth factor receptor mediated FRA-1
induction in non-oncogenic HBE cells ... We found that the
PI3K through p21 activated kinase 1
regulates FRA-1 proto-oncogene induction by CS and the subsequent activation of the Elk1 and cAMP-response element binding protein transcription factors that are bound to the promoter in HBE cells ... We found that the
PI3K through p21 activated kinase 1
regulates FRA-1 proto-oncogene induction by CS and the subsequent activation of the
Elk1 and cAMP-response element binding protein transcription factors that are bound to the promoter in HBE cells
Chadborn et al., J Cell Sci 2006
:
Sema3A suppresses
PI3K signalling concomitant with the activation of GSK-3, which depends on the phosphatase activity of PTEN
Hsieh et al., J Cell Physiol 2006
:
Moreover, S1P stimulated activation of NF-kappaB promoter activity was blocked by phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 and helenalin, but not by U0126, suggesting that
involvement of
PI3K/Akt in the activation of
NF-kappaB
Al-Rasheed et al., J Am Soc Nephrol 2006
(Diabetic Nephropathies) :
Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen activated protein kinase
mediated C-peptide and
insulin activation of NF-kappaB ...
Phosphatidylinositol 3-kinase but not extracellular signal regulated mitogen activated protein kinase
mediated C-peptide and insulin activation of
NF-kappaB
Simó et al., Cereb Cortex 2007
(MAP Kinase Signaling System) :
Our findings demonstrate that Reelin triggers
ERK signaling in an SFK/mDab1- and
PI3K dependent manner and that ERK activation is required for Reelin dependent transcriptional activation and the detachment of neurons migrating from the SVZ
Takai et al., J Cell Biochem 2006
:
These results suggest that
PI3K/Akt plays a part in the sphingosine 1-phosphate stimulated induction of
HSP27 , maybe independently of p38 MAP kinase, in osteoblasts
Sun et al., Toxicol Appl Pharmacol 2006
:
Serine 1179 phosphorylation of endothelial
nitric oxide synthase caused by 2,4,6-trinitrotoluene through
PI3K/Akt signaling in endothelial cells
Tal-Or et al., J Cell Biochem 2006
:
The
PI3K inhibitor LY294002 and the MEK inhibitor PD98059
caused a partial inhibition of the Ras induced
ErbB4 receptor phosphorylation
Kokkinakis et al., Cancer Lett 2006
(Neoplasms) :
The response of tumors to MET-stress depends on their mutational status, however, it always involves inhibition of CDK1 and in most cases the upregulation of p21, p27, GADDs and 14-3-3sigma in
response to upregulation of TGF-beta, IRF-1, TNF-alpha, Rb and/or
MDA-7 and the downregulation of
PI3K , RAS and NF-kappaB ... The response of tumors to MET-stress depends on their mutational status, however, it always involves inhibition of CDK1 and in most cases the upregulation of p21, p27, GADDs and 14-3-3sigma in
response to upregulation of TGF-beta, IRF-1,
TNF-alpha , Rb and/or MDA-7 and the downregulation of
PI3K , RAS and NF-kappaB ... The response of tumors to MET-stress depends on their mutational status, however, it always involves inhibition of CDK1 and in most cases the upregulation of p21, p27, GADDs and 14-3-3sigma in
response to upregulation of TGF-beta,
IRF-1 , TNF-alpha, Rb and/or MDA-7 and the downregulation of
PI3K , RAS and NF-kappaB
Friedrichsen et al., J Endocrinol 2006
:
We conclude that incretin induced beta-cell replication is dependent on cAMP/PKA, p42 MAPK and
PI3K activities, which may
involve transcriptional induction of
cyclin D1
Kondo et al., Oral Oncol 2006
(Carcinoma, Squamous Cell...) :
We found that both
PI 3-K inhibitors, wortmannin and LY294002, markedly
suppressed the phosphorylation of
Akt and accelerated Fas mediated apoptosis in OSCC cells ... Although
PI 3-K inhibitors did not
affect the
Fas expression of OSCC cells, cellular FLICE-inhibitory protein ( c-FLIP ) levels were markedly reduced by PI 3-K inhibitor treatment
Frey et al., J Biol Chem 2006
:
Phosphatidylinositol 3-kinase gamma signaling through protein kinase Czeta
induces NADPH oxidase mediated oxidant generation and
NF-kappaB activation in endothelial cells
Lee et al., Mol Pharmacol 2006
(Asthma...) :
This study aimed to determine the
effect of
PI3K inhibitors and PTEN on
VEGF expression in allergen induced airway inflammation
Maurer et al., Mol Cell 2006
:
S159 phosphorylation of MCL-1 was induced by
IL-3 withdrawal or
PI3K inhibition and prevented by AKT or inhibition of GSK-3, and it led to increased ubiquitinylation and degradation of MCL-1 ... S159 phosphorylation of
MCL-1 was
induced by IL-3 withdrawal or
PI3K inhibition and prevented by AKT or inhibition of GSK-3, and it led to increased ubiquitinylation and degradation of MCL-1
Ganesan et al., Blood 2006
(Inflammation) :
Interestingly, whereas
IL-6 production
required activation of both
PI3K and Ras/Erk pathways, IL-1beta production was dependent only on Ras/Erk activation, suggesting that SHIP may also regulate the Ras/Erk pathway in macrophages ... Inhibition of Ras/Erk or
PI3K suppressed the enhanced production of
IL-6 in SHIP-deficient macrophages
Fritz et al., J Immunol 2006
:
Induction of
VCAM-1 by OSM was
diminished by pharmacological inhibitors of
PI3K ( LY294002 ) but not inhibitors of ERK1/2 ( PD98059 ) or p38 MAPK ( SB203580 )
Hennig et al., J Nutr Biochem 2006
(Inflammation) :
Furthermore, inhibition of ERK activity by PD98059 and
PI3K/Akt activity by LY294002 or wortmannin significantly
reduced the LA-induced activation of
nuclear factor kappa B (NF-kappaB)
Guo et al., J Steroid Biochem Mol Biol 2006
(Endometrial Neoplasms) :
PI3K inhibitor, LY294002, stopped the activating Akt in a dose dependent manner and 50 microM LY294002 completely
blocked the activation of
Akt induced by E2
Bonnans et al., J Exp Med 2006
:
In human neutrophils,
leukotriene B4 (LTB4) triggered rapid decreases in PSDP and reciprocal increases in
PI3K activity
Sanchez-Lockhart et al., J Immunol 2006
:
CD28 signaling through
PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC, activation of NF-kappaB, and
induction of
IL-2 transcription ... CD28 signaling through
PI3K results in the recruitment of protein kinase C (PKC)theta to the cSMAC,
activation of
NF-kappaB , and induction of IL-2 transcription
Yu et al., Acta Biochim Biophys Sin (Shanghai) 2006
:
Insulin also strongly
activated both
PI3K and the downstream effector Akt
Bailey et al., J Am Soc Nephrol 2006
(Kidney Failure, Chronic...) :
The low IRS-1 associated
PI3-K activity in muscle was not
due to a decrease in
IRS-1 protein, but there was a higher amount of the PI3-K p85 subunit protein without a concomitant increase in the p110 catalytic subunit, offering a potential explanation for the lower IRS-1 associated PI3-K activity
Stojanovic et al., J Biol Chem 2006
:
Here we show that
PI3K mediated
Akt activation plays an important role in agonist stimulated platelet NO synthesis and cGMP elevation
Yun et al., Pharmacol Res 2006
:
Taken together, these experiments show that the enhanced phosphorylation of
Akt/PKB by OA is
dependent on
PI3K and suggest that this signaling event may be important for the regulation of OA-induced VSMC proliferation ... Taken together, these experiments show that the enhanced phosphorylation of
Akt/PKB by OA is
dependent on
PI3K and suggest that this signaling event may be important for the regulation of OA-induced VSMC proliferation
Yadav et al., J Immunol 2006
(Mycobacterium Infections) :
This cPKC and
PI3K activation was
dependent on
SPK and PI-PLC ... This cPKC and
PI3K activation was
dependent on SPK and
PI-PLC
Martínez-Salgado et al., Exp Cell Res 2006
:
PI3K-Akt pathway activation may be
involved in the increase in
ECM synthesis observed in the absence of H- and N-Ras
Rodriguez-Viciana et al., Mol Cell 2006
(Carcinoma...) :
Furthermore, in tumor cells with Ras gene mutations, inhibition of
Shoc2 expression
inhibits MAPK, but not
PI3K activity
Barbee et al., Int Immunol 2006
(Calcium Signaling) :
Since
PI3K can
affect activation of
Btk , which in turn potentiates calcium fluxes, during B cell development, our results suggest that PI3K could play a role in the regulation of Itk kinases in T cells, and that both cell types share a common signaling network to modulate calcium responses downstream of their antigen receptor
Choi et al., Int Immunopharmacol 2006
:
However, many aspects of the
PI3K negative
regulation of
NF-kappaB activation remain to be clarified ... The present study was conducted to shed light on cell-type specificity, stimulus specificity, and upstream mechanisms of the enhanced
NF-kappaB activation by
PI3K inhibitors
Rhee et al., J Biol Chem 2006
:
We demonstrate that silencing TLR5 expression in nontransformed human colonic epithelial cells blocks flagellin induced PI3K activation, indicating specific
activation of
PI3K by
flagellin/TLR5 engagement ... Indeed, we demonstrate that the adaptor molecule MyD88 associates with
TLR5 and silencing MyD88 expression
blocks PI3K activation by disrupting the association between TLR5 and p85 ... Indeed, we demonstrate that the adaptor molecule
MyD88 associates with TLR5 and silencing MyD88 expression
blocks PI3K activation by disrupting the association between TLR5 and p85 ... Additionally, we determine that blocking
PI3K activation
reduces interleukin-8 production induced by flagellin in human colonic epithelial cells
Akiyama et al., FEBS J 2006
:
The
PI3K inhibitor, LY294002,
blocked cartducin stimulated
Akt phosphorylation and a decrease in cartducin induced DNA synthesis in N1511 cells was also observed
Wood et al., J Cell Biol 2006
:
In contrast, using both laser ablation and a novel wounding assay that allows localized treatment with inhibitory drugs, we show that
PI3K is essential for hemocyte chemotaxis toward wounds and that Pvf signals and
PDGF/VEGF receptor expression are not
required for this rapid chemotactic response
Bertram et al., Cancer Res 2006
(Prostatic Neoplasms) :
Here we report that apoptotic cell death of PTEN-deficient LNCaP and
PC3 prostate cancer cells
induced by the
PI3K inhibitor LY294002 can be abrogated by disrupting Fas/Fas ligand (FasL) interactions with recombinant Fas : Fc fusion protein or FasL neutralizing antibody ( Nok-1 ), or by expressing dominant negative Fas associated death domain
Kuo et al., J Immunol 2006
:
Our results reveal that class III PI3K specifically regulates CpG oligodeoxynucleotide ( ODN ) -induced cytokine and NO production as well as NF-kappaB activation, whereas class I
PI3K regulates both CpG ODN- and LPS induced
IL-12 production and NF-kappaB activation ... Our results reveal that class III PI3K specifically regulates CpG oligodeoxynucleotide ( ODN ) -induced cytokine and NO production as well as NF-kappaB activation, whereas class I
PI3K regulates both CpG ODN- and LPS induced IL-12 production and
NF-kappaB activation ... Furthermore, experiments with MyD88 overexpressing fibroblast cells transfected with dominant negative mutants of PI3K demonstrate that class III
PI3K regulates CpG ODN mediated signaling upstream of
MyD88 , while class I PI3K regulation is downstream of MyD88
Yu et al., J Immunol 2006
:
Such effect of inhibiting PI3K with wortmannin was mimicked by the PI3K inhibitor LY294002, and, conversely, a constitutively active
PI3K prevented
p38 activation in response to flagellin
Komori et al., Clinical calcium 2006
:
Phosphoinositide 3-kinase
(PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2
upregulates PI3K subunits (
p85 and p110 beta ) and Akt ... Phosphoinositide 3-kinase
(PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2
upregulates PI3K subunits ( p85 and p110 beta ) and
Akt ... Phosphoinositide 3-kinase
(PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2
upregulates PI3K subunits ( p85 and
p110 beta ) and Akt
Slomiany et al., J Pharmacol Exp Ther 2006
(Anoxia) :
IGF-1 stimulated VEGF promoter activity was phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR ( mammalian target of rapamycin ) -dependent, whereas
VEGF secretion was only partially
reduced by inhibition of
PI3K/Akt/mTOR and HIF-1 activities
Leung et al., FEBS Lett 2006
:
Rg1 increased the phosphorylation of GR,
phosphatidylinositol-3 kinase (PI3K) , Akt/PKB and endothelial nitric oxide synthase (eNOS) leading to increase nitric oxide ( NO ) production in human umbilical vein endothelial cell
Bridle et al., J Lab Clin Med 2006
:
Both
IGF-1 and PDGF
increased ERK,
PI3-K and p70-S6-K activity ... When evaluating potential crosstalk between these signaling pathways, we observed that
PI3-K is
required for
p70-S6-K activation by IGF-1 and PDGF, and is partially responsible for PDGF induced ERK activation ... When evaluating potential crosstalk between these signaling pathways, we observed that
PI3-K is
required for p70-S6-K activation by
IGF-1 and PDGF, and is partially responsible for PDGF induced ERK activation
Abramova et al., Tsitologiia 2005
(Cell Transformation, Neoplastic) :
Inhibition of
PI3K leads to
p27 ( Kip1 ) accumulation and cell cycle arrest, consequently
Bae et al., Cancer Res 2006
(Adenocarcinoma...) :
The inhibition of
PI3K/Akt signaling also
prevented Sp1 activation
Zhan et al., Cancer Res 2006
(Breast Neoplasms...) :
The ability of heterodimers to induce invasion required the
ErbB1 kinase activity and
required activation of
PI3K , Ras/mitogen activated protein kinase, and phospholipase Cgamma1 signaling pathways
Kin et al., J Immunol 2006
:
In this study, we show that
CD86 stimulation on an activated B cell
increases the activity of
PI3K and the phosphorylation of phosphoinositide dependent kinase 1, Akt, and IkappaB kinase alphabeta
Forti et al., An Acad Bras Cienc 2006
(Adrenal Cortex Neoplasms...) :
We previously reported that this genetic lesion leads to high constitutive levels of
activation of the
c-Ki-Ras-GTP -- >
PI3K -- > Akt signaling pathway ( Forti et al. 2002 ) ... We previously reported that this genetic lesion leads to high constitutive levels of
activation of the
c-Ki-Ras-GTP -- >
PI3K -- > Akt signaling pathway ( Forti et al. 2002 )
Rosner et al., Am J Pathol 2006
(Atherosclerosis) :
IFN-gamma also stimulated Akt activity, and both Fas trafficking and
Stat1 activation were
inhibited by blocking
PI3K , Akt, or Jak-2 ... IFN-gamma also stimulated
Akt activity, and both Fas trafficking and Stat1 activation were
inhibited by blocking
PI3K , Akt, or Jak-2
Irarrazabal et al., Proc Natl Acad Sci U S A 2006
:
Inhibiting
PI3K-IA either by expressing a dominant negative of its regulatory subunit, p85, or by small interfering RNA mediated knockdown of its catalytic subunit, p110alpha,
reduces high NaCl induced increases in
TonEBP/OREBP transcriptional activity and transactivation, but not nuclear translocation of TonEBP/OREBP, or increases in its abundance ... High NaCl induced increase in
TonEBP/OREBP activity is
reduced equally by inhibition of ATM or
PI3K-IA , and the effects are not additive
Martinez et al., Diabetes 2006
:
The use of inhibitors demonstrated that glucose induced
Foxo1 phosphorylation was
dependent upon depolarization, calcium influx, and
PI3K signaling
Chen et al., Diabetes 2006
:
Antioxidant
N-acetyl-l-cysteine (NAC) prevented mercury induced insulin secretion inhibition and Akt phosphorylation but not increased
PI3K activity ... Inhibition of
PI3K/Akt activity with PI3K inhibitor or by expressing the dominant negative p85 or Akt
prevented mercury induced
insulin secretion inhibition but not ROS production ... These results indicate that both
PI3K and ROS independently regulated Akt signaling related, mercury
induced insulin secretion inhibition
Mori et al., Virus Genes 2006
(Burkitt Lymphoma) :
Akt phosphorylation and cell growth were
inhibited by
PI3-K specific inhibitor LY294002 in a dose dependent manner
Harokopakis et al., J Immunol 2006
:
A dominant negative mutant of
Rac1 also
inhibited the lipid kinase activity of
PI3K suggesting that Rac1 acts upstream of PI3K in this proadhesive pathway
Díaz-Montero et al., Eur J Cancer 2006
(Osteosarcoma) :
PI3-K/Akt mediated anoikis resistance of human osteosarcoma cells
requires Src activation ... The activity of
Akt was found to be upregulated in anoikis resistant SAOSar cells and the pharmacological inhibition of
PI3-K activity
restored sensitivity to anoikis resistant cells, reconfirming the critical role of PI3-K/Akt pathway in cell survival
Wu et al., Neurosci Lett 2006
(Brain Ischemia) :
Down-regulation of PTEN by sodium orthovanadate inhibits
ASK1 activation via
PI3-K/Akt during cerebral ischemia in rat hippocampus
Zanin-Zhorov et al., J Clin Invest 2006
:
The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2,
led to activation of PKC,
PI3K , and p38, and were further enhanced by inhibition of
ERK ... The enhancing effects of
HSP60 costimulation on Tregs involved innate signaling via TLR2,
led to activation of PKC,
PI3K , and p38, and were further enhanced by inhibition of ERK
Demirjian et al., Biochim Biophys Acta 2006
(MAP Kinase Signaling System) :
On the other hand, the
PI3-K inhibitor, LY294002, and epidermal growth factor receptor (EGFR)-specific inhibitor, AG1478, did not
suppress the release of
TNF-alpha
Tang et al., Mol Cancer Res 2006
(Breast Neoplasms...) :
Furthermore, the
PI3K-specific inhibitor LY294002
inhibited VEGF production by EMMPRIN overexpressing cells in a dose- and time dependent manner
Li et al., Cell Death Differ 2007
(Neuroblastoma) :
Previously, we found
BDNF activation of TrkB through
PI3K/Akt protects NB from etoposide/cisplatin induced cell death ... Previously, we found BDNF
activation of
TrkB through
PI3K/Akt protects NB from etoposide/cisplatin induced cell death
Xu et al., Am J Physiol Lung Cell Mol Physiol 2006
(Hyperoxia...) :
Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia induced cell death in lung epithelial cells through reduction of ROS,
activation of
ERK/MAPK , and
PI3K-Akt cell survival signaling pathways ... Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia induced cell death in lung epithelial cells through reduction of ROS,
activation of
ERK/MAPK , and
PI3K-Akt cell survival signaling pathways
Callegari et al., Int J Mol Med 2006
:
The incubation with specific inhibitors of intracellular kinases showed that
PI3K is mainly
involved in the Ox-HDL3 dependent
Cox-2 induction
Wolff et al., Comb Chem High Throughput Screen 2006
:
Upon
stimulation of the hIR with
insulin-like growth factor-1 (IGF-1) ,
PI3K was activated to phosphorylate phosphatidylinositol ( PtdIns ) -4,5-bisphosphate at the 3-position, resulting in the recruitment of AKT1-EGFP to the plasma membrane
Tessier et al., J Biol Chem 2006
:
Both a functional PX domain and
PI3K activation are
necessary for phosphorylation of
SGK3 at two regulatory sites ( Thr-320 and Ser-486 ) and subsequent induction of kinase activity
Suuronen et al., Neurochem Int 2006
(Inflammation) :
Our studies on signaling pathways revealed that
PI3K inhibitors LY294002 and Wortmannin
blocked the
TSA induced pro-inflammatory response but surprisingly did not affect the okadaic acid induced response
Sugano et al., J Neurochem 2006
:
Enhancement of
insulin induced
PI3K/Akt/GSK-3beta and ERK signaling by neuronal nicotinic receptor/PKC-alpha/ERK pathway : up-regulation of IRS-1/-2 mRNA and protein in adrenal chromaffin cells ... Thus, stimulation of nAChRs up-regulated expression of IRS-1/IRS-2 via Ca ( 2+ ) -dependent sequential activation of cPKC-alpha and ERK, and enhanced
insulin induced
PI3K/Akt/GSK-3beta and ERK signaling pathways
Rojo et al., Free Radic Biol Med 2006
:
Then, we observed with the use of a Sp1-Gal4 chimera that
PI3K regulates the transactivating capacity of
Sp1
Hanai et al., J Cell Biochem 2006
:
Taken together, these results strongly suggest that
PI3K/Akt negatively
regulates the PDGF-BB stimulated
IL-6 synthesis in osteoblasts
Yang et al., Cell Microbiol 2006
(MAP Kinase Signaling System) :
Furthermore, the inhibition of
PI3K-Akt , but not ERK 1/2 pathway, attenuated M. tbc
induced S6K1 phosphorylation, whereas PI3K inhibition enhanced p38 phosphorylation and apoptosis signal regulating kinase 1 activity during exposure to M. tbc ... Furthermore, the inhibition of PI3K-Akt, but not ERK 1/2 pathway, attenuated M. tbc induced S6K1 phosphorylation, whereas
PI3K inhibition
enhanced p38 phosphorylation and apoptosis signal regulating kinase 1 activity during exposure to M. tbc ... Furthermore, the inhibition of
PI3K-Akt , but not ERK 1/2 pathway, attenuated M. tbc
induced S6K1 phosphorylation, whereas PI3K inhibition enhanced p38 phosphorylation and
apoptosis signal regulating kinase 1 activity during exposure to M. tbc
Rodríguez-Barbero et al., Kidney Int 2006
:
Extracellular signal regulated kinase ( ERK ) 1/2,
p38 MAPK, and
PI3K pathway
inhibition blunted TGF-beta1 induced COX-2 overexpression
Saegusa et al., Mol Immunol 2007
:
The enhancement
effect of
PI3K inhibitors on IL-12
p70 production almost completely disappeared by the treatment with anti-IL-10 mAb ... The enhancement
effect of
PI3K inhibitors on
IL-12 p70 production almost completely disappeared by the treatment with anti-IL-10 mAb ...
PI3K inhibitors
suppressed the activation of
extracellular regulated kinase (ERK) , a member of the mitogen activated protein kinases, by CpG-ODN ... A specific ERK inhibitor, U0126, as well as
PI3K inhibitors, differentially
regulated IL-10 and IL-12
p70 productions ... A specific ERK inhibitor, U0126, as well as
PI3K inhibitors, differentially
regulated IL-10 and IL-12 p70 productions ... These results suggest that
PI3K positively and negatively
regulates the production of CpG-ODN induced IL-10 and IL-12
p70 , respectively, and negatively regulates IL-12 p70 production in macrophages through ERK mediated IL-10 induction ... These results suggest that
PI3K positively and negatively
regulates the production of CpG-ODN induced
IL-10 and IL-12 p70, respectively, and negatively regulates IL-12 p70 production in macrophages through ERK mediated IL-10 induction ... These results suggest that
PI3K positively and negatively regulates the production of CpG-ODN induced IL-10 and IL-12 p70, respectively, and negatively
regulates IL-12 p70 production in macrophages through ERK mediated IL-10 induction
Brunt et al., Arterioscler Thromb Vasc Biol 2006
:
Inhibition of
PI3K-Akt reduced induction of
HO-1 protein expression by H2O2 and blocked its anti-apoptotic effects
Redondo-Muñoz et al., Blood 2006
(Leukemia, B-Cell...) :
This effect was mediated by
alpha4beta1 integrin and
required PI3-K/Akt signaling ... Moreover, B-CLL cells formed podosomes upon adhesion to FN-H89, VCAM-1, or fibronectin
; MMP-9 localized to podosomes in a
PI3-K dependent manner and degraded a fibronectin/gelatin matrix ... Moreover, B-CLL cells formed podosomes upon adhesion to FN-H89, VCAM-1, or fibronectin ;
MMP-9 localized to podosomes in a
PI3-K dependent manner and degraded a fibronectin/gelatin matrix
Parsa et al., PLoS Pathog 2006
(Gram-Negative Bacterial Infections) :
Inhibition of
PI3K/Akt resulted in suppression of F. novicida
induced cytokine production through the inhibition of
NFkappaB
Cao et al., Biochem J 2006
:
MEK [ MAPK ( mitogen activated protein kinase ) /ERK ( extracellular-signal regulated kinase ) kinase ] /ERK inhibitor U0126 and
PI3K ( phosphoinositide 3-kinase ) inhibitor LY294002 also
inhibited EGF induced
AQP3 expression and cell migration
Risinger et al., J Biol Chem 2006
:
Both PDGF-BB and
IGF-I activated
PI3K/Akt to similar degrees ; however, only PDGF-BB concomitantly stimulated an inhibitory signaling pathway that antagonized the effects of Akt but did not alter the extent or duration of Akt activation ... Both
PDGF-BB and IGF-I
activated PI3K/Akt to similar degrees ; however, only PDGF-BB concomitantly stimulated an inhibitory signaling pathway that antagonized the effects of Akt but did not alter the extent or duration of Akt activation
Massheimer et al., Steroids 2006
:
However,
PLC activation was
dependent on
PI3K since presence of LY 294002 in the incubation medium abolished estrone induced DAG increment
Moeller et al., Nuclear receptor signaling 2006
:
We recently described an extranuclear mechanism of TH action that consists of the association of TH-liganded
TRbeta with p85alpha [ regulatory subunit of phosphatidylinositol 3-kinase (PI3K) ] in the cytosol and subsequent
activation of the
PI3K , generating phosphatidylinositol 3,4,5-triphosphate [ PtdIns ( 3,4,5 ) P3 ]
Kim et al., Biochem Biophys Res Commun 2006
:
Involvement of HDAC1 and the
PI3K/PKC signaling pathways in NF-kappaB activation by the
HDAC inhibitor apicidin ...
Involvement of HDAC1 and the
PI3K/PKC signaling pathways in
NF-kappaB activation by the HDAC inhibitor apicidin
Furuya et al., Autophagy 2005
:
Furthermore, they suggest a connection between Beclin 1-associated Class III
PI3K/Vps34 dependent autophagy, but not
VPS , function and the mechanism of Beclin 1 tumor suppressor action in human breast cancer cells
Lee et al., Am J Physiol Heart Circ Physiol 2006
(Inflammation...) :
The
PI3K inhibitor and a dominant negative mutant of Akt
suppressed Akt and eNOS phosphorylation and NO production ... The
PI3K inhibitor and a dominant negative mutant of Akt
suppressed Akt and
eNOS phosphorylation and NO production
Wang et al., Biochemistry 2006
:
Here we demonstrate that
PAR-2 can
increase PI3K activity through a Galphaq/Ca ( 2+ ) -dependent pathway involving PYK2 and a Src-family kinase, while inhibiting
PI3K activity through a beta-arrestin dependent mechanism, and that beta-arrestin-1 can directly associate with and inhibit the catalytic activity of p110alpha ... Here we demonstrate that PAR-2 can increase
PI3K activity through a Galphaq/Ca ( 2+ ) -dependent pathway involving PYK2 and a Src-family kinase, while inhibiting PI3K activity through a beta-arrestin dependent mechanism, and that beta-arrestin-1 can directly associate with and
inhibit the catalytic activity of
p110alpha
Wendel et al., Cancer Res 2006
(Lymphoma) :
We now show that reduced dosage of
PTEN , a negative
regulator of
PI(3)K signaling, is sufficient to activate Akt, but has only a modest effect on lymphomagenesis in the same model
Shen et al., J Am Soc Nephrol 2006
:
Inhibition of
PI3K with LY294002
prevented EGF induced increases in
GAPDH and pax2 abundance in NRK-52E renal tubular cells
Benson et al., Eur J Immunol 2006
:
Rapid CD40 rescue did not require
NF-kappaB activation and was independent of de novo protein synthesis, but was
dependent upon active
PI3 K
Bishop et al., J Endocrinol 2006
(Lymphoma) :
In summary, PRL stimulated phosphorylation of
mTOR is
mediated by
PI3K
Ilan et al., Int J Biochem Cell Biol 2006
(Disease Progression...) :
Heparanase enhances Akt signaling and
stimulates PI3K- and p38 dependent endothelial cell migration and invasion
Nakamae-Akahori et al., Immunology 2006
:
These findings are consistent with the fact that
G-CSF selectively
activates MEK/ERK and
PI3K , but not p38, in neutrophils
Engelman et al., J Clin Invest 2006
(Lung Neoplasms) :
Moreover, continued
activation of
PI3K signaling by the
PIK3CA oncogenic mutant, p110alpha E545K, was sufficient to abrogate gefitinib induced apoptosis
Chesler et al., Cancer Res 2006
(Neuroblastoma) :
Consistent with these observations,
PI3K inhibition in MYCN amplified human neuroblastoma cell lines
resulted in decreased levels of
Mycn protein without affecting levels of MYCN mRNA and caused decreased proliferation and increased apoptosis
Bousquet et al., EMBO J 2006
(Neoplasms, Experimental) :
Somatostatin , acting through sst2,
inhibits PI3K activity by disrupting a pre existing complex comprising the sst2 receptor and the p85 PI3K regulatory subunit ... Mutating sst2-Y71 disabled sst2 to interact with p85 and
somatostatin to
inhibit PI3K , consequently abrogating sst2 's ability to suppress cell survival and tumor growth ... Mutating sst2-Y71 disabled sst2 to interact with
p85 and somatostatin to
inhibit PI3K , consequently abrogating sst2 's ability to suppress cell survival and tumor growth
Bussolati et al., J Mol Med (Berl) 2006
(Carcinoma, Renal Cell...) :
As TEC were shown to display a basal upregulation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, we evaluated the possible regulation of TSP-1 by this pathway by using LY294002 and wortmannin, the
PI3K inhibitors, and rapamycin, the
mammalian target of rapamycin (mTOR) inhibitor
Chiang et al., Oncol Res 2005
(Carcinoma, Hepatocellular) :
FAS expression in HepG2 cells was strongly
inhibited by
PI3K inhibitor LY294002 and JNK inhibitor II and slightly inhibited by p38 inhibitor SB203580 and MEK inhibitor PD98059, separately
Hwang et al., Int J Hematol 2006
:
IFN-gamma did not enhance
SDF-1 induced activation of
PI3K/Akt or up-regulate the expression of CXCR4 or its function in bone marrow CD34+ cells ...
IFN-gamma did not
enhance SDF-1 induced activation of
PI3K/Akt or up-regulate the expression of CXCR4 or its function in bone marrow CD34+ cells
Jang et al., Cell Immunol 2006
:
The IL-4 induced
ANT3 expression is
dependent on tyrosine kinase, NF-kappaB,
PI3K/Akt , and Erk pathways
Villarreal et al., Mol Cell Biochem 2006
:
These results suggest that Ins and Ang II modulate
IRS-4 tyr-phosphorylation in a
PI3K dependent manner
Gouëffic et al., Cardiovasc Res 2006
:
Hyaluronan induces vascular smooth muscle cell migration through RHAMM mediated
PI3K dependent
Rac activation ... HA-induced migration depends exclusively on RHAMM mediated
PI3K dependent
Rac activation
Romano et al., Endocrinology 2006
:
Either specific pharmacological
PI3K and Akt inhibitors ( LY294002, Akt I, and phosphoinositide analog-6 ) or Akt dominant negative mutant ( K179M )
enhanced ERK-1/2 phosphorylation in unstimulated GH4C1 cells ... Either specific pharmacological
PI3K and Akt inhibitors ( LY294002, Akt I, and phosphoinositide analog-6 ) or Akt dominant negative mutant ( K179M )
enhanced ERK-1/2 phosphorylation in unstimulated GH4C1 cells ... Under the same conditions,
PI3K and Akt inhibition also both
increased Raf-1 kinase activity and the levels of GTP bound ( active form ) monomeric G protein
Rap1 , which suggests that a down-regulation of the ERK-1/2 cascade is induced by the PI3K/Akt signaling pathway in unstimulated cells ... Under the same conditions,
PI3K and Akt inhibition also both
increased Raf-1 kinase activity and the levels of GTP bound ( active form ) monomeric G protein Rap1, which suggests that a down-regulation of the ERK-1/2 cascade is induced by the PI3K/Akt signaling pathway in unstimulated cells ... Although the PRL promoter was not affected by either PI3K/Akt inhibition or activation,
PRL release increased in
response to the pharmacological
PI3K/Akt inhibitors in unstimulated GH4C1 and rat pituitary primary cells
Yang et al., BMC cell biology 2006
:
We found, however, that neither
PI3K , AKT, GSK3, nor proliferative signaling activity in general is
responsible for the S phase decline in
cyclin D1 levels
Miki et al., Basic Res Cardiol 2007
(MAP Kinase Signaling System...) :
EPO induced
PI3K dependent phosphorylation of
Akt in Sham but not in post-MI. EPO increased phosphorylation levels of ERK1/2 both in Sham and post-MI, but this phosphorylation was diminished by a PI3K inhibitor in Sham but not in post-MI
Uddin et al., Blood 2006
(Lymphoma, B-Cell...) :
AKT was phosphorylated in 5 of 5 DLBCL cell lines and inhibition of
PI3K caused dephosphorylation/inactivation of constitutively active AKT, FOXO transcription factor, and GSK3 in LY-sensitive cell lines
Pan et al., Biochem Pharmacol 2006
(Cocarcinogenesis...) :
We found that acacetin also inhibited
LPS induced
activation of
PI3K/Akt and p44/42, but not p38 MAPK ... Taken together, these results show that acacetin down
regulates inflammatory
iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation
PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation associated tumorigenesis ... Taken together, these results show that acacetin down
regulates inflammatory iNOS and
COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation
PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation associated tumorigenesis
Sun et al., Cytokine 2006
:
Furthermore, both the PI3K inhibitor LY294002 and the dominant negative AKT ( DN-AKT ) abolished the inhibitory effects of insulin, demonstrating that the inhibition of
Smad2 activation by insulin was
PI3K/AKT dependent
Zhang et al., Biochem Pharmacol 2007
(Prostatic Neoplasms) :
In PC-3 cells, CMEP has been found to inhibit only
AKT activation at both normal and serum-starvation conditions, not to
inhibit PI3K , PDK1, or MAPK
Hwang et al., Carcinogenesis 2007
:
Taken together, 9Z,11E-CLA
inhibits NF-kappaB driven-COX-2 expression by blocking the IKK and
PI3K-Akt signaling in TPA treated hairless mouse skin in vivo, which may account for its previously reported anti-tumor promoting effects ... Taken together, 9Z,11E-CLA
inhibits NF-kappaB
driven-COX-2 expression by blocking the IKK and
PI3K-Akt signaling in TPA treated hairless mouse skin in vivo, which may account for its previously reported anti-tumor promoting effects
Leibowitz-Amit et al., Cancer Res 2006
(Breast Neoplasms) :
In contrast, the level of phosphatidylinositol 3-kinase (PI3K) increases following Mimp induction and the level of phosphorylated
PI3K in
response to
HGF/SF is unaffected by the exogenous induction of Mimp
He et al., J Immunol 2006
:
Expression of
IL-12p40 required activation of the p38 MAPK and
PI3K ... Expression of
IL-12p40 required activation of the p38 MAPK and
PI3K
Xuan Nguyen et al., Biochem Biophys Res Commun 2006
(Prostatic Neoplasms) :
Employing the PI3K inhibitor and a variety of mutants PI3K, we showed that nuclear translocation of
Akt was
mediated by activation of
PI3K , and Akt phosphorylation status in the nucleus required PI3K activity ... Thus the activity of
PI3K might
contribute to the nuclear translocation of
Akt , and that Akt phosphorylation is essential for its nuclear retention under NGF stimulation conditions
Punn et al., Mol Endocrinol 2006
:
UCN I effect on
p38 MAPK phosphorylation was more transient, returned to basal within 40 min and was
dependent on epidermoid growth factor receptor transactivation, but not
PI3-K/Akt activation ... UCN I effect on p38
MAPK phosphorylation was more transient, returned to basal within 40 min and was
dependent on epidermoid growth factor receptor transactivation, but not
PI3-K/Akt activation
Vlotides et al., Mol Endocrinol 2006
(Pituitary Neoplasms) :
Phosphatidylinositol 3 kinase , protein kinase C, and MAPK, but not c-Jun N-terminal kinase and Janus activating kinase signaling
regulated EGF induced Pttg1, as well as
proliferating cell nuclear antigen mRNA expression and entry into S-phase ...
Phosphatidylinositol 3 kinase , protein kinase C, and MAPK, but not c-Jun N-terminal kinase and Janus activating kinase signaling
regulated EGF induced
Pttg1 , as well as proliferating cell nuclear antigen mRNA expression and entry into S-phase
Li et al., Free Radic Biol Med 2006
:
Peroxynitrite induces HO-1 expression via
PI3K/Akt dependent
activation of
NF-E2 related factor 2 in PC12 cells
Hale et al., Proc Natl Acad Sci U S A 2006
:
Additionally, it was found that expression of
NS1 alone was
sufficient to constitutively activate
PI3K , causing the phosphorylation of a downstream mediator of PI3K signal transduction, Akt
Li et al., Int J Mol Med 2006
:
Further, we found that
PI3K inhibitors, LY294002 and Wortmannin,
inhibited HIF-1alpha and
VEGF expression induced by UV radiation ... Further, we found that
PI3K inhibitors, LY294002 and Wortmannin,
inhibited HIF-1alpha and VEGF expression induced by UV radiation
Mannella et al., J Neurosci 2006
(Alzheimer Disease...) :
E2-induced phosphorylation of Akt, was first apparent at 10 min and maximal at 30 min. Simultaneously, E2-induced pERK1/2 was first apparent at 5-10 min and maximal at 30 min. Inhibition of
PI3K completely blocked E2 activation of pAkt at 10 and 30 min and
blocked E2 activation of
ERK1/2 at 10 min, which revealed a PI3K independent activation of ERK at 30 min. Double immunocytochemical labeling for pERK1/2 and pAkt demonstrated that E2 induced both signaling pathways in the same neurons
Fernandez-Gomez et al., Neurobiol Dis 2006
(Nerve Degeneration) :
Moreover, phosphatidylinositol 3-kinase (PI3K) inhibitors attenuated pyruvate induced cytoprotection indicating that
PI3K mediated
Akt activation is necessary for pyruvate to induce cytoprotection
Choudhury et al., Metabolism 2006
:
These effects were blocked by
JAK2 inhibition as well as
PI3K inhibition
Slomiany et al., Inflammopharmacology 2006
:
The inhibition by PAF antagonist of the LPS induced reduction in mucin synthesis was countered by wortmannin, an
inhibitor of
PI3K , as well as by
ERK inhibitor, PD98059
Lahair et al., Antioxid Redox Signal 2006
:
In contrast, hydrogen peroxide induced phosphorylation of Akt on serine 473 ( S473 ) was downregulated by both PI3K and CaM-K inhibition, indicating that hydrogen peroxideinduced phosphorylation of
Akt on S473 was largely
dependent on both
PI3K and a CaM-K activity
Ellson et al., EMBO J 2006
:
Wortmannin inhibition of the S. aureus oxidase response correlates with inhibition of phagosomal PtdIns3P accumulation and overlaps with the reduction in this response caused by the R58A mutation, suggesting
PI3K regulation of this response is substantially
dependent on PtdIns3P binding to
p40(phox)
Baregamian et al., J Surg Res 2006
(Enterocolitis, Necrotizing) :
Wortmannin, an inhibitor of PI3-K, was used to show
PI3-K dependent mechanism of action for
IGF-1 ... A better understanding of the exact role of
IGF-1 mediated activation of
PI3-K may allow us to facilitate the development of novel therapy against NEC
Omori et al., Immunity 2006
:
PI3K dependent activation of the
serine-threonine kinase , Akt, suppressed CSR, in part, through the inactivation of the Forkhead Box family ( Foxo ) of transcription factors ...
PI3K dependent
activation of the serine-threonine kinase,
Akt , suppressed CSR, in part, through the inactivation of the Forkhead Box family ( Foxo ) of transcription factors
Guenou et al., Am J Pathol 2006
(Acrocephalosyndactylia) :
Down-regulation of ubiquitin ligase
Cbl induced by twist haploinsufficiency in Saethre-Chotzen syndrome
results in increased
PI3K/Akt signaling and osteoblast proliferation ... This was associated with decreased ubiquitin mediated degradation of
phosphatidyl inositol 3 kinase (PI3K) and
increased PI3K expression and
PI3K/Akt signaling ... This provides genetic and biochemical evidence for a role for
Cbl mediated
PI3K signaling in the altered osteoblast phenotype induced by Twist haploinsufficiency in SCS
Lasunskaia et al., J Leukoc Biol 2006
(Tuberculosis) :
Mycobacteria directly induce cytoskeletal rearrangements for macrophage spreading and polarization through
TLR2 dependent
PI3K signaling ... The obtained data demonstrate that the direct effect of mycobacteria on macrophage shape might be mediated through
TLR2 dependent
PI3K activation
Leung et al., J Biol Chem 2006
:
In addition, the GR antagonist RU486 was able to inhibit
Rg1 induced
PI3K/Akt and beta-catenin activation
Bach et al., Blood 2007
:
PI3K regulates
pleckstrin-2 in T-cell cytoskeletal reorganization
Yamamoto et al., Mol Carcinog 2006
(Carcinoma, Hepatocellular...) :
Inhibition of PI3 kinase (PI3K) by Ly294002 in mouse HCC cells in vitro suppressed the nuclear shift of cyclin D1 as well as cell proliferation, while
PI3K activation by
PTEN suppression failed to induce nuclear shift of cyclin D1, suggesting that PI3K activation is essential but not sufficient for the cyclin D1 nuclear shift
Kumar et al., Mol Cell Biol 2006
:
Inhibition of late-G ( 1 )
PI3K activity
results in low c-Myc and cyclin A expression, impaired
Cdk2 activity, and reduced loading of MCM2 ( minichromosome maintenance protein ) onto chromatin ... Inhibition of late-G ( 1 )
PI3K activity
results in low
c-Myc and cyclin A expression, impaired Cdk2 activity, and reduced loading of MCM2 ( minichromosome maintenance protein ) onto chromatin ... Inhibition of late-G ( 1 )
PI3K activity
results in low c-Myc and
cyclin A expression, impaired Cdk2 activity, and reduced loading of MCM2 ( minichromosome maintenance protein ) onto chromatin
Swainson et al., Blood 2007
:
Glut-1 is directly
regulated by
PI3K and, indeed, inhibiting PI3K activity abrogates IL-7 induced proliferation
Orme et al., Nat Cell Biol 2006
:
The Drosophila class I
PI(3)K , Dp110, is
activated by nutrient-responsive
insulin signalling and modulates growth, oogenesis and metabolism ... Furthermore,
insulin can not maximally
activate PI(3)K signalling in Dp110 ( RBD ) imaginal discs and Dp110 ( RBD ) flies are small
Middleton et al., J Exp Med 2006
(Myeloproliferative Disorders) :
These data identify 12/15-LO as an important suppressor of MPD via its role as a critical upstream effector in the regulation of
PI3-K dependent
ICSBP phosphorylation
De Gregorio et al., Oncogene 2007
:
Similarly, binding of
PI3K to p21Ras and
activation of
AKT , a downstream PI3K target, were severely impaired in cells expressing the p85A mutant ... This latter mutant did not affect the
epidermal growth factor stimulated
PI3K activity ... We suggest that ( 1 ) TSH-cAMP induced
PKA phosphorylates p85alpha ( PI3K ) at serine 83, ( 2 ) phosphorylated p85alpha ( PI3K ) binds RIIbeta-PKA and targets PKAII to the membrane, and ( 3 ) PI3K activity and p21Ras binding to PI3K increase and
activate PI3K downstream targets
Utomo et al., J Immunol 2006
:
The FcgammaR mediated oxidative burst defect in Vav-deficient cells was linked to aberrant Rac activation as well as Rac- and actin-polymerization independent, but
PI3K dependent , phosphorylation of the NADPH oxidase component
p40(phox)
Chiou et al., Pediatr Res 2006
:
PTX and wortmannin, a
PI3 K inhibitor , not only inhibited the PDGF activated phosphorylation of Akt but also suppressed p70S6 K expression and IkappaBalpha degradation, inhibiting nuclear translocation and the DNA binding activity of NF-kappaB
Di Segni et al., J Mol Neurosci 2006
:
Taken together, these results indicate that in PC12-ErbB4 cells, the
NRG induced neuroprotective effect from MPP+ treatment, requires
PI3K/PKB/Akt and Ras/MapK signaling networks
Faraj et al., J Endocrinol 2006
(Diabetes Mellitus, Type 2...) :
In healthy young men, adiponutrin expression is upregulated [ corrected ] by hyperinsulinemia and is related to basal and/or
insulin stimulated p85alpha
PI3K , HKII, adiponectin, and leptin expression levels
Kolb et al., Int J Cancer 2007
(Pancreatic Neoplasms) :
HRGs induced phosphorylation of different
ErbB receptors as well as
activation of MAPK, p38MAPK, JNK and
PI3K in a cell- and ligand-specific manner
Hosoi et al., Eur J Pharmacol 2007
:
Inhibitory effect of 4- ( 2-aminoethyl ) -benzenesulfonyl fluoride, a serine protease inhibitor, on
PI3K inhibitor
induced CHOP expression
Pathak et al., J Immunol 2006
:
TLR4/PI3K dependent ERK1/2 and p38
MAPK signaling converged upon activation of mitogen- and stress activated protein kinase 1 ( MSK1 ) ...
TLR4/PI3K dependent
ERK1/2 and p38 MAPK signaling converged upon activation of mitogen- and stress activated protein kinase 1 ( MSK1 )
Tjokroprawiro et al., Acta Med Indones 2006
(Diabetes Mellitus, Type 2...) :
PPARgamma also
mediates increased production of Adiponectin and the insulin signaling intermediate
PI3K , and both actions lead to increase insulin sensitivity
Yoon et al., Mol Cancer Ther 2006
(Breast Neoplasms...) :
H-Ras did not increase MMP-9 in the
presence of a
PI3K inhibitor, LY294002, and a NF-kappaB inhibitor, SN50 ... H-Ras did not increase
MMP-9 in the
presence of a
PI3K inhibitor, LY294002, and a NF-kappaB inhibitor, SN50
Watson et al., Neoplasia (New York, N.Y.) 2006
(Adenocarcinoma...) :
We conclude that inhibition of c-Met may be a useful therapeutic strategy for EA. Factors other than receptor overexpression, such as
c-Met dependent
PI3K/Akt signaling, may be predictive of an individual tumor 's response to c-Met inhibition
Cruz et al., J Biol Chem 2007
(Inflammation) :
In parallel, ATP mediated ROS dependent
PI3K is
required for activation of
caspase-1 and secretion of IL-1beta and IL-18
Parhar et al., Mol Cell Biochem 2007
:
p65 ( Rel A ) Ser536 phosphorylation was not
affected by the
PI3K inhibitors but was dose-dependently attenuated by TPCK ... p65 (
Rel A ) Ser536 phosphorylation was not
affected by the
PI3K inhibitors but was dose-dependently attenuated by TPCK
Vantler et al., FEBS Lett 2006
:
Characterization of the downstream signaling events revealed that
PI3K activates the protein kinase
Akt , which in turn phosphorylates and thus inactivates proapoptotic Forkhead transcription factors
Tissier et al., J Mol Cell Cardiol 2007
(Myocardial Infarction...) :
In conclusion, genistein exerts pharmacological postconditioning with a similar potency as 17beta-estradiol through a pathway involving
activation of the
estrogen receptor , of
PI3K/Akt and mitochondrial preservation
Smyth et al., J Immunol 2006
(Inflammation) :
Furthermore, inhibition of
PI3K by use of LY294002
reduces expression of
IL-6 at both the mRNA and protein level in murine fibroblasts, and we suggest that PI3K is required for activation of PKCdelta
Tanaka et al., Cancer Res 2006
(Anoxia...) :
On the other hand, Akt, the pathway of which can up-regulate HIF-1alpha expression, was activated in the mouse lesions, whereas HIF-1alpha was markedly down-regulated in the mouse hepatocellular carcinoma ( HCC ) cell lines after treatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, indicating that
HIF-1alpha expression is
dependent on
PI3K/Akt signaling
Aparicio et al., Mol Reprod Dev 2007
:
Inhibition of
PI3-K did
affect neither the capacitation status nor AR nor protein
p32 tyrosine phosphorylation of boar spermatozoa incubated in TBM or TCM
Cho et al., Immunol Lett 2007
(Arthritis, Rheumatoid) :
Moreover
PI3K/Akt inhibitor, NF-kappaB inhibitor, and FK506 significantly
inhibited IL-15 induced
IL-17 production in CD4+ T cells
Tortorella et al., J Gerontol A Biol Sci Med Sci 2006
:
These results indicate that defective
PI3-K/Akt/ERK1/2 activation, likely
dependent on elevated
SOCS1 and SOCS3 levels, may affect the GM-CSF capacity to delay neutrophil apoptosis in elderly persons ... These results indicate that defective
PI3-K/Akt/ERK1/2 activation, likely
dependent on elevated SOCS1 and
SOCS3 levels, may affect the GM-CSF capacity to delay neutrophil apoptosis in elderly persons
Lanthier et al., Biochem Cell Biol 2006
:
Moreover, we found that PIMT expression returned to the basal level when cells were replated on a substratum after detachment, though downregulation of
PIMT expression could be partly
prevented by the
PI3K inhibitors LY294002 and wortmannin, as well as by the proteasome inhibitors MG-132, lactacystin, and beta-lactone
Mukai et al., Am J Physiol Heart Circ Physiol 2007
:
The increase in PAI-1 was due to transcriptional and posttranscriptional mechanisms as
PI3K inhibitors
increased PAI-1 promoter activity and mRNA stability ...
PI3K inhibitors
augmented TNF-alpha- and insulin induced phosphorylation of these MAPKs
Chen et al., J Biol Chem 2007
:
Iron induced
TAK1 activity is not
affected by the
PI3K or MEK1 inhibitor, suggesting TAK1 is upstream of PI3K and MEK1 ... In conclusion, MEK1, TAK1, NF-kappa inducing kinase, and
PI3K are
required for iron induced
IKK activation in hepatic macrophages and TAK1, PI3K, and p21ras physically interact in caveolae to initiate signal transduction
Vanni et al., Cell cycle (Georgetown, Tex.) 2006
:
Inhibition of
PI3K induces
Rac activation and membrane ruffling in proto-Dbl expressing cells ... Furthermore, we investigated the signaling molecules involved in proto-Dbl induced cell transformation and motility and observed that inhibition of
PI3K in proto-Dbl expressing cells
induces an increase in
p38 activity and a decrease in ERK phosphorylation ... Furthermore, we investigated the signaling molecules involved in proto-Dbl induced cell transformation and motility and observed that inhibition of
PI3K in proto-Dbl expressing cells
induces an increase in p38 activity and a decrease in
ERK phosphorylation
Ghosh-Choudhury et al., J Biol Chem 2007
(MAP Kinase Signaling System) :
Expression of dominant negative
PI3K and PTEN, an inhibitor of PI3K signaling, significantly
attenuated lovastatin induced transcription of
BMP-2 ... Expression of dominant negative PI3K and
PTEN , an
inhibitor of
PI3K signaling, significantly attenuated lovastatin induced transcription of BMP-2
Molnarfi et al., J Immunol 2007
:
In contrast,
PI3K inhibition
increased the production of
IL-1beta protein in both CE ( sHUT ) - and LPS activated monocytes, the enhancement being drastically higher in the former
Liu et al., J Exp Med 2007
(Anaphylaxis...) :
Here, we report that
RasGRP1 plays an important role in FcepsilonRI mediated
PI3K activation and mast cell function
Wong et al., Diabetologia 2007
(Diabetes Mellitus, Type 2) :
The protein/lipid phosphatase
Pten ( phosphatase and tensin homologue deleted on chromosome 10 )
attenuates PI3K signalling by dephosphorylating the phosphatidylinositol 3,4,5-trisphosphate generated by PI3K
McMullen et al., Proc Natl Acad Sci U S A 2007
(Cardiomyopathy, Dilated...) :
PI3K ( p110alpha ) signaling negatively
regulated G protein coupled receptor stimulated extracellular responsive kinase and Akt ( via PI3K, p110gamma ) activation in isolated cardiomyocytes ...
PI3K ( p110alpha ) signaling negatively
regulated G protein coupled receptor stimulated extracellular responsive kinase and
Akt ( via PI3K, p110gamma ) activation in isolated cardiomyocytes
Sherry et al., J Immunol 2007
(Diabetes Mellitus, Type 2) :
LPS dependent stimulation of
PI3K activity, ERK1/2 activation, and p38 kinase activity was greater in PerMphi from db/db mice as compared with db/+ mice
Storm et al., J Biol Chem 2007
:
Furthermore, GSK-3 mutants mimicked the
effects of
PI3K or GSK-3 inhibition on
Nanog expression
El Mabrouk et al., Biochim Biophys Acta 2007
:
These results suggest that OSM stimulated
ADAMTS-4 and MMP-13 expression is
mediated by ERK1/2, JAK3/STAT1/3 and
PI3K/Akt and by cross talk between these pathways ... These results suggest that OSM stimulated ADAMTS-4 and
MMP-13 expression is
mediated by ERK1/2, JAK3/STAT1/3 and
PI3K/Akt and by cross talk between these pathways
Bogush et al., J Biol Chem 2007
(Huntington Disease) :
We demonstrated that both the
PI3K/Akt/mammalian target of rapamycin and the cdk5/p35 signal transduction pathways
contribute to the induction of
DARPP-32 protein levels by BDNF and that the effects are on both the transcriptional and translational levels
Kaul et al., Cell Signal 2007
(Glioblastoma) :
Introduction of normal PTEN together with H-Ras ( G12V ) into U251 glioblastoma cells reduced the
PI3K dependent activation of
Akt , but had no effect on vacuolation
Lavery et al., J Neurosci 2007
:
Our results raise the possibility that neurofibroma formation in individuals with neurofibromatosis might result in part from a
Ras-PI3K-Akt dependent inhibition of
FOXO within Schwann cells
Ehrhardt et al., J Virol 2007
:
NS1 binds to and
activates PI3K , which results in the activation of the PI3K effector Akt
Wang et al., Am J Physiol Cell Physiol 2007
:
Treatment of cells with dexamethasone for 24 h : 1 ) suppressed IRS-1 associated
PI3K activity and Akt phosphorylation, 2 ) increased the level of the PI3K p85 regulatory subunit but not the p110 catalytic subunit, and 3 )
induced the phosphorylation of
IRS-1 on inhibitory Ser ( 307 ) ... Inhibition of
PI3K using LY-294002
increased the transcription of the BCKD E2 subunit but not the E1alpha subunit or
BCKD kinase
Zhande et al., Am J Physiol Heart Circ Physiol 2007
:
EPO caused a prolonged activation of
nuclear factor (NF)-kappaB , which was
blocked by inhibition of
PI3K , but not by inhibition of mitogen activated protein ( MAP ) /ERK kinase ( MEK ), suggesting that EPO activated NF-kappaB requires PI3K activity
Radhakrishnan et al., J Immunol 2007
:
Analysis of human or mouse DC treated with the B7-DC cross linking Ab revealed
PI3K dependent phosphorylation of
AKT accompanied by mobilization of NF-kappaB
Leslie et al., Curr Biol 2007
:
Expression either of PTEN lacking the PDZ binding site or of the
PTEN C2 domain, or
inhibition of
PI3K through specific inhibitors, does not inhibit EMT, but results in a loss of both cell polarity and directional migration of mesoderm cells
Nakatani et al., Biochem Biophys Res Commun 2007
:
Treatment of 3Y1 cells with AVP resulted in transient activation of p44/42 mitogen activated protein kinase ( MAPK ) and cPLA(2)alpha, and phosphatidylinositol 3-kinase (PI3K) inhibitor blocked not only AVP induced PGE ( 2 ) synthesis but also MAPK activation, suggesting that
PI3K is
involved in the AVP induced
MAPK and cPLA(2)alpha activation, which initiates the production of PGE ( 2 ) ... Treatment of 3Y1 cells with AVP resulted in transient activation of p44/42 mitogen activated protein kinase ( MAPK ) and cPLA(2)alpha, and phosphatidylinositol 3-kinase (PI3K) inhibitor blocked not only AVP induced PGE ( 2 ) synthesis but also MAPK activation, suggesting that
PI3K is
involved in the AVP induced MAPK and
cPLA(2)alpha activation, which initiates the production of PGE ( 2 )
Harvey et al., Arterioscler Thromb Vasc Biol 2007
(Atherosclerosis) :
AKT was the downstream
target for
PI3K action ... These studies provide novel insights into the
role of
PI3K/AKT and CK2 in
IFN-gamma signaling relevant to changes in macrophage gene expression during atherosclerosis
Wang et al., J Biomed Sci 2007
:
In conclusion, A20 attenuates neointimal formation after arterial injury as well as cell proliferation and migration in response to TNF-alpha in VSMCs through blocking
PI3K/Akt/GSKbeta dependent activation of
CREB
Kanda et al., Eur J Immunol 2007
:
Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9,
CXCL10 , and CXCL11 production and NF-kappaB, STAT1, and IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and
CXCL11 production and NF-kappaB, STAT1, and IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and CXCL11 production and NF-kappaB,
STAT1 , and IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and CXCL11 production and NF-kappaB, STAT1, and IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and CXCL11 production and NF-kappaB, STAT1, and
IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced
CXCL9 , CXCL10, and CXCL11 production and NF-kappaB, STAT1, and IRF-1 activities ... Inhibitors of
PI3 K , p38 MAPK, and MEK
suppressed IL-18 plus IFN-gamma induced CXCL9, CXCL10, and CXCL11 production and
NF-kappaB , STAT1, and IRF-1 activities
Arcaro et al., Cell Signal 2007
(Carcinoma, Small Cell) :
Together our data demonstrate that lipid rafts
play a key role in the activation of
PI3K signalling by facilitating the interaction of
Src with specific PI3K isoforms
Moriyama et al., Immunol Lett 2007
(Lymphoma, B-Cell) :
The BCR induced rapid expression of
c-FLIP was not affected by inactivation of NF-kappaB, but was
inhibited by either treatment with a PI3K inhibitor, LY294002, or expression of a dominant negative
PI3K p85 subunit, both of which suppressed phosphorylation of Akt and sensitized BCR stimulated A20 cells to Fas mediated apoptosis
Spillman et al., Gynecol Oncol 2007
(MAP Kinase Signaling System...) :
The
PI3K/Akt pathway inhibitor wortmannin decreased the amount of ser-80 MKK4 by 50 %, and
inhibited EGF stimulation of MKK4 ser-80 phosphorylation by 60 %
Zhang et al., J Immunol 2007
:
Small interfering RNA mediated knockdown of SHIP1 expression increased
PI3K dependent
Akt activation and subsequently decreased inflammatory cytokine expression, suggesting GC-mediated up-regulation of SHIP1 expression is responsible for the augmentation in inflammatory cytokine production following LPS stimulation
Frossi et al., J Immunol 2007
:
Selective activation of
Fyn/PI3K and p38 MAPK
regulates IL-4 production in BMMC under nontoxic stress condition
Pivoriūnas et al., Mol Cell Biochem 2007
(Leukemia) :
Here, we report a novel finding that
PI 3-K inhibition by LY294002 significantly
increases p21WAF1/Cip1 expression in PMA stimulated human leukemia cells NB4 and THP1
Camacho-Leal et al., J Cell Physiol 2007
(MAP Kinase Signaling System) :
Inhibition of
PI3-K and ILK, but not MAPK,
prevented the
alpha5beta1 integrin activation ... Conversely, anti-alpha5 antibody inhibited the
PI3-K mediated activation of
Akt , implying the involvement of outside-in and inside-out signaling in integrin activation
Ohsawa et al., Glia 2007
:
ATP stimulation increased
Akt phosphorylation in the microglia, and the increase was
reduced by the
PI3K inhibitors and a P2Y ( 12 ) R antagonist
Lin et al., J Cell Physiol 2007
(Lung Neoplasms) :
We initially observed that IL-1beta induced
ICAM-1 promoter activity was
attenuated by the inhibitors of Src ( PP1 ), PDGFR ( AG1296 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), revealed by reporter gene assay, Western blotting, and RT-PCR analyses ... The
involvement of Src and
PI3-K/Akt in IL-1beta induced
ICAM-1 expression was significantly attenuated by transfection of A549 cells with dominant negative plasmids of Src, p85 and Akt, respectively ... Src, PDGFR, and
PI3K/Akt mediated the effects of
IL-1beta because pretreatment with PP1, AG1296, and wortmannin also abrogated IL-1beta stimulated Src, PDGFR, and Akt phosphorylation, respectively
Hsieh et al., J Rheumatol 2007
(Osteoarthritis, Knee) :
Enzyme linked immunosorbent assay and gelatin zymography were used to investigate the
effects of ERK 1/2 inhibitor U0126, JNK and p38 inhibitor SB203580, and
PI3K inhibitor LY294002 on the secretion of u-PA, PAI-1,
MMP-2 , and MMP-9 in early osteoarthritic tissue cultures, with or without interleukin 1alpha (IL-1alpha) and lipopolysaccharide (LPS) induction ... Enzyme linked immunosorbent assay and gelatin zymography were used to investigate the
effects of ERK 1/2 inhibitor U0126, JNK and p38 inhibitor SB203580, and
PI3K inhibitor LY294002 on the secretion of u-PA, PAI-1, MMP-2, and
MMP-9 in early osteoarthritic tissue cultures, with or without interleukin 1alpha (IL-1alpha) and lipopolysaccharide (LPS) induction ... Enzyme linked immunosorbent assay and gelatin zymography were used to investigate the
effects of ERK 1/2 inhibitor U0126, JNK and p38 inhibitor SB203580, and
PI3K inhibitor LY294002 on the secretion of u-PA,
PAI-1 , MMP-2, and MMP-9 in early osteoarthritic tissue cultures, with or without interleukin 1alpha (IL-1alpha) and lipopolysaccharide (LPS) induction
Ho et al., J Virol 2007
:
However, Rta transduced
PI 3-K activity
plays a minor role in
DcR3 expression
Voss et al., Mol Pharmacol 2007
:
PI3K inhibitors eliminated these effects downstream of PAR1, but they
had no effect on
PAR4 signaling
Dhar et al., Cancer Res 2007
(Breast Neoplasms) :
Because a pure anti-ER ICI 182,780 is not only able to suppress the up-regulation of WISP-2/CCN5 mRNA expression by IGF-1, it also suppresses the
PI3K/Akt activity
induced by
IGF-1 in MCF-7 cells ; we anticipate that the membrane ER receptor may participate in this event
Folgiero et al., Cancer Res 2007
(Breast Neoplasms...) :
Given that
ErbB-2 can
activate PI3K only when it heterodimerizes with other members of the epidermal growth factor receptor family, these data imply that other receptors cooperate in this process
Bahlis et al., Blood 2007
(Multiple Myeloma) :
We have found that direct activation of myeloma cell
CD28 by anti-CD28 mAb alone
induces activation of
PI3K and NFkappaB, suppresses MM cell proliferation, and protects against serum starvation and dexamethasone ( dex ) -induced cell death
Thamilselvan et al., FASEB J 2007
(Colonic Neoplasms...) :
PI3K inhibitor ( LY294002 )
prevented pressure stimulated Akt Ser473 and FAK Tyr397, but not FAK576 or
Src416 phosphorylation ...
PI3K inhibitor ( LY294002 )
prevented pressure stimulated Akt Ser473 and FAK
Tyr397 , but not FAK576 or Src416 phosphorylation
Ahmad et al., Biochem J 2007
:
Another
PI3K inhibitor, LY294002, and the tyrosine kinase inhibitor, Genistein, also
inhibited insulin induced activation of
PDE3B and its co-immunoprecipitation with PKB
Shin et al., J Gen Virol 2007
:
The
PI3K-specific inhibitor LY294002 could
suppress Akt phosphorylation, suggesting that influenza A virus induced Akt phosphorylation is PI3K dependent
Lee et al., Cell cycle (Georgetown, Tex.) 2007
(Cell Transformation, Neoplastic) :
Here we discuss our recent study indicating that activation of the phosphoinositide 3-kinase (PI3K) signaling pathway through inactivating mutations in PTEN or activating mutations in PIK3CA causes functional activation of p53 signaling in human cells. ( 1 ) ur data suggest that activation of p53 is a fail-safe mechanism triggered by loss of
PTEN or oncogenic
activation of
PI3K , and furthermore, that these events provide selective pressure to mutate p53
Nielsen-Preiss et al., Endocrinology 2007
:
In addition,
PI3K inhibition in GnRH neuronal cells
diminished Gas6 induced
Rac activation
Fumagalli et al., J Immunol 2007
:
An increase in intracellular Ca ( 2+ ) concentration and phosphorylation of Akt/PKB occurred normally in fMLP stimulated hck-/-fgr-/- neutrophils, indicating that activation of both phosphoinositide-specific phospholipase C and
PI3K is
independent of Hck and
Fgr ... An increase in intracellular Ca ( 2+ ) concentration and phosphorylation of Akt/PKB occurred normally in fMLP stimulated hck-/-fgr-/- neutrophils, indicating that activation of both phosphoinositide-specific phospholipase C and
PI3K is
independent of
Hck and Fgr
Cao et al., Cell Signal 2007
(MAP Kinase Signaling System...) :
We found that
PI3K inhibitor wortmannin or LY294002
blocked COX-2 expression induced by IGF-I
Cui et al., J Neurochem 2007
:
Furthermore, inhibitors of
PI3K ( LY294002 and Wortmannin ), MEK1 ( PD98059 and U0126 ), and Src family tyrosine kinases ( PP2 ) decreased IGF-I induced proliferation, and
blocked ERK1/2 activation
Xia et al., J Biol Chem 2007
(Neoplasms) :
Collectively, these findings demonstrate that
p21 ( RAS ), through its downstream effector
PI3K ,
induces PKCdelta expression and that this increase in PKCdelta activity, acting through Akt, is required for cell survival
Marzec et al., Oncogene 2007
(Lymphoma, T-Cell) :
Accordingly, whereas the low-dose
PI3K inhibitor wortmannin and Akt inhibitor III profoundly
inhibited Akt phosphorylation, they had a very modest effect on S6rp and 4E-BP1 phosphorylation
Walker et al., Am J Physiol Cell Physiol 2007
:
PI3K activation is
required for PMA directed activation of cSrc by
AFAP-110
Wu et al., Eur J Pharmacol 2007
(Neurotoxicity Syndromes) :
The effect of erythropoietin was mediated by the phosphatidylinositol 3-kinase (PI3K) signaling pathway since erythropoietin failed to rescue cells from
MPP ( + ) insult in the
presence of the
PI3K inhibitor, LY 294002
Datta et al., Cancer Res 2007
(Carcinoma, Hepatocellular...) :
Suppression of MT-1 and MT-2A by ectopic expression of the constitutively active PI3K or
AKT and their
up-regulation by dominant negative
PI3K or AKT mutant confirmed negative regulation of MT expression by PI3K/AKT signaling pathway
Hale et al., Biochem Soc Trans 2007
(Influenza, Human) :
Activation of PI3K in virus infected cells is mediated by the viral NS1 protein, which binds directly to the p85beta regulatory subunit of PI3K and causes the
PI3K dependent phosphorylation of
Akt ( protein kinase B )
Gulati et al., Biochem Soc Trans 2007
:
Nutrient overload induces constitutive S6K1 ( S6 kinase 1 ) activation, which leads to insulin resistance by suppressing
insulin induced class I
PI3K ( phosphoinositide 3-kinase ) signalling [ Um, Frigerio, Watanabe, Picard, Joaquin, Sticker, Fumagalli, Allegrini, Kozma, Auwerx and Thomas ( 2004 ) Nature 431, 200-205 ]
Luo et al., J Pharmacol Exp Ther 2007
:
The stimulation of
Akt phosphorylation was
inhibited in a concentration dependent manner by the
PI3K inhibitor, 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 )
Liu et al., J Exp Med 2007
(Toxoplasmosis) :
We further show that DGKzeta negatively controls the phosphatidylinositol 3-kinase (PI3K)-Akt pathway and that inhibition of
PI3K activity or treatment with PA can
restore lipopolysaccharide induced
IL-12 production by DGKzeta-deficient Mphi
Renner et al., Carcinogenesis 2007
(Adenocarcinoma...) :
Additionally, we describe that the phosphorylation of AKT and
eIF4G , as well as the elevation of the Mst1 and RanBP2 protein levels, can be
inhibited in vivo in transgenic animals by the
PI3K inhibitor LY294002 ... Additionally, we describe that the phosphorylation of
AKT and eIF4G, as well as the elevation of the Mst1 and RanBP2 protein levels, can be
inhibited in vivo in transgenic animals by the
PI3K inhibitor LY294002 ... Additionally, we describe that the phosphorylation of AKT and eIF4G, as well as the elevation of the
Mst1 and RanBP2 protein levels, can be
inhibited in vivo in transgenic animals by the
PI3K inhibitor LY294002 ... Additionally, we describe that the phosphorylation of AKT and eIF4G, as well as the elevation of the Mst1 and
RanBP2 protein levels, can be
inhibited in vivo in transgenic animals by the
PI3K inhibitor LY294002
Naito et al., Nagoya J Med Sci 2005
:
AG-490, a
Jak-2 inhibitor, or LY294002, a
PI3K inhibitor , similarly suppressed the augmented production of hyarulonan
Lilja et al., J Neurosci Res 2007
(Neuroblastoma) :
By blocking phosphatidylinositol-3-kinase [ PI(3)K ] or mitogen activated protein kinase ( MAPK ) signaling, we concluded that the increase in total TRPV1 protein content induced by
IGF-I was
controlled by
PI(3)K signaling, whereas insulin seemed to regulate TRPV1 protein expression via both PI(3)K and MAPK pathways
Kozuma et al., Journal of thrombosis and haemostasis : JTH 2007
:
We thus hypothesized that
PI3 K inhibits the activation of caspase-3 and consequent cleavage of
Bcl-xL ... We thus hypothesized that
PI3 K inhibits the activation of
caspase-3 and consequent cleavage of Bcl-xL
Trucy et al., Cell Immunol 2006
:
CD4 binding also
increases interactions between
PI3K and activated PKCzeta and PDK1
Cuevas et al., J Hepatol 2007
:
Changes in
ERK phosphorylation in IRS-4 depleted cells were
independent of ras/raf/MEK1/2- and
PI3K/Akt-cascades
Jin et al., Cancer Res 2007
(Cell Transformation, Neoplastic) :
Here, we define some aspects of the molecular mechanisms regulating
ETV6-NTRK dependent Ras-Erk1/2 and
PI3K-Akt activation ... Here, we define some aspects of the molecular mechanisms regulating
ETV6-NTRK dependent Ras-Erk1/2 and
PI3K-Akt activation ... Suppression of
c-Src by RNA interference in NIH3T3-ETV6-NTRK3 cells
resulted in markedly decreased expression of cyclin D1 and suppression of activation of Ras-Erk1/2 and
PI3K-Akt
Lee et al., Development 2007
:
Akt was rapidly phosphorylated when GDNF was added to the GS cell culture, and the addition of a chemical inhibitor of
PI3K prevented GS cell self-renewal
So et al., Mol Immunol 2007
(MAP Kinase Signaling System) :
In cytokine producing Jurkat T cells, we have found that IL-4 induces activation of Erk and Akt, and the IL-4 induced
STAT6 activity is
suppressed by inhibitors of Erk and
PI3K
Lengyel et al., Steroids 2007
:
The present work shows that
PI3K plays a crucial role in the phosphorylation and inactivation of
FOXO1 in vivo, indicating that the regulation of this transcription factor is a more complex event in uterine cells requiring further investigations
Ruggiero et al., BMC molecular biology 2007
:
Our study identified a set of transcripts that are targets of
KSRP and whose expression is
increased by
PI3K-AKT activation
Wrann et al., J Immunol 2007
(Sepsis) :
In addition,
PI3K inhibition
resulted in strongly elevated TLR-4 mediated generation of
IL-1beta and IL-8 in neutrophils when these cells were co-stimulated with C5a ... In addition,
PI3K inhibition
resulted in strongly elevated TLR-4 mediated generation of IL-1beta and
IL-8 in neutrophils when these cells were co-stimulated with C5a
Zhang et al., Planta Med 2007
(Osteoporosis) :
Furthermore, puerarin stimulated osteoblastic growth,
Akt activation and redistribution were significantly blocked by the specific
PI3K inhibitor, LY294002 ... These results strongly suggested that puerarin stimulated osteoblastic proliferation and
Akt activation in a
PI3K dependent manner
Saal et al., Proc Natl Acad Sci U S A 2007
(Carcinoma) :
Taking advantage of the observation that loss of
PTEN , the negative
regulator of
PI3K , results in robust activation of this pathway, we developed and validated a microarray gene expression signature for immunohistochemistry ( IHC ) -detectable PTEN loss in breast cancer ( BC )
Zhu et al., Oncogene 2007
(Gastrointestinal Stromal Tumors) :
Activated signaling intermediates were identified by immunoaffinity purification of tyrosine phosphorylated proteins in GIST cells before and after treatment with KIT inhibitors, and these analyses show that GRB2, SHC, CBL and MAPK activation are largely KIT dependent in GISTs, whereas
PI3-K , STAT1 and STAT3 activation are partially
KIT dependent
Jung et al., Invest Ophthalmol Vis Sci 2007
:
Upregulation of TGF-beta induced
tissue transglutaminase expression by
PI3K-Akt pathway activation in human subconjunctival fibroblasts
Zhang et al., J Neurosci Res 2007
(Ion Channel Gating...) :
Inhibitors of PKC, tyrosine kinase, and
PI3K were all able to inhibit the INa, but none of them could
prevent the
GnRH response
Geering et al., Proc Natl Acad Sci U S A 2007
:
These results argue against a
role of free
p85 in
PI3K signaling and provide insights into the nonredundant functions of the different class IA PI3K isoforms
Don et al., Br J Pharmacol 2007
:
Furthermore,
MIP-1alpha induced cell migration and
PI3K-p110gamma translocation were also inhibited by cryptotanshinone in a concentration dependent manner ... Furthermore,
MIP-1alpha induced cell migration and
PI3K-p110gamma translocation were also inhibited by cryptotanshinone in a concentration dependent manner
Smith et al., J Bone Joint Surg Am 2007
(Prosthesis Failure) :
The
PI3K inhibitor
reduced TNF-alpha production by 70 % in response to titanium with adherent endotoxin without increasing cytotoxicity ... High concentrations of endotoxin-free titanium particles resulted in a small delayed increase in
TNF-alpha production that was completely
blocked by the
PI3K inhibitor
Zhu et al., Biochem Biophys Res Commun 2007
:
PI3K is negatively
regulated by
PIK3IP1 , a novel p110 interacting protein ...
PI3K is negatively
regulated by
PIK3IP1 , a novel p110 interacting protein
Wiseman et al., J Immunol 2007
(MAP Kinase Signaling System) :
Perforin dependent cryptococcal microbicidal activity in NK cells requires
PI3K dependent
ERK1/2 signaling
Joshi et al., FASEB J 2007
:
Here, using pharmacological inhibition of
PI3K , adenoviral
mediated T-cad-overexpression , siRNA mediated T-cad-depletion, and agonistic antibody mediated ligation, we demonstrate signaling by T-cad through PI3K-Akt-GSK3beta pathways in EC ... Here, using pharmacological inhibition of
PI3K , adenoviral
mediated T-cad-overexpression , siRNA mediated T-cad-depletion, and agonistic antibody mediated ligation, we demonstrate signaling by T-cad through PI3K-Akt-GSK3beta pathways in EC
Benitez et al., Br J Cancer 2007
(Breast Neoplasms...) :
Immunoprecipitation and kinase assays showed that RES inhibited AR- and
ERalpha dependent
PI3K activities in LNCaP and PC-3, respectively
Ray et al., Int J Oncol 2007
(Breast Neoplasms...) :
MCF-7 cells expressed higher levels of Ob-Rb, Jak2,
PI3K , Stat3 and p-Stat3 in a dose dependent manner to 50 ng/ml at 24 h ; and
IGF-IRalpha increased at 24 h. Cyclin D1 and Cox-2 levels increased with leptin treatment
Sancho et al., Int J Mol Med 2007
(Obesity, Morbid) :
In addition,
GLP-1 and Ex-4
stimulated PI3K and MAPKs, similar to insulin, but not PKB ... In addition,
GLP-1 and Ex-4
stimulated PI3K and MAPKs, similar to insulin, but not PKB
Liu et al., Biochim Biophys Acta 2007
(MAP Kinase Signaling System) :
We propose that the inhibition of
PI(3)K by wortmannin in mouse macrophages enhances the PI-PLC downstream signals, and subsequently
increases the
LPS induction of iNOS expression independently of Akt pathway ... We propose that the inhibition of
PI(3)K by wortmannin in mouse macrophages enhances the PI-PLC downstream signals, and subsequently
increases the LPS induction of
iNOS expression independently of Akt pathway
Yano et al., J Biol Chem 2007
:
ANG II
induced a significant increase in
PI3K activity, which was abolished by co-treatment with losartan or 2',5'-dideoxyadenosine ( 2',5'-DOA, an adenylyl cyclase inhibitor ) but not by PD123319 ( an AT-2R antagonist ) or H89 ( a protein kinase A (PKA) inhibitor )
Etkovitz et al., Biol Reprod 2007
:
The increases in
PIP ( 2 ( 4,5 ) ) and F-actin intracellular levels during sperm capacitation were
mediated by PI4K but not by
PI3K activity ... On the other hand, activation of PKC by phorbol myristate acetate
enhanced PIP ( 2 ( 4,5 ) ) and F-actin formation mediated by PI4K activity, while the
PI3K activity and intracellular PIP ( 3 ( 3,4,5 ) ) levels were reduced
Giani et al., Am J Physiol Heart Circ Physiol 2007
:
The specific JAK2 inhibitor AG-490 blocked
ANG- ( 1-7 ) -induced JAK2 and IRS-1 phosphorylation but had no effect on ANG- ( 1-7 ) -induced phosphorylation of Akt, indicating that activation of cardiac Akt by ANG- ( 1-7 ) appears not to involve the recruitment of JAK2 but proceeds through the receptor Mas and
involves PI3K
Xu et al., J Cell Biochem 2008
(MAP Kinase Signaling System) :
Furthermore, the antiapoptotic effect of lovastatin on mitochondrial apoptotic pathway was effectively abrogated by both
PI3K inhibitor, LY294002 and
ERK1/2 inhibitor , U0126 ... The activation of
ERK1/2 was
inhibited by a
PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not inhibit phosphorylation of Akt and GSK3 beta ... The activation of ERK1/2 was inhibited by a
PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not
inhibit phosphorylation of
Akt and GSK3 beta ... The activation of ERK1/2 was inhibited by a
PI3K inhibitor, LY294002, but U0126, a ERK1/2 inhibitor did not
inhibit phosphorylation of Akt and
GSK3 beta
Lee et al., J Neurochem 2007
:
Consistent with neurotrophic effects,
tPA activated Raf-K/ERK, PKC and
PI3-K/Akt , 5-60 min after treatment
Liu et al., Clin Chim Acta 2007
:
Role of ERK1/2 and
PI3-K in the regulation of CTGF induced
ILK expression in HK-2 cells ... Chemical inhibitors were used to assess the
role of MEK/ERK1/2,
PI3-K , and P38 MAPK signaling pathways in induction of
ILK by CTGF ... CTGF induced
ILK expression was partially
reduced by inhibiting ERK1/2 and
PI3-K activation
Riera et al., Reproduction 2007
:
In summary, results presented herein demonstrate that
IL1beta stimulates
PI3K/PKB- , P70S6K-, and ERK1/2 dependent pathways in rat Sertoli cells
Ma et al., Mol Endocrinol 2007
:
BRCA1 underexpression also enhanced estrogen-inducible
ER-alpha activity in a
PI3K/Akt dependent manner
Raghu et al., J Virol 2007
(Herpesviridae Infections) :
RhoA-GTPase activation was
inhibited by
PI3-K inhibitors, demonstrating that PI3-K is upstream to RhoA-GTPase
O'Connor et al., J Immunol 2007
(Diabetes Mellitus, Type 2) :
In this study, we report that normal IL-4 dependent elaboration of IL-1 receptor antagonist (IL-1RA) requires
IRS-2 mediated
PI3K activity in primary macrophages ... Inhibition of
PI3K with wortmannin or blockage of IRS-2/PI3K complex formation with a cell permeable IRS-2 derived tyrosine phosphopeptide
inhibited IL-4 dependent
IL-1RA production in db/+ macrophages ... Examination of IL-4 signaling in db/db macrophages revealed that
IL-4 dependent
IRS-2/PI3K complex formation and IRS-2 tyrosine phosphorylation was reduced compared with db/+ macrophages ... These results indicate that in the db/db mouse model of T2D, macrophage expression of
SOCS-3 is increased, and impaired IL-4 dependent
IRS-2/PI3K formation
induces a state of IL-4 resistance that disrupts IL-4 dependent production of IL-1RA ... These results indicate that in the db/db mouse model of T2D, macrophage expression of SOCS-3 is increased, and impaired
IL-4 dependent
IRS-2/PI3K formation induces a state of IL-4 resistance that disrupts IL-4 dependent production of IL-1RA
Yoshii et al., Nat Neurosci 2007
:
BDNF induces transport of PSD-95 to dendrites through
PI3K-AKT signaling after NMDA receptor activation
Boisvert et al., Mol Immunol 2007
:
Inhibition studies indicated that activation of ERK and JNK MAPKs and
PI3K/AKT are necessary for both TCR- and TCR+alpha2 beta1 integrin dependent IFN-gamma production and that Coll I
increases TCR dependent activation of
ERK and JNK MAPKs, and AKT ... Inhibition studies indicated that activation of ERK and JNK MAPKs and
PI3K/AKT are
necessary for both TCR- and TCR+alpha2 beta1 integrin dependent
IFN-gamma production and that Coll I increases TCR dependent activation of ERK and JNK MAPKs, and AKT
Amin et al., Arthritis Rheum 2007
(Arthritis, Rheumatoid) :
Additionally, RA ST fibroblast IL-18 induced
MCP-1/CCL2 production was
mediated by JNK,
PI3K , and NFkappaB
Canabal et al., Am J Physiol Regul Integr Comp Physiol 2007
(Acute Disease...) :
Hyperglycemia induced inhibition of
AMPK reduces
PI3K signaling by activating the mammalian target of rapamycin (mTOR)
Chuang et al., Endocrinology 2007
(Diabetes Mellitus, Experimental...) :
MAPK/ERK inhibitor PD98059
inhibited the
PI3K activity, Akt phosphorylation, and lipid accumulation triggered by HG ...
MAPK/ERK inhibitor PD98059
inhibited the
PI3K activity, Akt phosphorylation, and lipid accumulation triggered by HG ...
PI3K inhibitor LY294002 did not
affect the HG-increased
ERK1/2 phosphorylation during adipogenesis
Hung et al., Stem Cells 2007
:
Also, addition of CdM ( Hyp ) activated the PI3K-Akt pathway ; the levels of p-Akt and several of its downstream targets were
increased by
CdM ( Hyp ), and both the increase in p-Akt and the increase in angiogenesis were blocked by an inhibitor of
PI3K-Akt or by expression of a dominant negative gene for PI3K ... Also, addition of CdM ( Hyp ) activated the PI3K-Akt pathway ; the levels of
p-Akt and several of its downstream targets were
increased by CdM ( Hyp ), and both the increase in p-Akt and the increase in angiogenesis were blocked by an inhibitor of
PI3K-Akt or by expression of a dominant negative gene for PI3K
Zhao et al., J Cell Biochem 2008
(Calcium Signaling...) :
Our results showed that YSL decreased the mRNA level and protein expression of
CaM ,
inhibited the activity of
PI3K , and reduced the mRNA level and protein expression of the PI3K regulatory subunit p85 and mRNA level of PI3K catalytic subunits p110alpha and p110gamma ... Our results showed that YSL decreased the mRNA level and protein expression of CaM,
inhibited the activity of
PI3K , and reduced the mRNA level and protein expression of the PI3K regulatory subunit
p85 and mRNA level of PI3K catalytic subunits p110alpha and p110gamma
Nakagawa et al., Oncol Rep 2007
(Carcinoma, Squamous Cell...) :
E-cadherin transfection increased phosphorylated Akt expression concomitantly with the increase in SCCA2 expression, and the increased
SCCA2 expression was
inhibited by a
PI3K inhibitor ... E-cadherin transfection increased phosphorylated
Akt expression concomitantly with the increase in SCCA2 expression, and the increased SCCA2 expression was
inhibited by a
PI3K inhibitor
Shukla et al., Int J Cancer 2007
(Neoplasm Invasiveness...) :
Immunoblot analysis of PI3K and total/activated levels of Akt showed increased protein levels of catalytic ( p110alpha/beta ) and regulatory ( p85 ) subunits of
PI3K and constitutive
Akt activation in high-grade tumors compared to low-grade tumor and benign tissue
Vivanco et al., Cancer Cell 2007
(Cell Transformation, Neoplastic) :
Furthermore,
PTEN deficiency sensitizes cells to JNK inhibition and negative feedback regulation of
PI3K was
impaired in PTEN null cells
Zeidan et al., J Pharmacol Exp Ther 2007
(Hypertrophy) :
Our results indicate that the activation of RhoA/ROCK and
PI3K/Akt plays a pivotal role in
leptin signaling, leading to the development of VSMC hypertrophy through a mechanism involving altered actin dynamics
Nizhynska et al., Dev Neurobiol 2007
:
Moreover, agrin induced activation of Rac and
Cdc42 is
impaired in the presence of
PI3-K inhibitors ... Moreover, agrin induced activation of
Rac and Cdc42 is
impaired in the presence of
PI3-K inhibitors
Yamaki et al., Exp Cell Res 2007
:
On the other hand, the regulation of anoikis by RhoG required phosphatidylinositol 3-kinase (PI3K) activity, and constitutively active RhoG bound to the PI3K regulatory subunit p85alpha and induced the
PI3K dependent phosphorylation of
Akt
Choi et al., J Clin Invest 2007
(Insulin Resistance...) :
Insulin resistance in these tissues was associated with reduced
insulin stimulated insulin receptor substrate 1- (IRS-1-) and IRS-2 associated
PI3K activity in muscle and liver, respectively
Roztocil et al., J Surg Res 2007
:
Migration assays were performed in the presence of K with and without the plasmin inhibitors ( aprotinin and -aminocaproic acid ), the Galphai inhibitor Pertussis toxin, the
MMP inhibitor ( GM6001 ), the
PI3-K inhibitors , Wortmannin and LY294002, and the MAPK inhibitors PD98089 ( MEK1 inhibitor ) and SB203580 ( p38 ( MAPK ) inhibitor ) ... Activation of
p38 ( MAPK ) and ERK 1/2 was completely
inhibited by the
PI3-K inhibitors ... Activation of p38 (
MAPK ) and ERK 1/2 was completely
inhibited by the
PI3-K inhibitors ... Activation of p38 ( MAPK ) and
ERK 1/2 was completely
inhibited by the
PI3-K inhibitors ... Activation of p38 ( MAPK ) and
ERK 1/2 was completely
inhibited by the
PI3-K inhibitors
Tomita et al., Biochem J 2007
(Leukemia, T-Cell) :
The
PI3K inhibitor LY294002
suppressed HIF-1alpha protein expression,
HIF-1 DNA binding and HIF-1 transcriptional activity in HTLV-1 infected T-cell lines ... The
PI3K inhibitor LY294002
suppressed HIF-1alpha protein expression, HIF-1 DNA binding and HIF-1 transcriptional activity in HTLV-1 infected T-cell lines ... The results of the present study suggest that
PI3K/Akt activation induced by Tax
leads to activation of
HIF-1 ... The results of the present study suggest that
PI3K/Akt activation
induced by
Tax leads to activation of HIF-1
Usluoglu et al., Eur J Immunol 2007
:
Different signal pathways mediate LPS induced expression of
IL-12 and
involve PI3K , MAPK and the transcription factor NF-kappaB
Caravatta et al., J Cell Physiol 2008
(Leukemia...) :
PI3-K/Akt dependent
activation of
cAMP-response element binding ( CREB ) protein in Jurkat T leukemia cells treated with TRAIL
Doepfner et al., Leukemia 2007
(Acute Disease...) :
Moreover, downregulation of the class Ia
PI3K isoforms p110beta and p110delta by RNA interference
impaired IGF-I stimulated
Akt activation, cell growth and survival in AML cells
Papakonstanti et al., EMBO J 2007
:
We now show that this relationship is in fact bidirectional, whereby
PI3K reciprocally
controls PTEN ... We report that the p110delta
PI3K negatively
regulates PTEN , through a pathway involving inhibition of RhoA ... This work identifies the RhoA/ROCK pathway as a major target of
p110delta mediated
PI3K signalling, and establishes for the first time that PI3K controls itself, via a feedback loop involving PTEN
Kato et al., Am J Physiol Lung Cell Mol Physiol 2007
(Inflammation) :
We conclude that whereas
PI3K is downstream of MUC1 activation and negatively
regulates TLR5 signaling, it is not responsible for MUC1 induced suppression of TLR5 signaling
Carelli et al., Mol Med 2007
(Angiomyolipoma...) :
Interestingly, single or simultaneous inhibition of
PI3K by LY294002 and ERK by PD98059 does not
prevent IGF-1 mediated survivin expression
Miyazaki et al., Am J Physiol Cell Physiol 2007
:
Moreover, Akt phosphorylation downstream of
PI3K , which was elicited by shear, was
attenuated by neomycin but not by
calpain inhibitor ( calpeptin )
Song et al., Gut 2007
(Adenocarcinoma...) :
Dominant negative ( DN )
AKT and LY294002 (
PI3K inhibitor ) or U0126 ( MEK-1/2 inhibitor ) blocked chenodeoxycholic acid ( CD ) and deoxycholic acid ( DC ) mediated COX-2 induction ... Unconjugated bile acids
induce CREB and AP-1 dependent COX-2 expression in Barrett 's oesophagus and OA through ROS mediated activation of
PI3K/AKT and ERK1/2 ... Unconjugated bile acids
induce CREB and
AP-1 dependent COX-2 expression in Barrett 's oesophagus and OA through ROS mediated activation of
PI3K/AKT and ERK1/2 ... Unconjugated bile acids
induce CREB and AP-1 dependent
COX-2 expression in Barrett 's oesophagus and OA through ROS mediated activation of
PI3K/AKT and ERK1/2
Afrasiabi et al., Mol Cell Endocrinol 2007
(Thyroid Neoplasms) :
Taken together,
SPC is an effective suppressor of thyroid cancer cell proliferation and migration, and this effect is, in part,
mediated by inhibition of both the
PI3K-Akt and the MAP kinase signalling pathways
Furuya et al., Mol Cell Biol 2007
(Thyroid Neoplasms) :
Since NCoR is known to modulate the actions of TRbeta mutants in vivo and in vitro, we asked whether
NCoR regulates PV-activated
PI3K signaling ... Overexpression of
NCoR in thyroid tumor cells of TRbetaPV/PV mouse
reduced PI3K signaling, as indicated by the decrease in the phosphorylation of its immediate downstream effector, p-AKT
Estrella et al., Int J Oncol 2007
(MAP Kinase Signaling System...) :
LPA stimulation of ovarian cancer cells markedly
increased the phosphorylation and activity of p38 ( MAPK ), p42/p44(MAPK), and
PI3K
Nurieva et al., J Immunol 2007
:
We found that
CD28 and ICOS
regulate sustained
PI3K activity in primary T cells, which is required for NFATc1 up-regulation ... We found that CD28 and
ICOS regulate sustained
PI3K activity in primary T cells, which is required for NFATc1 up-regulation ... Costimulation of T cells potentiated transcription of the
Nfatc1 gene P1 promoter in a
PI3K dependent manner
Tang et al., J Immunol 2007
:
Leptin mediated
IL-6 production was
attenuated by OBRl receptor antisense oligonucleotide,
PI3K inhibitor ( Ly294002 and wortmannin ), Akt inhibitor ( 1L-6-hydroxymethyl-chiro-inositol-2- ( ( R ) -2-O-methyl-3-O-octadecylcarbonate ) ), NF-kappaB inhibitor ( pyrrolidine dithiocarbamate ), IkappaB protease inhibitor ( L-1-tosylamido-2-phenylenylethyl chloromethyl ketone ), IkappaBalpha phosphorylation inhibitor ( Bay 117082 ), or NF-kappaB inhibitor peptide
Hu et al., Diabetes 2007
(Diabetes Mellitus, Experimental) :
In cultured C2C12 myotubes, acute suppression of
PI3K activity
led to decreased
PTEN expression, while palmitic acid increased PTEN in myotubes in a p38 dependent fashion
Oka et al., J Invest Dermatol 2008
(Melanoma...) :
Furthermore, the introduction of PKC-betaII suppressed
HGF induced activation of
PI3K , and attenuated the in vitro invasion activity of the melanoma cells
Mainou et al., J Virol 2007
(Cell Transformation, Viral...) :
CTAR1 is necessary for
LMP1 mediated transformation as well as activation of
PI3K signaling and induction of cell cycle markers associated with G ( 1 ) /S transition
Nakamura et al., Rheumatol Int 2007
(Sjogren's Syndrome) :
EGF activates
PI3K-Akt and NF-kappaB via distinct pathways in salivary epithelial cells in Sjögren 's syndrome ... Chemical inhibition of
PI3K-Akt by LY294002/wortmannin did not affect EGF mediated NF-kappaB p65 nuclear translocation ; and
NF-kappaB inhibition by Bay 11-7082 did not
suppress Akt phosphorylation ... Chemical inhibition of
PI3K-Akt by LY294002/wortmannin did not affect EGF mediated NF-kappaB p65 nuclear translocation ; and NF-kappaB inhibition by Bay 11-7082 did not
suppress Akt phosphorylation ... Chemical inhibition of
PI3K-Akt by LY294002/wortmannin did not
affect EGF mediated NF-kappaB
p65 nuclear translocation ; and NF-kappaB inhibition by Bay 11-7082 did not suppress Akt phosphorylation
Ramshaw et al., Blood 2007
:
These results reveal a previously unrecognized negative signaling role for Tyr577 in beta ( c ) and demonstrate that uncoupling
Shc from cytokine receptors
enhances PI3K signaling as well as survival and proliferation
Kin et al., J Immunol 2007
:
However, the mechanism by which
CD86 activates
PI3K in a B cell and the relevance of CD86 stimulation in vivo remains unknown
Yang et al., Blood 2007
(Multiple Myeloma) :
This study was undertaken to elucidate the mechanisms underlying
anti-beta2M mAb induced
PI3K/Akt and ERK inhibition and the inability of IL-6 and IGF-I to protect myeloma cells from mAb induced apoptosis
Chavarría et al., Dev Neurobiol 2007
:
Differential, age dependent MEK-ERK and
PI3K-Akt activation by
insulin acting as a survival factor during embryonic retinal development ...
Insulin activated both the
PI3K-Akt and the MEK-ERK pathways
Park et al., J Biol Chem 2007
:
Specifically,
NGF enhanced TrkA phosphorylation,
PI3K activity, and Akt phosphorylation
Tung et al., Cell Signal 2007
:
In this study, we identified a
requirement for PDGFR,
PI3-K/Akt , p38 MAPK, JNK, and NF-kappaB in the regulation of
VCAM-1 expression by rat vascular smooth muscle cells ( VSMCs ) in response to viral infection
Guijarro et al., Carcinogenesis 2007
:
Furthermore, activation of
AKT by MAP17 as measured by Thr308 phosphorylation was
independent of
PI3K activity
Wang et al., Biochem J 2007
:
We have shown previously that PAR-2 simultaneously promotes
Galphaq/Ca2+ dependent activation and beta-arrestin-1 dependent inhibition of class IA
PI3K ( phosphoinositide 3-kinase ), and we sought to characterize further the role of beta-arrestins in the regulation of PI3K activity ... We have shown previously that
PAR-2 simultaneously
promotes Galphaq/Ca2+ dependent activation and beta-arrestin-1 dependent inhibition of class IA
PI3K ( phosphoinositide 3-kinase ), and we sought to characterize further the role of beta-arrestins in the regulation of PI3K activity ... In the present study we have demonstrated that : ( i ) PAR-2 increases p110alpha- and p110beta associated lipid kinase activities, and both p110alpha and p110beta are inhibited by over-expression of either beta-arrestin-1 or -2 ; ( ii ) both beta-arrestin-1 and -2 directly inhibit the p110alpha catalytic subunit in vitro, whereas only beta-arrestin-2 directly inhibited p110beta ; ( iii ) examination of upstream pathways revealed that PAR-2 induced
PI3K activity
required the small GTPase Cdc ( cell-division cycle)42, but not tyrosine phosphorylation of
p85 ; and ( iv ) beta-arrestins inhibit PAR-2 induced Cdc42 activation ... In the present study we have demonstrated that : ( i ) PAR-2 increases p110alpha- and p110beta associated lipid kinase activities, and both p110alpha and p110beta are inhibited by over-expression of either beta-arrestin-1 or -2 ; ( ii ) both beta-arrestin-1 and -2 directly inhibit the p110alpha catalytic subunit in vitro, whereas only beta-arrestin-2 directly inhibited p110beta ; ( iii ) examination of upstream pathways revealed that PAR-2 induced
PI3K activity
required the small GTPase
Cdc ( cell-division cycle)42, but not tyrosine phosphorylation of p85 ; and ( iv ) beta-arrestins inhibit PAR-2 induced Cdc42 activation ... In the present study we have demonstrated that : ( i ) PAR-2 increases p110alpha- and p110beta associated lipid kinase activities, and both p110alpha and p110beta are inhibited by over-expression of either beta-arrestin-1 or -2 ; ( ii ) both beta-arrestin-1 and -2 directly inhibit the p110alpha catalytic subunit in vitro, whereas only beta-arrestin-2 directly inhibited p110beta ; ( iii ) examination of upstream pathways revealed that
PAR-2 induced
PI3K activity required the small GTPase Cdc ( cell-division cycle)42, but not tyrosine phosphorylation of p85 ; and ( iv ) beta-arrestins inhibit PAR-2 induced Cdc42 activation
Luo et al., J Gene Med 2007
(Carcinoma) :
The PKA and
PI3K signal transduction pathways are likely
involved in enhanced
Cx43 expression as inhibitors of these pathways prevented Cx43 upregulation
Elia et al., Biochim Biophys Acta 2007
:
Taken together, we suggest that Shh acts in an autocrinic manner in adult myoblasts, and provide first evidence of a
role for
PI3K/Akt in
Shh signaling during myoblast differentiation
Lee et al., FEBS Lett 2007
:
The enhanced
MMP-2 activity was significantly
attenuated not only by a
PI3K inhibitor but also by an Akt inhibitor
Shao et al., Carcinogenesis 2007
(Adenocarcinoma...) :
Moreover,
OPN expression was strongly increased in Ras induced transformation of intestinal epithelial cells in a
PI3K dependent manner
Jossin et al., Mol Cell Biol 2007
:
We show that the mTor ( mammalian target of rapamycin ) -S6K1 ( S6 kinase 1 ) pathway is activated by Reelin and that this depends on
Dab1 ( Disabled-1 ) phosphorylation and
activation of
PI3K and Akt ( protein kinase B )
Barber et al., J Biol Chem 2007
:
Activation of
PI3K alone is not
sufficient to promote significant membrane translocation of
P-Rex1 ... Co-expression of P-Rex1 with either Gbetagamma or PI3K caused only an insignificant increase in P-Rex1 membrane localization, whereas Gbetagamma and
PI3K together synergistically
caused a robust increase in membrane localized
P-Rex1 to 23 % of the total
Toulany et al., Mol Cancer Res 2007
(Neoplasms) :
Therefore, the role of K-Ras activity for a direct ( i.e., through
activation of
PI3K by
K-Ras ) or an indirect stimulation of PI3K-AKT signaling ( through K-Ras activity dependent EGFR ligand production ) was investigated by means of small interfering RNA and inhibitor approaches as well as ELISA measurements of EGFR ligand production ... Knocking down
K-Ras expression by specific small interfering RNA markedly
affected autocrine production of AREG, but not
PI3K-AKT signaling, after treatment of K-RAS mutated or wild-type cells with EGFR ligands or exposure to ionizing radiation ... These results indicate that
PI3K mediated activation of
AKT in K-RASmt human tumor cells as a function of EGFR ligand or radiation stimulus is independent of a direct function of K-Ras enzyme activity but depends on a K-Ras mediated enhanced production of EGFR ligands ( i.e., most likely AREG ) through up-regulated extracellular signal regulated kinase-1/2 signaling
Tétreault et al., J Cell Physiol 2008
:
Epidermal growth factor receptor dependent
PI3K-activation promotes restitution of wounded human gastric epithelial monolayers ... In conclusion, the present results indicate that
EGFR dependent
PI3K activation promotes restitution of wounded human gastric epithelial monolayers
Luo et al., Eur J Neurosci 2007
(Optic Nerve Injuries) :
In this study we showed that : ( i ) the RGC protection was pathway inhibition dependent ; ( ii ) inhibition of PI3K/akt and
JAK/STAT , but not MEK/ERK, activated macrophages in the eye, ( iii ) macrophage removal from the eye using clodronate liposomes significantly impeded PI3K/akt and JAK/STAT inhibition
induced RGC survival and axon regeneration whereas it only slightly affected MEK/ERK inhibition dependent protection ; ( iv ) in the absence of recruited macrophages in the eye, inhibition of PI3K/akt or JAK/STAT did not influence RGC survival ; and ( v ) strong
PI3K/akt , JAK/STAT and MEK/ERK pathway activities were located in RGCs but not macrophages after ON injury ... In this study we showed that : ( i ) the RGC protection was pathway inhibition dependent ; ( ii ) inhibition of PI3K/akt and JAK/STAT, but not
MEK/ERK , activated macrophages in the eye, ( iii ) macrophage removal from the eye using clodronate liposomes significantly impeded PI3K/akt and JAK/STAT inhibition
induced RGC survival and axon regeneration whereas it only slightly affected MEK/ERK inhibition dependent protection ; ( iv ) in the absence of recruited macrophages in the eye, inhibition of PI3K/akt or JAK/STAT did not influence RGC survival ; and ( v ) strong
PI3K/akt , JAK/STAT and MEK/ERK pathway activities were located in RGCs but not macrophages after ON injury ... In this study we showed that : ( i ) the RGC protection was pathway inhibition dependent ; ( ii ) inhibition of PI3K/akt and
JAK/STAT , but not MEK/ERK, activated macrophages in the eye, ( iii ) macrophage removal from the eye using clodronate liposomes significantly impeded PI3K/akt and JAK/STAT inhibition
induced RGC survival and axon regeneration whereas it only slightly affected MEK/ERK inhibition dependent protection ; ( iv ) in the absence of recruited macrophages in the eye, inhibition of PI3K/akt or JAK/STAT did not influence RGC survival ; and ( v ) strong
PI3K/akt , JAK/STAT and MEK/ERK pathway activities were located in RGCs but not macrophages after ON injury
Nie et al., Mech Dev 2007
:
PI3K and Erk MAPK
mediate ErbB signaling in Xenopus gastrulation
Zhao et al., Biochem Biophys Res Commun 2007
(Diabetes Mellitus...) :
PI3K inhibitor, LY294002
attenuated ghrelin 's inhibitory effect on
caspase-3 activity
Donahue et al., Eur J Immunol 2007
:
We used flow cytometry and magnetic cell sorting to examine the requirement for
PI3K and mTOR in
responses of splenic B cell subsets to
BCR and LPS stimulation ... We used flow cytometry and magnetic cell sorting to examine the requirement for
PI3K and mTOR in
responses of splenic B cell subsets to BCR and
LPS stimulation
Liu et al., Am J Physiol Cell Physiol 2007
(Hypertrophy) :
Ouabain induced activation of
ERK1/2 was
prevented by Src, EGFR, and MEK inhibitors, but not by
PI3K inhibitors
Jana et al., J Immunol 2007
:
Involvement of NF-kappaB activation in LPS-, Abeta-, PrP-, poly IC-, Tat-, and MPP+-, but not IFN-gamma-, induced microglial expression of iNOS and stimulation of IkappaBalpha expression and inhibition of NF-kappaB activation by gemfibrozil via the PI3K pathway suggests that gemfibrozil inhibits the activation of NF-kappaB and the expression of proinflammatory molecules in microglia via
PI3K mediated up-regulation of
IkappaBalpha
Girart et al., J Immunol 2007
(Melanoma) :
Excitingly, IFN-gamma secretion was significantly increased when NK cells were stimulated with poly ( I:C ) or loxoribine and IL-12, and
NKG2D engagement was induced by coculture with MICA+ tumor cells in a
PI3K dependent manner
Endo et al., Cancer Res 2007
:
IGFs and
insulin enhanced the endoplasmic reticulum ( ER ) stress response as monitored by induction of the CCAAT/enhancer binding protein homologous protein ( CHOP ) proteins and the X box protein-1 splicing under hypoxic conditions, and this response was
suppressed by inhibiting
PI3K and mTOR activity
Fang et al., Cell Signal 2007
(Neovascularization, Pathologic...) :
Reconstitution of
PTEN , the molecular
inhibitor of
PI3K in PC-3 cells inhibited angiogenesis and tumor growth
Kim et al., Biol Pharm Bull 2007
:
Water extract of Korean red ginseng stimulates angiogenesis by activating the
PI3K/Akt dependent
ERK1/2 and eNOS pathways in human umbilical vein endothelial cells ... Water extract of Korean red ginseng stimulates angiogenesis by activating the
PI3K/Akt dependent ERK1/2 and
eNOS pathways in human umbilical vein endothelial cells ... Inhibition of
PI3K activity by wortmannin completely
inhibited KRGE induced angiogenesis and phosphorylation of Akt,
ERK1/2 , and eNOS, indicating that PI3K/Akt activation is an upstream event of the KRGE mediated angiogenic pathway ... Inhibition of
PI3K activity by wortmannin completely
inhibited KRGE induced angiogenesis and phosphorylation of
Akt , ERK1/2, and eNOS, indicating that PI3K/Akt activation is an upstream event of the KRGE mediated angiogenic pathway ... Inhibition of
PI3K activity by wortmannin completely
inhibited KRGE induced angiogenesis and phosphorylation of Akt, ERK1/2, and
eNOS , indicating that PI3K/Akt activation is an upstream event of the KRGE mediated angiogenic pathway ... This study demonstrated that KRGE stimulates in vitro and in vivo angiogenesis through the activation of the
PI3K/Akt dependent
ERK1/2 and eNOS signal pathways and their cross talk ... This study demonstrated that KRGE stimulates in vitro and in vivo angiogenesis through the activation of the
PI3K/Akt dependent ERK1/2 and
eNOS signal pathways and their cross talk
Stommel et al., Science 2007
(Brain Neoplasms...) :
We hypothesized that multiple RTKs are coactivated in these tumors and that redundant inputs drive and maintain downstream signaling, thereby limiting the efficacy of therapies targeting single RTKs. Tumor cell lines, xenotransplants, and primary tumors indeed show multiple concomitantly activated RTKs. Combinations of RTK inhibitors and/or RNA interference, but not single agents, decreased signaling, cell survival, and anchorage independent growth even in glioma cells deficient in
PTEN , a frequently inactivated
inhibitor of
PI3K
Tamburini et al., Blood 2008
(Leukemia, Myeloid, Acute) :
This
RAD001 induced
PI3K/Akt up-regulation was due to an up-regulated expression of the IRS2 adaptor
Reséndiz et al., Journal of thrombosis and haemostasis : JTH 2007
:
Akt phosphorylation approximately 60 s after PAR1 stimulation became entirely
dependent on the purinergic receptor P2Y(12) and the activation of
PI3K ... Akt phosphorylation approximately 60 s after PAR1 stimulation became entirely dependent on the
purinergic receptor P2Y(12) and the
activation of
PI3K
Mandl et al., Mol Cell Biol 2007
:
PI3K dependent activation of
Akt is critical for myoblast differentiation induced by serum withdrawal, suggesting that in these cells PI3K signaling is activated in an unconventional manner
Westra et al., Ann N Y Acad Sci 2007
(Arthritis, Rheumatoid) :
The
effect of inhibitors of the
PI3K and the ERK pathway on
HIF-1alpha protein expression was measured ... Furthermore, it was shown that cytokine induced mRNA expression of
HIF-1alpha was
inhibited by the
PI3K inhibitor
Belaiba et al., Mol Biol Cell 2007
(Anoxia) :
Together, these findings provide a novel mechanism in which hypoxia induces HIF-1alpha mRNA expression via the
PI3K/AKT pathway and
activation of
NFkappaB ... Furthermore, inhibition of the phosphatidylinositol 3-kinase (PI3K)/AKT but not extracellular signal regulated kinase 1/2 pathway blocked the hypoxia dependent induction of HIF-1alpha mRNA and HIF-1alpha promoter activity, suggesting involvement of a
PI3K/AKT regulated
transcription factor
Smith et al., Cell Signal 2007
:
Use of second generation inhibitors that can discriminate between individual PI3K isoforms, revealed that PI3Kgamma was the major contributor to
CXCL12 induced migration and
PI3K/Akt signaling ( as assessed by S6 phosphorylation )
Zhao et al., Life Sci 2007
(Hypoxia-Ischemia, Brain...) :
We found that the effect of EA on
TRPM7 was also
inhibited by a
PI3K inhibitor, while an ERK inhibitor had no effect
Martin et al., J Biol Chem 2007
(Hyperplasia) :
Rapamycin inhibits S6K1 dependent IRS-1 serine phosphorylation,
increases IRS-1 protein levels, and promotes association of tyrosine phosphorylated IRS-1 with
PI3K
Iwase et al., Int J Oncol 2007
(Carcinoma, Squamous Cell...) :
We found that two
PI 3-K inhibitors, wortmannin and LY294002, markedly
suppressed the phosphorylation of
Akt in OSCC cells ...
Caspase-3 and -9 inhibitors, but not a caspase-8 inhibitor,
reduced anticancer drug mediated apoptosis in
PI 3-K inhibitor treated OSCC cells, suggesting that the apoptotic pathway induced by the combination of anticancer drug therapy and PI 3-K inhibition may be functionally related to the intrinsic apoptotic pathway in OSCC cells ... Expression of Bcl-2, cellular inhibitor of apoptosis protein-1 (
cIAP-1 ), and X-linked IAP was down-regulated, and expression of Bax was
up-regulated by
PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated ... Expression of Bcl-2, cellular
inhibitor of apoptosis protein-1 ( cIAP-1 ), and X-linked IAP was down-regulated, and expression of Bax was
up-regulated by
PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated ... Expression of Bcl-2, cellular inhibitor of apoptosis protein-1 ( cIAP-1 ), and
X-linked IAP was down-regulated, and expression of Bax was
up-regulated by
PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated ... Expression of Bcl-2, cellular inhibitor of apoptosis protein-1 ( cIAP-1 ), and X-linked IAP was down-regulated, and expression of
Bax was
up-regulated by
PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated ...
Caspase-3 and -9 inhibitors, but not a caspase-8 inhibitor,
reduced anticancer drug mediated apoptosis in
PI 3-K inhibitor treated OSCC cells, suggesting that the apoptotic pathway induced by the combination of anticancer drug therapy and PI 3-K inhibition may be functionally related to the intrinsic apoptotic pathway in OSCC cells ... Expression of
Bcl-2 , cellular inhibitor of apoptosis protein-1 ( cIAP-1 ), and X-linked IAP was down-regulated, and expression of Bax was
up-regulated by
PI 3-K inhibitors, while that of Bcl-xL, Bak and cIAP-2 was not attenuated
Keum et al., Carcinogenesis 2008
:
3MP-ITC activated
ERK1/2 and JNK1/2 and the activation of antioxidant response element ( ARE ) by 3MP-ITC was significantly
attenuated by chemical inhibition of PKC and
PI3K signaling pathways in HepG2C8 cells
Pinheiro da Silva et al., Nat Med 2007
(Escherichia coli Infections...) :
Decreased
PI3K activity inhibits E. coli phagocytosis and
increases TNF-alpha production through
Toll-like receptor 4 ... Decreased
PI3K activity inhibits E. coli phagocytosis and
increases TNF-alpha production through Toll-like receptor 4
Yang et al., Biochem J 2008
(Breast Neoplasms) :
Inhibition of EGFR,
PI3K ( phosphoinositide 3-kinase ; kinases required for Rac activation by HRG ) or MEK [ MAPK ( mitogen activated protein kinase ) /ERK ( extracellular-signal regulated kinase ) kinase ] also
blocked the up-regulation of
cyclin D1 and p21(Cip1) by HRG
Wagner et al., J Am Soc Nephrol 2007
:
Activation of
ERK1/2 is partially
dependent on
PI3-K , and both the PI3-K and MEK-ERK1/2 pathways contribute to PI3-K dependent mitogenesis
Zhang et al., J Immunol 2007
(Body Weight) :
Inflammatory cytokine overexpression by 11betaHSD1 ( -/- ) splnMphi results from an increased activation of NF-kappaB- and MAPK signaling cascades and an attenuated
PI3K dependent
Akt activation
Hehlgans et al., Int J Radiat Biol 2007
:
On the basis of the presented data, a precise correlation of adhesion-, serum- and
PI3K mediated changes in PI3K/AKT and
FAK/Paxillin/p130Cas signaling cascades was not found ... On the basis of the presented data, a precise correlation of adhesion-, serum- and
PI3K mediated changes in
PI3K/AKT and FAK/Paxillin/p130Cas signaling cascades was not found ... On the basis of the presented data, a precise correlation of adhesion-, serum- and
PI3K mediated changes in PI3K/AKT and
FAK/Paxillin/p130Cas signaling cascades was not found ... On the basis of the presented data, a precise correlation of adhesion-, serum- and
PI3K mediated changes in PI3K/AKT and
FAK/Paxillin/p130Cas signaling cascades was not found
Lu et al., Diabetes 2008
(Diabetes Mellitus, Type 2) :
Inhibition of
PI3K with wortmannin or suppression of Akt activation with dominant negative Akt
inhibited FGF2 expression
Liu et al., Pathophysiology : the official journal of the International Society for Pathophysiology / ISP 2007
:
Work with genetic manipulations, as well as pharmacological agents with cell culture models, have demonstrated that the cardiotonic steroid stimulated endocytosis of the plasmalemmal Na/K-ATPase requires caveolin and clathrin as well as the activation of c-Src, transactivation of the
EGFR and
activation of
PI3K
Kim et al., Biogerontology 2008
:
Insulin induced
PI3K/Akt activation is known to inhibit a family of Forkhead transcription factors ( FOXO ), which can lead to increased oxidative stress in several model organisms
Park et al., J Cell Biochem 2008
:
But our study revealed, through p53 mutant-type as well as p53 null cell lines, that neither the
PI3K/Akt nor the p53 signaling pathway is
required for quercetin induced
HIF-1alpha accumulation
Huang et al., J Immunol 2007
:
Requirement for both JAK mediated
PI3K signaling and
ACT1/TRAF6/TAK1 dependent NF-kappaB
activation by IL-17A in enhancing cytokine expression in human airway epithelial cells ... Requirement for both JAK mediated
PI3K signaling and
ACT1/TRAF6/TAK1 dependent NF-kappaB
activation by IL-17A in enhancing cytokine expression in human airway epithelial cells ... Requirement for both
JAK mediated
PI3K signaling and ACT1/TRAF6/TAK1 dependent NF-kappaB activation by IL-17A in enhancing cytokine expression in human airway epithelial cells ... Requirement for both JAK mediated
PI3K signaling and
ACT1/TRAF6/TAK1 dependent NF-kappaB
activation by IL-17A in enhancing cytokine expression in human airway epithelial cells ... However, both JAK inhibitor I and
PI3K inhibitor
had no effect on the DNA binding activities of
p65 and p50 to NF-kappaB consensus sequences
Kim et al., J Immunol 2007
(Asthma...) :
Our results also showed that
PI3K inhibitors or AdPTEN
down-regulated a
transcription factor , NF-kappaB activity, and BAY 11-7085 substantially reduced the increased levels of IL-17 after TDI inhalation ... Our results also showed that
PI3K inhibitors or AdPTEN down-regulated a transcription factor, NF-kappaB activity, and BAY 11-7085 substantially
reduced the increased levels of
IL-17 after TDI inhalation ... Our results also showed that
PI3K inhibitors or AdPTEN
down-regulated a transcription factor,
NF-kappaB activity, and BAY 11-7085 substantially reduced the increased levels of IL-17 after TDI inhalation
Walter et al., Biochem Biophys Res Commun 2008
(Carcinoma, Hepatocellular) :
This suppressive effect of insulin on
SeP expression was
attenuated by inhibitors of
PI3K
Jin et al., J Biol Chem 2008
(Cell Transformation, Neoplastic) :
Here we define some aspects of the molecular mechanisms regulating
TrkC dependent Ras-Erk1/2 and
PI3K/Akt activation ... Suppression of
c-Src by RNA interference in highly metastatic 4T1 mammary cancer cells, which express endogenous TrkC,
resulted in markedly decreased expression of cyclin D1 and suppression of activation of Ras-Erk1/2 and
PI3K-Akt
Hügl et al., JOP : Journal of the pancreas 2007
(Insulinoma) :
PI3'K activation was
essential for
prolactin and glucose stimulated INS-1 cell proliferation
Tucker et al., Cell Signal 2008
:
Inhibition of either Src or FAK activity attenuated both laminin and/or
NGF induced
PI 3-K/Akt and MEK/MAPK signalling pathways, as well as neurite growth
Yu et al., J Neurochem 2008
:
Moreover, SKF83959 treatment significantly inhibited H2O2 activated
glycogen synthase kinase-3beta ( GSK-3beta ) which was associated with the drug 's neuroprotective effect, but this inhibition was
attenuated by SCH23390 and a selective
PI 3-K inhibitor
Di Fulvio et al., Cell Signal 2008
:
Transient expression of PLD2 in COS7 cells with either the WT or with a Y179F mutant, resulted in an increased basal phosphorylation of
AKT in residues T308 and S473, in a
PI3K dependent manner ... Transient expression of
PLD2 in COS7 cells with either the WT or with a Y179F mutant, resulted in an increased basal phosphorylation of AKT in residues T308 and S473, in a
PI3K dependent manner ... PLD2-Y179F caused an increase in phosphorylation of p42/p44
ERK and in the expression of G0/G1 phase transition markers ( p21 CIP, PCNA ), and these effects, too, were
dependent on
PI3K ...
PLD2-Y179F caused an increase in phosphorylation of p42/p44 ERK and in the expression of G0/G1 phase transition markers ( p21 CIP, PCNA ), and these effects, too, were
dependent on
PI3K
Garçon et al., Blood 2008
:
CD28 provides T-cell costimulation and
enhances PI3K activity at the immune synapse independently of its capacity to interact with the p85/p110 heterodimer ... Using a quantitative imaging based assay, we show that the
PI3K activity at the T cell-APC contact area is
dependent on the
p110delta , but not the p110gamma, isoform of PI3K
Sampaio et al., Mol Cell Biol 2008
:
Indeed, by up- and down-regulation of signal strength in different cell lines and through different methods, we observed that Gab1/Shp2 and
Ras/ERK1-2 in concert become independent of PI3K upon strong epidermal growth factor receptor (EGFR) stimulation and
dependent on
PI3K upon limited EGFR activation ... Indeed, by up- and down-regulation of signal strength in different cell lines and through different methods, we observed that
Gab1/Shp2 and Ras/ERK1-2 in concert become independent of PI3K upon strong epidermal growth factor receptor (EGFR) stimulation and
dependent on
PI3K upon limited EGFR activation ... Indeed, by up- and down-regulation of signal strength in different cell lines and through different methods, we observed that
Gab1/Shp2 and Ras/ERK1-2 in concert become independent of PI3K upon strong epidermal growth factor receptor (EGFR) stimulation and
dependent on
PI3K upon limited EGFR activation
Aiba et al., Blood 2008
:
Together, our data suggest that BCAP and CD19 have complementary roles in
BCR mediated
PI3K activation, thereby, at least in part, contributing to B-cell development
Marzec et al., Blood 2008
(Lymphoma, T-Cell, Cutaneous) :
The mTORC1,
PI3K/Akt , and MEK/ERK pathways could also be
activated by
IL-2 in the primary leukemic, mitogen preactivated CTCL cells
Hale et al., J Biol Chem 2008
:
Overall, these data suggest a model by which
NS1 activates
PI3K catalytic activity by masking a normal regulatory element specific to the p85beta inter-SH2 domain
Zhu et al., Kidney Int 2008
:
Stable transfection of rat nephrin in the podocytes with podocin led to nephrin tyrosine phosphorylation,
PI3K dependent phosphorylation of
Akt , increased Rac1 activity, and an altered actin cytoskeleton with decreased stress fibers and increased lamellipodia
Kwon et al., Biochem Biophys Res Commun 2008
:
Moreover, inhibitors of Ras ( sulindac sulfide and farnesyltransferase inhibitor I ) or
PI3K/Akt ( wortmannin ),
reduced the amounts of Akt1 and Ki-Ras in the nucleus as well as partial
NF-kappaB activity
Saffar et al., J Allergy Clin Immunol 2008
:
Phosphatidylinositol 3-kinase and p38 mitogen activated protein kinase
regulate induction of
Mcl-1 and survival in glucocorticoid treated human neutrophils
Nishimoto et al., J Neurosci Res 2008
(Brain Ischemia...) :
These findings suggest that AMPA activates
PI3K-Akt and subsequently
inhibits GSK3beta and that inactivated GSK3beta attenuates glutamate induced caspase-3 cleavage and neurotoxicity
Metlakunta et al., Endocrinology 2008
(Body Weight...) :
Leptin ( ip ) significantly
increased hypothalamic
PI3K activity and phosphorylated signal transducer and activator of transcription 3 ( p-STAT3 ) levels in LFD fed mice but not in DIO mice
Zhang et al., Am J Respir Cell Mol Biol 2008
(MAP Kinase Signaling System) :
Acrolein
induces heme oxygenase-1 through PKC-delta and
PI3K in human bronchial epithelial cells
Burnham et al., Microbiology 2007
:
Western blot analysis revealed that phosphorylation of host-cell
Akt and glycogen synthase kinase-3 ( GSK-3 ) occurs in response to GBS infection, and that this is
mediated upstream by
PI3K ... Western blot analysis revealed that phosphorylation of host-cell Akt and
glycogen synthase kinase-3 ( GSK-3 ) occurs in response to GBS infection, and that this is
mediated upstream by
PI3K
Plum et al., Cell Metab 2007
(Thinness) :
Enhanced
leptin stimulated
Pi3k activation in the CNS promotes white adipose tissue transdifferentiation ... These data provide direct genetic evidence that
leptin stimulated
Pi3k signaling in the CNS regulates energy expenditure via activation of SNA to perigonadal WAT leading to BAT-like differentiation of WAT
Babbin et al., J Immunol 2007
:
Taken together, theses results support a novel role for FPR stimulation in enhancing intestinal epithelial cell restitution through
PI3K dependent activation of Rac1 and
Cdc42 ... Taken together, theses results support a novel role for FPR stimulation in enhancing intestinal epithelial cell restitution through
PI3K dependent activation of
Rac1 and Cdc42
Lambert et al., J Immunol 2007
:
To test the hypothesis that
PI3K , which acts upstream of mammalian target of rapamycin, might also be
involved in LMP1 dependent
IL-10 production, we generated B cell lines expressing signaling-inducible chimeric LMP1 ... Our results show that induced LMP1 signaling elicits both p38- and
PI3K dependent
IL-10 production in EBV- B cells ... We also demonstrate that the LMP1 dependent p38 and
PI3K activation
regulates IL-10 induction through discrete mechanisms ... We also demonstrate that the
LMP1 dependent p38 and
PI3K activation regulates IL-10 induction through discrete mechanisms
Fernández et al., Biochim Biophys Acta 2008
:
We analyzed IGF-I signalling on astrocytes through the canonical phosphatidylinositol 3-kinase (PI3K)/Akt pathway and focused on possible changes in PTEN, a phosphatase that modulates
IGF-I signalling by inhibiting Akt activation and, in turn is positively
regulated by
PI3K ... Subsequent recovery of reduced PTEN required also
activation by
IGF-I of
PI3K to recruit in this case protein kinase A (PKA) which stimulated Egr-1 levels and, consequently PTEN synthesis
Miyamoto et al., Cell Death Differ 2008
:
HK-II contains consensus sequences for phosphorylation by Akt and
LIF treatment
induces PI3K- and Akt dependent HK-II phosphorylation
Koeberle et al., Cell Death Differ 2008
:
NTN
required PI3K activity to upregulate
GLAST-1 and did not affect GLT-1 levels ...
NTN required
PI3K activity to upregulate GLAST-1 and did not affect GLT-1 levels
Raufman et al., J Cell Physiol 2008
(Colonic Neoplasms) :
Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating
EGFR dependent
PI3K/Akt signaling ... Both EGFR kinase and
PI3K inhibitors
attenuated DCT induced Akt phosphorylation and
Akt activation, as demonstrated by reduced phosphorylation of a GSK-3-paramyosin substrate ... DCT induced
PI3K/Akt activation
resulted in downstream phosphorylation of GSK-3 ( Ser ( 21/9 ) ) and
BAD ( Ser ( 136 ) ), and nuclear translocation ( activation ) of NF-kappaB, thereby confirming that DCT induced activation of PI3K/Akt signaling regulates both proproliferative and prosurvival signals ...
DCT induced
PI3K/Akt activation resulted in downstream phosphorylation of GSK-3 ( Ser ( 21/9 ) ) and BAD ( Ser ( 136 ) ), and nuclear translocation ( activation ) of NF-kappaB, thereby confirming that DCT induced activation of PI3K/Akt signaling regulates both proproliferative and prosurvival signals ... Collectively, these results indicate that
DCT induced activation of post-EGFR
PI3K/Akt signaling stimulates both colon cancer cell survival and proliferation
Reddy et al., J Cell Physiol 2008
:
Interleukin-18 stimulates fibronectin expression in primary human cardiac fibroblasts via
PI3K-Akt dependent
NF-kappaB activation
Tu et al., J Biol Chem 2008
:
Inhibition of
CaR expression
blocked the Ca ( 2+ ) ( o ) -induced tyrosine phosphorylation of beta-, gamma-, and p120-catenin, PI3K, and the tyrosine kinase Fyn and the association of Fyn with E-cadherin and
PI3K
Malyala et al., J Comp Neurol 2008
:
We found that the
PI3K inhibitors wortmannin and LY294002 significantly
reduced the estrogen mediated
GABA(B) receptor desensitization in POMC arcuate neurons, suggesting that PI3K signaling is a critical downstream mediator of the estrogen mediated rapid effects
Muñoz-Alonso et al., J Pharmacol Exp Ther 2008
(Melanoma) :
By using inhibitors, we found that JNK and p38 MAPK activation depends on Rac1 but not on phosphatidylinositol 3-kinase (PI3K), whereas
AKT activation is independent of Rac1 but
requires PI3K activity ... Plitidepsin cytotoxicity diminishes by Rac1 inhibition or by the blockage of JNK and p38
MAPK using 4- ( 4-fluorophenyl ) -2- ( 4-methylsulfinylphenyl ) -5- ( 4-pyridyl ) 1H-imidazole ( SB203580 ), but not by
PI3K inhibition using wortmannin or 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 ) ... Plitidepsin cytotoxicity diminishes by
Rac1 inhibition or by the blockage of JNK and p38 MAPK using 4- ( 4-fluorophenyl ) -2- ( 4-methylsulfinylphenyl ) -5- ( 4-pyridyl ) 1H-imidazole ( SB203580 ), but not by
PI3K inhibition using wortmannin or 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 )
Liu et al., PloS one 2007
:
We showed that H ( 2 ) O ( 2 ) induces rCMECs apoptosis mainly through the PI3K/ERK pathway, since a
PI3K inhibitor ( LY294002 )
blocked ERK activation caused by H ( 2 ) O ( 2 ) and a specific inhibitor of MEK ( U0126 ) protected cells from apoptosis
Mehta et al., Growth Factors 2007
(MAP Kinase Signaling System) :
HB-EGF- and EGF induced HUVEC migration and capillary tube formation were
dependent upon activation of
PI3K , MAPK and eNOS ...
HB-EGF- and EGF induced HUVEC migration and capillary tube formation were
dependent upon activation of
PI3K , MAPK and eNOS
Ramos-Nino et al., Molecular cancer 2007
(Mesothelioma) :
Cell lines with
PI3K dependent
Fra-1 expression were SV40 positive and expressed the lowest basal Fra-1 levels
Matsuzaki et al., Am J Respir Cell Mol Biol 2008
:
The activities of
PI3K and AKT were
required for normal
Abca3 gene expression in vitro
Yasui et al., J Vasc Res 2008
:
These data suggest that K ( ATP ) channel activation by
insulin is
mediated by
PI3-K
Xu et al., J Clin Invest 2008
(Seizures...) :
Leptin is a hormone that reduces excitability in some hypothalamic neurons via
leptin receptor activation of the JAK2 and
PI3K intracellular signaling pathways
Fivaz et al., Curr Biol 2008
:
Here, we use live FRET imaging in hippocampal neurons and show that the activity of the small
GTPase HRas , an upstream
regulator of
PI3K , markedly increases in the nascent axonal growth cone upon symmetry breaking
Filiz et al., Int J Biochem Cell Biol 2008
:
Furthermore, CQ inhibited H2O2 mediated up-regulation of
p53 activity in the M17 cells and this was
dependent on
PI3K activation
Kondadasula et al., Blood 2008
:
Studies with specific chemical inhibitors revealed that the activation of
ERK was
dependent on the activation of
PI3-K , whose activation was dependent on Syk, and that sequential activation of these molecules was required for NK cell IFN-gamma production in response to FcR and IL-12 stimulation
Méndez-Samperio et al., Cell Immunol 2007
(Tuberculosis) :
Importantly, the
PI3K activation was
dependent on
SPK
Lau et al., J Immunol 2008
:
We postulated that
Syk regulates
PI3K activation and HRV endocytosis in the airway epithelium ... HRV induced
PI3K activation was
dependent on
Syk ; Syk knockdown by small interfering RNA significantly decreased phosphorylation of the PI3K substrate Akt
Moshal et al., J Cell Physiol 2008
(Hyperhomocysteinemia) :
The result suggested that Hcy downregulated CYP2J2 protein expression and dephosphorylated
PI3K dependent
AKT signal
Lin et al., Toxicol Appl Pharmacol 2008
:
LPS stimulated
Src , PYK2, EGFR, and Akt phosphorylation and VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110 ... LPS stimulated Src, PYK2, EGFR, and Akt phosphorylation and
VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110 ... LPS stimulated Src, PYK2,
EGFR , and Akt phosphorylation and VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110 ... LPS stimulated Src, PYK2, EGFR, and
Akt phosphorylation and VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110 ... LPS stimulated Src,
PYK2 , EGFR, and Akt phosphorylation and VCAM-1 expression were
attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ),
PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110
Irino et al., J Neurosci Res 2008
:
These results indicate that Akt activation is dependent on the
PI3K pathway and a
PLC mediated
increase in intracellular calcium and suggest that Akt activation is involved in ADP induced microglial chemotaxis
Baki et al., J Neurosci 2008
(Alzheimer Disease...) :
Expression of exogenous WT PS1 or constitutively active
Akt in PS1-/- neurons
stimulates PI3K signaling and suppresses both caspase-3 activity and dendrite retraction ... Expression of exogenous WT
PS1 or constitutively active Akt in PS1-/- neurons
stimulates PI3K signaling and suppresses both caspase-3 activity and dendrite retraction ... Familial Alzheimer disease ( FAD ) mutations suppress the ability of PS1 to promote
PI3K/AKT signaling, prevent phosphorylation/inactivation of GSK-3 and
promote activation of
caspase-3
Weisberg et al., Blood 2008
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) :
Potentiation of antileukemic therapies by the dual
PI3K/PDK-1 inhibitor, BAG956 :
effects on
BCR-ABL- and mutant FLT3 expressing cells ... Potentiation of antileukemic therapies by the dual
PI3K/PDK-1 inhibitor, BAG956 :
effects on
BCR-ABL- and mutant FLT3 expressing cells ... We investigated the ability of
BAG956 , a dual
PI3K/PDK-1 inhibitor , to be used in combination with inhibitors of BCR-ABL and mutant FLT3, as well as with the mTOR inhibitor, rapamycin, and the rapamycin derivative, RAD001
Sugimoto et al., Leuk Res 2008
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
The Abl kinase inhibitors and
PI3K inhibitor, LY294002,
induced the expression of
HOXA10 , and it enhanced apoptosis in CML cells
Yeh et al., Biochem Pharmacol 2008
(Chondrosarcoma) :
Taken together, these results suggest that the
TGF-beta1 acts through
PI3K/Akt , which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of alphavbeta3 integrins and contributing the migration of chondrosarcoma cells
Yang et al., Life Sci 2008
:
PI3K-GSK3beta signaling may be
responsible for
insulin stimulation of ET-1 production associated with insulin resistance and hyperinsulinemia
Lee et al., Endocrinology 2008
:
Protein kinase C-zeta, a downstream effector of phosphatidylinositol 3-kinase (PI3K), phosphorylates insulin receptor substrate (IRS)-1 on serine residues impairing activation of
PI3K in
response to
insulin ... Significant
insulin stimulated increases in
PI3K activity was coimmunoprecipitated with all IRS isoforms ... In cells overexpressing PKC-zeta there was marked inhibition of
insulin stimulated
PI3K activity associated with IRS-1, -3 and -4 but not IRS-2
Tanabe et al., J Periodontal Res 2008
:
Phosphatidylinositol-3'-kinase inhibitors added during the tolerance-induction period markedly
attenuated the increase in
interleukin-1 beta secretion but had no effect on tumor necrosis factor-alpha
Xing et al., Journal of neuroinflammation 2008
(Encephalitis) :
Elevations of phosphorylated PPAR-gamma, PI3K, and
Akt levels were observed with pioglitazone treatment, and inhibition of
PI3K activity
enhanced LPS induced NO production
Gáspár et al., J Cereb Blood Flow Metab 2008
(Ion Channel Gating) :
Long-term BMS treatment induced a
PI3K dependent increase in the expression and activity of
catalase without affecting manganese SOD and copper/zinc dependent SOD
Autret et al., J Virol 2008
:
JNK inhibition is associated with
PI3K dependent negative regulation of the
apoptosis signal regulating kinase 1 , which acts upstream from JNK in PV-infected IMR5 cells
Yao et al., Ophthalmic Res 2008
:
TGF-beta2 activated
PI3K/Akt in a time dependent manner, but not extracellular signal regulated kinase and p38 MAPK ... The activation of
PI3K/Akt was
necessary for the TGF-beta(2) stimulated downregulation of
connexin 43 , which in turn was necessary for TGF-beta2 induced EMT in HLEB-3 cells
Guiducci et al., J Exp Med 2008
:
PI3K is
critical for the nuclear translocation of
IRF-7 and type I IFN production by human plasmacytoid predendritic cells in response to TLR activation ... We show that
PI3K is
activated by
TLR stimulation in primary human pDCs and demonstrate, using specific inhibitors, that PI3K is required for type I IFN production by pDCs, both at the transcriptional and protein levels
Zhao et al., Biochem Pharmacol 2008
:
In addition, the pharmacological inhibitors of
PI3K ( wortmannin and LY294002 )
enhance phosphorylation of NF-kappaB
p65 on Ser529 and Ser536 residues, which result in enhanced p65 transactivation activity
MacKinnon et al., J Immunol 2008
:
Galectin-3 binds to CD98, and exogenous galectin-3 or cross linking
CD98 with the mAb 4F2
stimulates PI3K activation and alternative activation ...
Galectin-3 binds to CD98, and exogenous galectin-3 or cross linking CD98 with the mAb 4F2
stimulates PI3K activation and alternative activation
Lee et al., Cell cycle (Georgetown, Tex.) 2008
(Prostatic Neoplasms) :
Inhibition of
PI3K with either LY294002 and wortmannin was
sufficient to cause upregulation of
ERK activity as measured by immunoblotting
Brady et al., Growth Horm IGF Res 2008
:
IGF-I and -II
caused significant increases in
PI3-K , but not MAPK, activity ...
IGF-I and -II caused significant increases in
PI3-K , but not MAPK, activity
Schonhoff et al., Hepatology 2008
:
CPT-cAMP stimulated nPKCdelta but not cPKCalpha or nPKCepsilon, and induced
PI3K dependent phosphorylation of
nPKCdelta at Thr ( 505 )
Bradley et al., J Cell Biochem 2008
:
M-CSF activates Ras to coordinate activation of PI3K and
Raf/MEK/ERK , since Ras inhibition decreased PI3K activation and
PI3K inhibition did not
block M-CSF mediated Ras activation
Kang et al., Oncogene 2008
(Neovascularization, Pathologic...) :
N-myc is a novel regulator of
PI3K mediated VEGF expression in neuroblastoma ... Our results show that N-myc plays an important role in the
PI3K mediated
VEGF regulation in NB cells
Wunderlich et al., Exp Dermatol 2008
:
Our findings indicate the
involvement of
PI3K in UVB mediated
HIF-1alpha upregulation
Banerjee et al., Biochemistry 2008
(Breast Neoplasms) :
Neutralization of VEGF action by its antibody or inhibition of
VEGF induced
PI3K/Akt kinase
activation by wortmannin, a PI3K/Akt specific inhibitor, results in inhibition of VEGF induced hAOSMC migration
Cosker et al., J Cell Sci 2008
:
Regulation of
PI3K signalling by the phosphatidylinositol transfer protein
PITPalpha during axonal extension in hippocampal neurons
Kim et al., Biochem Biophys Res Commun 2008
:
MT-III increased
PI3K/Akt and ERK1/2 phosphorylation according to Western blot analysis
Rafail et al., Thromb Res 2008
(Inflammation...) :
Inhibition studies revealed that the effect of
leptin on TF expression is
mediated , at least in part, by JAK2 and
PI3K
Venkatachalam et al., Am J Physiol Heart Circ Physiol 2008
(Hyperglycemia) :
Resveratrol inhibits high glucose induced
PI3K/Akt/ERK dependent
interleukin-17 expression in primary mouse cardiac fibroblasts ... HG
induces phosphoinositide 3- kinase
[PI3K ; inhibited by adenoviral ( Ad ) .dominant negative ( dn ) PI3Kp85 ], Akt ( inhibited by Ad.dnAkt1 ), and ERK ( inhibited by PD-98059 ) activation and induces IL-17 expression via PI3K -- >
Akt -- > ERK dependent signaling
Ding et al., Exp Cell Res 2008
:
In addition, we have also analyzed the
roles of
PI3K and its downstream kinases Akt and atypical PKC in
TRB3 expression
Bouchard et al., Apoptosis 2008
:
Hence, beta1 integrin/Fak/Src signaling translates into integrated mediating functions of
p38beta activation and
regulation of Bcl-2 homologs by
PI3-K/Akt-1 and MEK/Erk, consequently determining their requirement ( or not ) for survival
Schabbauer et al., Mol Immunol 2008
(Rhabdoviridae Infections) :
TLR4/CD14 mediated
PI3K activation is an essential component of interferon dependent VSV resistance in macrophages ...
TLR4/CD14 mediated
PI3K activation is an essential component of interferon dependent VSV resistance in macrophages
Tsuboi et al., Biochem J 2008
:
Co-expression of CD148 reduced p85 phosphorylation induced by active Src, and
attenuated the increases in
PI3K activity, yet
CD148 did not alter the basal PI3K activity
Wang et al., J Biol Chem 2008
(Ovarian Neoplasms) :
KLF8 promoter activity and mRNA levels are induced by expression of constitutively active ( CA ) phosphatidylinositol 3-kinase (PI3K) or CA-Akt but are
repressed by dominant negative Akt or the
PI3K inhibitor LY294002
Kinderlerer et al., J Biol Chem 2008
:
Although
CD59 induction was
independent of
PI3-K , ERK1/2 and nitric oxide, an RNA interference approach demonstrated dependence upon an ERK5/KLF2 signaling pathway
Wei et al., Am J Physiol Cell Physiol 2008
:
The data illustrated that PD-98059, a MEK ( MAPK kinase ) inhibitor, LY-294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, and H-89, a protein kinase A (PKA) inhibitor, substantially decreased the induction of ODC catalytic activity and ODC mRNA expression induced by IL-4 and IL-13, suggesting positive
regulation of the
ODC gene by ERK,
PI3K , and PKA pathways
Zhu et al., Oncogene 2008
(Prostatic Neoplasms) :
In our previous study, we found that inhibition of
PI3K activity
suppressed the
androgen receptor (AR) mediated gene expression in prostate cancer cells
Dufour et al., Bone 2008
:
Biochemical and molecular analyses revealed that the attenuated
PI3K signaling induced by FGFR2 activation is
due to increased
Cbl-PI3K molecular interaction mediated by the Cbl Y731 residue, which results in increased PI3K ubiquitination and proteasome degradation ... Biochemical and molecular analyses revealed that the attenuated
PI3K signaling
induced by
FGFR2 activation is due to increased Cbl-PI3K molecular interaction mediated by the Cbl Y731 residue, which results in increased PI3K ubiquitination and proteasome degradation
Watanabe et al., Pancreas 2008
:
The
role of
PI3K in
PDX-1 expression and duct cell differentiation with pancreatic regeneration in mice after partial pancreatectomy ( Px ) was examined using either wortmannin, a pharmacological PI3K inhibitor, or small interfering RNA directed to the p85alpha regulatory subunit of PI3K
Hill et al., J Clin Invest 2008
(Body Weight) :
Acute effects of
leptin require
PI3K signaling in hypothalamic proopiomelanocortin neurons in mice ... It has been proposed that
leptin action
requires PI3K activity
Lee et al., Int Immunopharmacol 2008
:
Interestingly, emodin induced the activation of phosphatidylinositol 3-kinase (PI3K), Akt and mitogen activated protein ( MAP ) kinases, but those inductions by emodin were completely inhibited by the PI3K inhibitor, LY294002, suggesting that the up-regulation of
BMP-2 by emodin could be
mediated through the activation of both Akt and MAP kinases by activating
PI3K ... Interestingly, emodin induced the activation of phosphatidylinositol 3-kinase (PI3K),
Akt and mitogen activated protein ( MAP ) kinases, but those inductions by emodin were completely
inhibited by the
PI3K inhibitor, LY294002, suggesting that the up-regulation of BMP-2 by emodin could be mediated through the activation of both Akt and MAP kinases by activating PI3K ... Interestingly, emodin induced the activation of phosphatidylinositol 3-kinase (PI3K), Akt and
mitogen activated protein ( MAP ) kinases , but those inductions by emodin were completely
inhibited by the
PI3K inhibitor, LY294002, suggesting that the up-regulation of BMP-2 by emodin could be mediated through the activation of both Akt and MAP kinases by activating PI3K ... Interestingly, emodin induced the activation of
phosphatidylinositol 3-kinase (PI3K) , Akt and mitogen activated protein ( MAP ) kinases, but those inductions by emodin were completely
inhibited by the
PI3K inhibitor, LY294002, suggesting that the up-regulation of BMP-2 by emodin could be mediated through the activation of both Akt and MAP kinases by activating PI3K
Cao et al., Cancer Lett 2008
(Ovarian Neoplasms) :
EGF plus EGFR inhibitor primed ovarian cancer cells display increased sensitivity to taxol induced cell death, resistant to
EGF induced cell migration and cell proliferation as well as ERK and
PI3K/AKT activation
Bénéteau et al., Mol Cancer Res 2008
:
Herein, we show that inhibition of the
PI3K signal by edelfosine
triggers a
Fas mediated apoptotic signal independently of the Fas/FasL interaction
Zhang et al., Free radical research 2008
:
Protection of chlorophyllin against oxidative damage by inducing HO-1 and
NQO1 expression
mediated by
PI3K/Akt and Nrf2 ... Protection of chlorophyllin against oxidative damage by inducing
HO-1 and NQO1 expression
mediated by
PI3K/Akt and Nrf2 ... In conclusion, this study proved that CHL exerts antioxidant effect by inducing HO-1 and
NQO1 expression
mediated by
PI3K/Akt and Nrf2 ... In conclusion, this study proved that CHL exerts antioxidant effect by inducing
HO-1 and NQO1 expression
mediated by
PI3K/Akt and Nrf2
Yoon et al., Biochem Biophys Res Commun 2008
:
Pharmacologically blocking
PI3K significantly
inhibited Akt and GSK3beta phosphorylation ... Pharmacologically blocking
PI3K significantly
inhibited Akt and
GSK3beta phosphorylation
Romão et al., J Neurochem 2008
:
MAPK ( PD98059 ) and
PI3K ( LY294002 ) inhibitors fully
prevented activation of
GFAP gene promoter by all treatments
Radhakrishnan et al., J Biol Chem 2008
(MAP Kinase Signaling System) :
In contrast to MAPK activation the
role of
Shc in modulating
PI3K in response to IGF-I has not been determined ... In contrast to MAPK activation the role of Shc in modulating
PI3K in
response to
IGF-I has not been determined ... In this study we show that impaired Shc association with Grb2 results in decreased Grb2-p85 association, SHPS-1-p85 recruitment, and
PI3K activation in
response to
IGF-I ... Cellular exposure to 25 mm glucose, which is required for Shc phosphorylation in response to IGF-I, resulted in enhanced Grb2 binding to p85,
activation of
PI3K activity, and increased
AKT phosphorylation as compared with cells exposed to 5 mm glucose ... Cellular exposure to 25 mm glucose, which is required for Shc phosphorylation in response to IGF-I, resulted in enhanced
Grb2 binding to p85,
activation of
PI3K activity, and increased AKT phosphorylation as compared with cells exposed to 5 mm glucose
Hennenlotter et al., Oncol Rep 2008
(Carcinoma, Renal Cell...) :
We concluded that a strong expression of PTEN in renal cell cancer did not block the
PI3K mediated phosphorylation of
Akt in the tumour specimens analysed
Xing et al., American journal of physiology. Renal physiology 2008
:
In contrast, PP1 and
PI3K inhibition
had no effect on cyclin E and
p21 ... These data reveal that Src is a crucial mediator of RPTC proliferation and Src mediated proliferation is associated with
PI3K dependent upregulation of
cyclin D1 and PI3K independent downregulation of p27 and p57
Lim et al., J Neurosci Res 2008
:
Thus, MAPK/ERK dependent p35 up-regulation and MAPK/ERK dependent and
PI3K/Akt dependent
Bcl2 up-regulation contribute to BDNF stimulated neural differentiation and to the survival of differentiated cells
Katsube et al., J Leukoc Biol 2008
:
The studies with pharmacological inhibitors suggest that calpain inhibition mediated
neutrophil migration is
mediated by activation of MEK/ERK, p38, JNK,
PI-3K/Akt , and Rac
Maganto-Garcia et al., Traffic 2008
(Trypanosomiasis) :
Assays carried out using a selective PI3K inhibitor ( LY294002 ) showed that the
PI3K activation is
essential for
Rab5 activation by T. cruzi infection and for the entrance and intracellular replication of T. cruzi in macrophages
Liu et al., Cell Microbiol 2008
(Coxsackievirus Infections...) :
Furthermore, silencing NF-kappaB with siRNAs significantly inhibited the phosphorylation of FAK and Akt, but not their total expression levels, indicating that
NF-kappaB activation is
required for the IGTP induced activation of FAK and
PI3K/Akt
Cheung et al., J Immunol 2008
(AIDS Dementia Complex) :
Using pharmacological inhibitors and small interfering RNA gene knockdown, we demonstrated that concomitant activation of Lyn, Pyk2, and class IA
PI3K are
required for gp120 induced
IL-1beta production
Zhu et al., Mol Cancer Ther 2008
(Acute Disease...) :
Cancer cell growth and progression are associated with high levels of
PI3K/Akt activation by loss of
PTEN expression and the inactivation of p53 by MDM2 overexpression
Lee et al., Mol Cells 2008
(Breast Neoplasms) :
In contrast, the
effect of the
PI3K/Akt inhibitor on
ER alpha was blocked in cells that were treated with LY294002 in the presence of the proteasome inhibitors
Zheng et al., J Immunol 2008
(HIV Infections) :
Late expression of
granulysin by microbicidal CD4+ T cells
requires PI3K- and STAT5 dependent expression of IL-2Rbeta that is defective in HIV infected patients ... We demonstrate that IL-2 initially
requires both STAT5 and
PI3K activation to increase expression of IL-2Rbeta, produce
granulysin , and kill C. neoformans ... We demonstrate that
IL-2 initially
requires both STAT5 and
PI3K activation to increase expression of IL-2Rbeta, produce granulysin, and kill C. neoformans
Wang et al., J Am Chem Soc 2008
:
To explore the specificity of these types of molecules, we have synthesized D-3-deoxydioctanoylphosphatidylinositol ( D-3-deoxy-diC8PI ), D-3,5-dideoxy-diC8PI, and D-3-deoxy-diC8PI-5-phosphate and their enantiomers, characterized their aggregate formation by novel high-resolution field cycling ( 31 ) P NMR, and examined their susceptibility to
phospholipase C (PLC) , their
effects on the catalytic activities of
PI3K and PTEN against diC8PI and diC8PI-3-phosphate substrates, respectively, and their ability to induce the death of U937 human leukemic monocyte lymphoma cells
Akpan et al., Brain Res 2008
(Chagas Disease) :
It also requires
TrkA dependent
PI3K and MAPK/Erk signaling pathways because PDNF stimulation of cholinergic transcripts is abolished by specific pharmacological inhibitors
Codina et al., Gen Comp Endocrinol 2008
:
Metabolic and mitogenic effects of IGF-II in rainbow trout ( Oncorhynchus mykiss ) myocytes in culture and the
role of
IGF-II in the
PI3K/Akt and MAPK signalling pathways
Kang et al., Int J Mol Med 2008
(Cell Transformation, Neoplastic) :
ERK and
PI3K/AKT inhibitors
inhibit ECM induced
ERK , AKT activation and cell proliferation ... ERK and
PI3K/AKT inhibitors
inhibit ECM induced ERK,
AKT activation and cell proliferation
Merino et al., Nephrol Dial Transplant 2008
(Kidney Diseases) :
This inflammatory response was mediated by intracellular signalling
dependent on NF-kappaB, p38 MARK or c-Jun
PI3K but not by
MEK1/2 activation
Sanderson et al., J Neurochem 2008
(Brain Ischemia...) :
We hypothesized that
insulin acts through
PI3-K , Akt, and Bcl-2 family proteins to inhibit cytochrome c release following transient global brain ischemia
McLaughlin et al., J Immunol 2008
(MAP Kinase Signaling System) :
EEA-1 provided a scaffold for recruitment of the p40(phox)-p67(phox) complex and
PI3K dependent
Akt1 phosphorylation of these two phox proteins
Kato et al., Biochem Biophys Res Commun 2008
:
OML induced
ERK phosphorylation was
inhibited by specific inhibitors of
PI3K and SFKs, and OML induced Akt phosphorylation was inhibited by a inhibitor of SFKs ... OML induced ERK phosphorylation was inhibited by specific inhibitors of
PI3K and SFKs, and OML induced
Akt phosphorylation was
inhibited by a inhibitor of SFKs
Chung et al., J Endocrinol 2008
:
Our data also suggest that
PI3K/Akt mediated inactivation of GSK-3beta and stabilization of
beta-catenin contribute to the anti-apoptotic effects of ghrelin
Lankat-Buttgereit et al., Biol Cell 2008
(Diabetes Mellitus, Type 2) :
The enhanced secretion of CgA and Sg II seemed to be mediated by an
activation of protein kinase
Akt via
PI3K ( phosphoinositide 3-kinase )
Shang et al., J Endocrinol 2008
:
Rb(1) induced glucose uptake as well as
GLUT1 and GLUT4 translocations was
inhibited by the
PI3K inhibitor ... Rb(1) induced glucose uptake as well as GLUT1 and
GLUT4 translocations was
inhibited by the
PI3K inhibitor
Sun et al., Proc Natl Acad Sci U S A 2008
:
Consistent with a TSC-Rheb-PLD signaling cascade, AMPK and
PI3K , both established
regulators of
TSC2 , appear to lie upstream of PLD as revealed by the effects of pharmacological inhibitors, and serum activation of PLD is also dependent on amino acid sufficiency
Hwang et al., Toxicol Appl Pharmacol 2008
:
Moreover,
MT-III induces Nrf2 nuclear translocation, which is upstream of MT-III induced HO-1 expression, and
PI3K and ERK1/2 activation, a pathway that is involved in induced Nrf2 nuclear translocation, HO-1 expression and neuroprotection
Ispanovic et al., Am J Physiol Cell Physiol 2008
:
ROCK inhibition rapidly
increased cell surface localization of MT1-MMP and increased
PI3K activity, which was required for MMP-2 activation
Le Guilloux et al., Rev Neurol (Paris) 2008
(Brain Neoplasms...) :
High expression of the EGF receptor by tumor cells,
activation of the
PI3K/Akt and the
Ras/Raf pathways represent interesting targets for new selective drugs under development
Dilly et al., Invest Ophthalmol Vis Sci 2008
(Disease Models, Animal) :
Light stress
induced the activation of
PI3K through activation and binding of
IGF-1R , which leads to activation of the Akt survival pathway in photoreceptors
Park et al., EMBO Rep 2008
:
Reconstitution of MEFs with RIP1 downregulates
p27 ( Kip1 ) levels in a
PI3K dependent manner
Cemeus et al., J Neurooncol 2008
(Brain Neoplasms...) :
Co-expression of EGFRvIII, a constitutively active mutant receptor expressed in 50 % of tumours, and
PTEN , an
inhibitor of
PI3K activity, by glioblastoma cells is associated with clinical response to these EGFR kinase inhibitors
Ki et al., Xenobiotica 2008
:
1. alpha-Lipoic acid ( alpha-LA ) activates antioxidant pathways and exerts insulin-like actions via phosphatidylinositol 3-kinase (PI3K), and previous studies from the authors ' laboratory support the essential role of
PI3K dependent
CCAAT/enhancer binding protein (C/EBP) activation in antioxidant defence responses ... 5. The results demonstrate that alpha-LA induces phase II enzymes via
PI3K dependent
C/EBPalpha and C/EBPbeta activation, and enhances the ability of insulin to promote target gene induction ... 5. The results demonstrate that alpha-LA induces phase II enzymes via
PI3K dependent C/EBPalpha and
C/EBPbeta activation, and enhances the ability of insulin to promote target gene induction
Chan et al., J Biol Chem 2008
(MAP Kinase Signaling System) :
PAK is
regulated by
PI3K , PIX, CDC42, and PP2Calpha and mediates focal adhesion turnover in the hyperosmotic stress induced p38 pathway
Black et al., Toxicol Appl Pharmacol 2008
:
While inhibition of
PI3K suppressed UVB induced
mPGES-1 and CRTH2 expression, JNK inhibition suppressed mPGES-1, PGIS, EP2 and CRTH2, and p38 kinase inhibition only suppressed EP1 and EP2
Huang et al., Int J Cardiol 2009
(Atherosclerosis) :
Metformin inhibits TNF-alpha induced IkappaB kinase phosphorylation, IkappaB-alpha degradation and IL-6 production in endothelial cells through
PI3K dependent
AMPK phosphorylation ... This effect was related to
PI3K dependent
AMPK phosphorylation
Rogers et al., Diabetes 2008
(Adenovirus Infections, Human...) :
In turn, the activation of
PI3K by Ad-36 was
independent of
insulin receptor signaling but dependent on Ras signaling recruited by Ad-36
John et al., Dev Biol 2008
:
Oocyte-specific ablation of Pten resulted in
PI3K induced Akt activation, Foxo3 hyperphosphorylation, and
Foxo3 nuclear export, thereby triggering primordial follicle activation, defining the steps by which the PI3K pathway and Foxo3 control this process ... Oocyte-specific ablation of Pten resulted in
PI3K induced
Akt activation , Foxo3 hyperphosphorylation, and Foxo3 nuclear export, thereby triggering primordial follicle activation, defining the steps by which the PI3K pathway and Foxo3 control this process
Méndez-Samperio et al., Peptides 2008
:
Moreover, there was increased activation of c-Jun N-terminal kinase (JNK) and phosphatidylinositol-3-kinase
(PI3K)/Akt in A549 cells infected with M. bovis BCG, and this JNK and
PI3K activation was
mediated through PKC ... Moreover, there was increased activation of
c-Jun N-terminal kinase (JNK) and phosphatidylinositol-3-kinase (PI3K)/Akt in A549 cells infected with M. bovis BCG, and this JNK and
PI3K activation was
mediated through PKC ... Moreover, there was increased activation of c-Jun N-terminal kinase (JNK) and
phosphatidylinositol-3-kinase (PI3K)/Akt in A549 cells infected with M. bovis BCG, and this JNK and
PI3K activation was
mediated through PKC ... Finally, we found that M. bovis BCG induced
HBD-2 mRNA gene expression in A549 cells was
dependent on JNK, and PI3K determined by real-time PCR analysis, which was attenuated by inhibitors of JNK ( SP600125 and AG126 ), and
PI3K ( wortmannin and Ly294002 )
Pincheira et al., J Immunol 2008
:
Stimulation with
TNF induces a time dependent change in the level of Jak2, c-Src, and
PI3K associated with TNFR1
Ramos-Nino et al., Mol Cancer Ther 2008
:
The novel drug combination of ranpirnase and rosiglitazone is a promising combination to treat cancers with increased
PI3K dependent
Fra-1 expression or Survivin
Rotshenker et al., Glia 2008
(Demyelinating Diseases...) :
S-trans, trans-farnesylthiosalicylic (FTS), which inhibits
Galectin-3/MAC-2 dependent activation of
PI3K through Ras, inhibited phagocytosis ... A role for
Galectin-3/MAC-2 dependent activation of
PI3K through Ras, mostly K-Ras, is thus suggested
He et al., Cancer Res 2008
(Carcinoma, Hepatocellular...) :
PIK3IP1 , a negative
regulator of
PI3K , suppresses the development of hepatocellular carcinoma ...
PIK3IP1 , a negative
regulator of
PI3K , suppresses the development of hepatocellular carcinoma
Palma-Nicolas et al., Biosci Rep 2008
(MAP Kinase Signaling System...) :
Pharmacological analysis revealed that the activation of ` conventional ' PKC isoforms is essential for proliferation, although thrombin induced phosphorylation of
ERK1/2 requires the activation of atypical PKCzeta by
PI3K ... Consistently, thrombin induced
ERK1/2 activation and RPE cell proliferation were
prevented completely by
PI3K or PKCzeta inhibition
Wang et al., J Surg Res 2009
(Breast Neoplasms) :
Moreover, a combination of TZDs and a specific Akt inhibitor may serve as a new approach to target Wnt/beta-catenin directly and via
PI3K/Akt action on
glycogen synthase-3beta
García et al., Leuk Res 2009
(Lymphoma) :
PI3K/Akt inhibition modulates multidrug resistance and
activates NF-kappaB in murine lymphoma cell lines
Zdychová et al., Experimental biology and medicine (Maywood, N.J.) 2008
(Diabetes Mellitus, Type 2...) :
Acute
PI3K inhibition with wortmannin ( 100 mug/kg )
attenuated renal
Akt and mTOR activities in ZO, but not in ZL rats ... Acute
PI3K inhibition with wortmannin ( 100 mug/kg )
attenuated renal Akt and
mTOR activities in ZO, but not in ZL rats
Touré et al., Biochem J 2008
(Ion Channel Gating) :
Finally, we found that blocking
RAGE with anti-RAGE antibodies or
inhibiting PI3K with PI3K inhibitors restored fMLP ( N-formylmethionyl-leucyl-phenylalanine ) -induced neutrophil migration on AGE-collagen
Cao et al., Cell Signal 2008
:
Inhibition of
EGFR also
suppresses UV-induced activation of
PI3K/AKT/mTOR/S6K and NF-kappaB signal transduction pathways
Hui et al., Mol Cell Biol 2008
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
As was the case for FOXO3a, the expression or knockdown of
p110alpha was
sufficient to amplify or reduce
PI3K/Akt activity, respectively
Abair et al., Blood 2008
(Neovascularization, Pathologic) :
Integrin alpha1beta1 dependent endothelial cell proliferation is primarily mediated by ERK activation, whereas migration and tubulogenesis require both p38
MAPK and
PI3K/Akt activation
Hoarau et al., PloS one 2008
(Hypersensitivity...) :
We found that 1 ) the PI3K pathway was positively involved in the prolonged DC survival induced by BbC50sn, LPS and Zymosan in contrast to p38MAPK and GSK3 which negatively regulated DC survival ; 2 ) p38MAPK and PI3K were positively involved in DC maturation, in contrast to ERK and GSK3 which negatively regulated DC maturation ; 3 ) ERK and
PI3K were positively
involved in
DC-IL-10 production, in contrast to GSK3 that was positively involved in DC-IL-12 production whereas p38MAPK was positively involved in both ; 4 ) BbC50sn induced a PI3K/Akt phosphorylation similar to Zymosan and a p38MAPK phosphorylation similar to LPS
Gingerich et al., Neuropharmacology 2008
:
Finally, we demonstrate that Src kinase acts upstream of the PI3K/Akt pathway based on our finding that the selective
Src inhibitor, PP2 ( 10microM ),
blocked the increases in nNOS phosphorylation levels, NO production, and
PI3K/Akt activity induced by ERbeta activation ... Finally, we demonstrate that Src kinase acts upstream of the PI3K/Akt pathway based on our finding that the selective Src inhibitor, PP2 ( 10microM ), blocked the increases in nNOS phosphorylation levels, NO production, and
PI3K/Akt activity
induced by
ERbeta activation
Pan et al., J Agric Food Chem 2008
:
We found that pterostilbene also inhibited
LPS induced
activation of
PI3K/Akt , extracellular signal regulated kinase 1/2 and p38 MAPK ... Taken together, these results show that pterostilbene down
regulates inflammatory
iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NFkappaB by interfering with the activation of
PI3K/Akt/IKK and MAPK ... Taken together, these results show that pterostilbene down
regulates inflammatory iNOS and
COX-2 gene expression in macrophages by inhibiting the activation of NFkappaB by interfering with the activation of
PI3K/Akt/IKK and MAPK
Sun et al., Toxicol Appl Pharmacol 2008
:
These data suggest a possible
role of calcium instead of
PI3K in CT-induced
COX-2 expression in cardiomyocytes
Liu et al., Mol Immunol 2008
:
These results suggest that
NAC activates mainly
PI3K to phosphorylate p65 and subsequently induces DNA binding activity of NF-kappaB, independent of its antioxidative function
Pisitkun et al., American journal of physiology. Renal physiology 2008
(MAP Kinase Signaling System) :
Akt activation was blocked by an inhibitor of
PI3K , LY294002
Tacheau et al., J Cell Physiol 2008
:
Using specific pharmacologic inhibitors for JNK, ERK, p38, and PI3K/AKT signaling pathways, we demonstrated the cooperative
role of p38 and
PI3K/AKT signaling in TGF-beta1 induced
Cx43 expression and gap junctional communication
Liu et al., Neoplasia (New York, N.Y.) 2008
:
On the basis of gene expression array studies, we identified Aurora A as one of the genes
regulated transcriptionally by
Akt inhibitors including Compound A. Inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, either by
PI3K inhibitor LY294002 or by Compound A, dramatically inhibits the promoter activity of Aurora A, whereas the mammalian target of rapamycin inhibitor has little effect, suggesting that Akt might be responsible for up-regulating Aurora A for mitotic progression
Hamamura et al., Cell Biol Int 2008
:
LY294002 did not suppress upregulation of TGFbeta mRNA induced by IGF2, so
IGF2 activates
PI3K and TGFbeta pathways
Creson et al., J Mol Neurosci 2009
(MAP Kinase Signaling System...) :
Evidence for
involvement of ERK,
PI3K , and RSK in induction of
Bcl-2 by valproate
Toulany et al., DNA repair 2008
(MAP Kinase Signaling System) :
PI3K-Akt signaling regulates basal, but MAP-kinase signaling
regulates radiation induced
XRCC1 expression in human tumor cells in vitro ...
XRCC1 expression induced by irradiation, however, was
independent of
PI3K/Akt signaling, but dependent of MAPK-ERK1/2
Snoeks et al., Infect Immun 2008
:
Additionally, inhibition of
PI3K attenuated LPS induced proinflammatory
interleukin-8 (IL-8)
Pan et al., Mol Nutr Food Res 2008
:
We found that 6-shogaol also inhibited
LPS induced
activation of
PI3K/Akt and extracellular signal regulated kinase 1/2, but not p38 mitogen activated protein kinase ( MAPK )
Kuijk et al., Blood 2008
(Mevalonate Kinase Deficiency) :
HMG-CoA reductase inhibition induces IL-1beta release through
Rac1/PI3K/PKB dependent
caspase-1 activation ... Here we show that inhibition of HMG-CoA reductase by simvastatin treatment, mimicking MKD, results in increased
IL-1beta secretion in a
Rac1/PI3K dependent manner ... IL-1beta release is mediated by caspase-1, and simvastatin treatment resulted in increased
caspase-1 activity in a
Rac1/PI3K dependent manner
Sherbakova et al., Mol Biol (Mosk) 2008
(Prostatic Neoplasms) :
Transfection of
PTEN into PTEN-deficient PC3 as well as rapamycin treatment
caused the inhibition of
PI3K/Akt/mTOR signaling and resulted in cell sensitization to the action of doxorubicin and vinblastine
Wang et al., Eur J Pharmacol 2008
:
These results described a novel mechanism by which the activation of
PI3K/Akt -- > NF-kappaB ( p65/p52 ) signaling pathway could
play a role in the
calbindin-D28K expression induced by GDNF
Larrea et al., Mol Cell Biol 2008
:
PI3K/PKB inhibition rapidly
reduced p27pT157 and
p27pT198 and dissociated cellular p27-cyclin D1-Cdk4 ...
PI3K/PKB inhibition rapidly
reduced p27pT157 and p27pT198 and dissociated cellular p27-cyclin D1-Cdk4
Fong et al., J Cell Physiol 2008
(Chondrosarcoma) :
Taken together, these results suggest that the
BMP-2 acts through
PI3K/Akt , which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of beta1 integrin and contributing the migration of human chondrosarcoma cells
Robertson et al., Regul Pept 2009
:
The increased migration and sprouting of endothelial cells, due to resistin, were blocked by wortmannin ( 100 nM ) and LY294002 ( 10 microM ), inhibitors of phosphatidylinositol-3-kinase (PI3K), and accompanied by
PI3K dependent phosphorylation of
Akt ; moreover, while the changes were not associated with altered production of nitric oxide ( NO ), resistin induced angiogenic responses were inhibited by IKK Inhibitor X ( 5 microM ), an inhibitor of activation of nuclear factor (NF)-kappaB
Wee et al., Proc Natl Acad Sci U S A 2008
(Colonic Neoplasms...) :
Down-regulation of
PIK3CA in colorectal cancer cells harboring mutations in PIK3CA
inhibited downstream
PI3K signaling and cell growth
Shair et al., Cancer Res 2008
:
However, constitutive activation of Akt alone did not alter cell growth, suggesting that both
PI3K/Akt and NF-kappaB activation are
required by
LMP1
Chalhoub et al., Annu Rev Pathol 2009
(Cell Transformation, Neoplastic...) :
PTEN regulates
PI3K signaling by dephosphorylating the lipid signaling intermediate PIP ( 3 ), but PTEN may have additional phosphatase independent activities, as well as other functions in the nucleus
Dal Col et al., Cell cycle (Georgetown, Tex.) 2008
(Lymphoma, Mantle-Cell) :
Here we show that inhibition of
PI3-K/Akt induces a 40 % decrease of cyclin D1 half-life as a
result of accumulation of the dephosphorylated/active form of
GSK-3beta within the nucleus, where this kinase can phosphorylate cyclin D1 on Thr286 thereby promoting its nuclear export
Rajalingam et al., PloS one 2008
(Chlamydia Infections...) :
Infection leads to the Raf/MEK/ERK mediated up-regulation and
PI3K dependent stabilization of the anti-apoptotic Bcl-2 family member
Mcl-1
Kim et al., Exp Mol Med 2008
(Ascites...) :
Both
LPA- and AOCP induced MEF cell migration was completely
attenuated by
PI3K inhibitor, LY294002
Ciraolo et al., Science signaling 2008
(Cell Transformation, Neoplastic...) :
Pharmacological and genetic analyses of p110beta function revealed that
p110beta catalytic activity is
required for
PI3K signaling downstream of heterotrimeric guanine nucleotide binding protein ( G protein ) -coupled receptors as well as to sustain long-term insulin signaling
Tabassam et al., Cell Microbiol 2009
:
Pharmacologic inhibitors of PI3K or mitogen activated protein kinase kinase ( MEK ), Akt knock-down and EGFR knock-down showed that H. pylori infection induced the
activation of
EGFR -- >
PI3K -- > PI3K dependent kinase 1 -- > Akt -- > extracellular signal regulated kinase signalling pathways, the inactivation of glycogen synthase kinase 3beta and interleukin-8 production
Abid et al., Arterioscler Thromb Vasc Biol 2008
:
Incubation of human coronary artery endothelial cells with HGF induced prolonged
PI3K/Akt dependent phosphorylation and nuclear exclusion of
FKHR/FOXO1
Choi et al., Stem Cells Dev 2008
(MAP Kinase Signaling System) :
Moreover, the pERK1/2 and pAkt upregulation induced by FGF-2 and -4 were completely abolished by treatment with the
MEK1/2 inhibitor, U0126 and the
PI3K inhibitor , LY294002 ... As a
consequence of
PI3K-Akt and ERK1/2, the upregulation of
c-Jun in the Sca-1 ( + ) BMMSCs, after stimulation with FGF-2 or FGF-4, was observed after 12 and 24 h
Chung et al., Biochem Biophys Res Commun 2008
(MAP Kinase Signaling System) :
The
PI3K inhibitor Wortmannin
suppressed icariin mediated angiogenesis and
Akt and eNOS activation without affecting ERK phosphorylation ... The
PI3K inhibitor Wortmannin
suppressed icariin mediated angiogenesis and Akt and
eNOS activation without affecting ERK phosphorylation
Tang et al., J Steroid Biochem Mol Biol 2008
(MAP Kinase Signaling System) :
Treatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), abolished ER-mediated up-regulation of a CYP7B1 promoter-luciferase reporter in HepG2 cells, whereas overexpression of
PI3K or Akt significantly
increased estrogenic up-regulation of
CYP7B1
Gogishvili et al., Eur J Immunol 2008
:
In p110delta ( D910A/D910A ) transgenic T cells, which are defective in
PI3K activation following
CD28 ligation, proliferation was comparable to that in wild-type cells
Zheng et al., J Neurosci Res 2009
:
Specifically,
PI3K and CaM dependent protein kinase (CaMK) activity were
required for Ca ( 2+ ) -stimulated
Arc transcription through regulating ERK signaling
Esposito et al., Mol Pharmacol 2008
:
However, phosphoinositide dependent kinase-1,
Akt/protein kinase B, and protein kinase Czeta activities were rapidly induced after SR141716 treatment of L6 cells in a
PI3K dependent manner ... However, phosphoinositide dependent kinase-1,
Akt/protein kinase B , and protein kinase Czeta activities were rapidly induced after SR141716 treatment of L6 cells in a
PI3K dependent manner ... However, phosphoinositide dependent kinase-1, Akt/protein kinase B, and
protein kinase Czeta activities were rapidly induced after SR141716 treatment of L6 cells in a
PI3K dependent manner
Soda et al., Cell Signal 2008
:
Previously we and others have shown that
TPO activates
PI3K and Akt and that this pathway is important for megakaryocyte growth
Lu et al., Microvasc Res 2009
(Lung Neoplasms...) :
Furthermore, lenalidomide inhibited
VEGF induced
PI3K-Akt pathway signaling, which is known to regulate adherens junction formation
Zhang et al., J Neuroimmunol 2008
(Disease Models, Animal) :
Our data demonstrated that
TLR4 negatively
regulates PI3K activity in wild type mice, leading to the observed the stress induced immune response ... Therefore, stress modulates the immune system through
TLR4 mediated
PI3K/Akt signaling
Dutta et al., Curr Biol 2008
:
Our data indicate that the Wts-pathway components Yki, Sd, and bantam fail to function in salivary glands and that
Wts regulates salivary gland cell death in a
PI3K dependent manner
Li et al., Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi 2008
(Hypoxia-Ischemia, Brain) :
To investigate the expression of hypoxia inducible factor 1alpha ( HIF-1alpha ) protein and the activation of phosphoinositide 3-kinase/Akt (PI3K/Akt) signaling pathway in neurons under hypoxia ischemia condition, and to elucidate the
role of
PI3K/Akt on
HIF-1alpha regulation in the developing neurons after hypoxia ischemia brain damage ( HIBD )
Li et al., J Neurochem 2008
:
The membrane binding of Akt1 to
rod outer segments (ROS) is insulin receptor
(IR)/PI3K dependent as demonstrated by reduced binding of Akt1 to ROS membranes of photoreceptor-specific IR knockout mice ... The membrane binding of
Akt1 to rod outer segments (ROS) is insulin receptor
(IR)/PI3K dependent as demonstrated by reduced binding of Akt1 to ROS membranes of photoreceptor-specific IR knockout mice
Tachado et al., J Biol Chem 2008
(HIV Infections...) :
Pharmacological inhibition of
PI3K ( LY294002 ) normalized TNF-alpha release in HIV+ macrophages and
augments ERK1/2
mitogen activated protein kinase phosphorylation in response to lipid A. Importantly, HIV+ macrophages demonstrated increased constitutive phosphatidylinositol 3,4,5-trisphosphate formation, increased phosphorylation of downstream signaling molecules Akt and glycogen synthase kinase-3beta ( GSK-3beta ) at Ser9, and reduced PTEN protein expression ... Taken together, these data demonstrate increased constitutive activation of the PI3K signaling pathway in HIV+ macrophages and support the concept that
PI3K activation ( by HIV proteins such as Nef ) may
contribute to reduced TLR4 mediated
TNF-alpha release in HIV+ human macrophages and impair host cell response to infectious challenge
Tachado et al., PloS one 2008
:
Furthermore,
PI3K activation
led to
Akt stimulation, a serine/threonine kinase, which was also inhibited by wortmannin and LY294002
Sagan et al., Biochem Biophys Res Commun 2008
(Nijmegen Breakage Syndrome) :
We provide evidence that the observed reduced
PI3K activity in NBS lymphoblasts is
caused by an impaired expression of the SFKs
LCK and/or HCK
Holmström et al., Exp Cell Res 2008
(MAP Kinase Signaling System) :
EGF stimulated
Erk1/2 activation
involved Src tyrosine kinases, but not PKC or
PI3K , whereas in PDGF induced Erk1/2 activation, PI3K, PKC ( probably the atypical zeta isoform ) and Src were involved sequentially ... EGF stimulated
Erk1/2 activation
involved Src tyrosine kinases, but not PKC or
PI3K , whereas in PDGF induced Erk1/2 activation, PI3K, PKC ( probably the atypical zeta isoform ) and Src were involved sequentially ... Both
EGF and PDGF
induced PI3K dependent Akt activation that was not involved in Erk1/2 activation ... Both EGF and PDGF induced
PI3K dependent
Akt activation that was not involved in Erk1/2 activation
Han et al., Toxicol Appl Pharmacol 2008
:
Phosphatidylinositol 3 (PI3)-kinase , its downstream signaling molecule, Akt, and mitogen activated protein kinases ( MAPK ) were also significantly
activated by the o, p'-DDT induced
AP-1 and CRE activation
Li et al., J Biol Chem 2008
:
Inhibition of
PI3K or mTOR
reduced the level of
Rap1B , which acts downstream of Rheb and mTOR
Hwang et al., Toxicol Appl Pharmacol 2008
:
Mechanism of phytoestrogen puerarin mediated cytoprotection following oxidative injury :
estrogen receptor dependent up-regulation of
PI3K/Akt and HO-1 ... Also, puerarin mediated increases in
PI3K activation and
HO-1 induction were reversed by co-treatment with ICI 182,780 and pertussis toxin
Song et al., Experimental biology and medicine (Maywood, N.J.) 2008
(Stomach Neoplasms) :
Furthermore,
PI3-K inhibitor LY294002
attenuated OPN mediated
Akt activation
Bedogni et al., J Clin Invest 2008
(Anoxia...) :
Hyperactivated
PI3K/Akt signaling
led to upregulation of
Notch1 through NF-kappaB activity, while the low oxygen content normally found in skin increased mRNA and protein levels of Notch1 via stabilization of HIF-1alpha
Jiang et al., Hepatology 2008
:
We found that
leptin induced the
PI3K dependent activation of Rac1, and that nicotinamide adenine dinucleotide phosphate, reduced form ( NADPH ) oxidase activation was also implicated in this process ... We found that leptin induced the
PI3K dependent activation of
Rac1 , and that nicotinamide adenine dinucleotide phosphate, reduced form ( NADPH ) oxidase activation was also implicated in this process
Matsuda et al., Blood 2009
:
Critical
role of class IA
PI3K for
c-Rel expression in B lymphocytes ... Nevertheless, both
PI3K and Btk are
required for the activation of
NF-kappaB , a critical transcription factor family for B-cell development and function ... The loss of
PI3K activity
results in marked reduction of
c-Rel and to a lesser extent RelA expression ... These results show that the
PI3K mediated control of
c-Rel expression is essential for B-cell functions
Zhang et al., Exp Brain Res 2009
:
The importance of the PI3K pathway was further confirmed by the activation of
Akt and anti-apoptotic Bcl-2 by cryptotanshinone in a
PI3K dependent manner ... The importance of the PI3K pathway was further confirmed by the activation of Akt and anti-apoptotic
Bcl-2 by cryptotanshinone in a
PI3K dependent manner
Kang et al., Eur J Pharmacol 2008
:
In contrast, a JNK 1/2 inhibitor ( SP600125 ) and
PI3K inhibitor ( wortmannin or LY294002 ) did not
block the induction of
IL-6 production by LPS
Graham et al., Prostate 2009
(Neoplasm Metastasis...) :
PI3K/Akt dependent transcriptional regulation and activation of
BMP-2-Smad signaling by NF-kappaB in metastatic prostate cancer cells ...
PI3K/Akt dependent transcriptional regulation and activation of
BMP-2-Smad signaling by NF-kappaB in metastatic prostate cancer cells ...
PI3K/Akt dependent transcriptional regulation and activation of BMP-2-Smad signaling by
NF-kappaB in metastatic prostate cancer cells ... Selective inhibition of
PI3K/Akt suppressed the NF-kappaB induced
BMP-2 promoter activity
Mellgren et al., Circ Res 2008
:
Our data demonstrate that
PDGFRbeta is required for the formation of 2 distinct cVSMC populations and that loss of
PDGFRbeta-PI3K signaling
disrupts epicardial cell migration
Maus et al., Cell Signal 2009
:
It has been shown in several model systems that
Gab/Dos family members may
regulate both the anti-apoptotic
PI3-K/Akt and the mitogenic Ras/MAPK pathways, still their role in B-cells have not been investigated in detail
Melstrom et al., Pancreas 2008
(Pancreatic Neoplasms) :
In addition, the inhibitory
effects of apigenin and the
PI3K inhibitors on
GLUT-1 are similar, indicating that the PI3K/Akt pathway is involved in mediating apigenin 's effects on downstream targets such as GLUT-1
Lesma et al., PloS one 2008
(Lymphangioleiomyomatosis...) :
In TSC2 ( -/- ) ASM cells specific
PI3K inhibitors ( e.g. LY294002, wortmannin ) and Akt1 siRNA
had little effect on S6 and
ERK phosphorylation
Guo et al., Stroke 2009
:
In contrast, neither inhibition of GSK-3beta nor inhibition of
PI3-K had any detectable effects on
VEGF levels in astrocytes
García-Maceira et al., Oncogene 2009
(Carcinoma, Hepatocellular) :
Moreover, silibinin reduced hypoxia induced
vascular endothelial growth factor ( VEGF ) release by HeLa and Hep3B cells, and this effect was
potentiated by the
PI3K/Akt inhibitor LY294002
Jeon et al., Pigment Cell Melanoma Res 2009
:
Stem cell factor induces ERM proteins phosphorylation through
PI3K activation to mediate melanocyte proliferation and migration ... Our results demonstrated that SCF induced ERM proteins phosphorylation on threonine residue and
Rac1 activation in cultured normal human melanocytes through the activation of
PI3K
Bieri et al., Mol Immunol 2009
:
Herewith, we demonstrated that the expression of
VE-cadherin is
dependent on mTOR and
PI3K signaling
Suh et al., J Cell Physiol 2009
:
In addition,
IL-6 increased EGFR/src/FAK,
PI3K/Akt phosphorylation and 2-DG uptake as well as GLUT-2 protein expression, which were blocked by AG 1478 ( EGF receptor inhibitor ), PP2 ( src family of tyrosine kinase inhibitor ), PI3K-specific siRNA, and a Akt inhibitor
Liu et al., Horm Metab Res 2009
:
In summary, these results suggest that visfatin induced
MCP-1 and IL-6 production
involve p38 MAPK,
PI3K , and ERK 1/2 pathways in human umbilical vein endothelial cells as determined by inhibition with specific inhibitors ... In summary, these results suggest that visfatin induced MCP-1 and
IL-6 production
involve p38 MAPK,
PI3K , and ERK 1/2 pathways in human umbilical vein endothelial cells as determined by inhibition with specific inhibitors
Kim et al., Mol Cancer Res 2008
(MAP Kinase Signaling System...) :
Inhibition of
PI3K also
suppressed SEK-1/MKK-4 and JNK activation, Bax and Bak activation, and
Bcl-2 down-regulation ... Inhibition of
PI3K also
suppressed SEK-1/MKK-4 and JNK activation, Bax and Bak activation, and Bcl-2 down-regulation ... Inhibition of
PI3K also
suppressed SEK-1/MKK-4 and JNK activation,
Bax and Bak activation, and Bcl-2 down-regulation
Jensen et al., PloS one 2008
(MAP Kinase Signaling System) :
We conclude that altered
insulin activation of the
PI3K/Akt but not the MAPK pathway precedes and may contribute to development of whole-body insulin resistance and type 2 diabetes in men with LBW
Furuya et al., Steroids 2009
(Thyroid Neoplasms) :
Conversely, lowering cellular
NCoR by siRNA knockdown in tumor cells
leads to over activated
PI3K-AKT signaling to increase cell proliferation and motility
Kuehn et al., J Immunol 2008
(Calcium Signaling...) :
The FcepsilonRI dependent
activation of
Btk and eicosanoid and ROS generation in bone marrow derived mast cells and human mast cells were similarly blocked by the
PI3K inhibitors, Wortmannin and LY294002, indicating that Btk regulated eicosanoid and ROS production occurs downstream of PI3K
Yan et al., Biochem J 2008
:
The
activation of the AGC ( protein kinase A/protein kinase G/protein kinase C ) -family kinase
SGK1 ( serum- and glucocorticoid induced kinase 1 ) by insulin via
PI3K ( phosphoinositide 3-kinase ) signalling has been appreciated for almost 10 years ... The
activation of the AGC ( protein kinase A/protein kinase G/protein kinase C ) -family kinase SGK1 ( serum- and glucocorticoid induced kinase 1 ) by
insulin via
PI3K ( phosphoinositide 3-kinase ) signalling has been appreciated for almost 10 years
Sun et al., FASEB J 2009
(Inflammation) :
Additionally,
phosphoinositide 3-kinase (PI3K)-Akt was also
activated by
SP/NK-1R in macrophages ... Kinetic analysis indicated that PKC isoforms
induced early
ERK1/2 activation, while
PI3K-Akt contributed to the pathway at later time points
Rosenberger et al., Hum Mutat 2009
(Abnormalities, Multiple...) :
Oncogenic HRAS mutations cause prolonged
PI3K signaling in
response to
epidermal growth factor in fibroblasts of patients with Costello syndrome
Rodríguez-Pérez et al., Int J Biochem Cell Biol 2009
:
Inhibitors of
PI3K and PKC essentially
blocked insulin-,
IGF-I- and EGF induced desensitizations
Howlett et al., PLoS Genet 2008
:
In humans, PI3K and group II mGluRs are implicated in epilepsy, neurofibromatosis, autism, schizophrenia, and other neurological disorders ; however, neither the link between group II mGluRs and PI3K, nor the role of
PI3K dependent regulation of
Foxo in the control of neuronal excitability, had been previously reported
Gayer et al., J Biol Chem 2009
:
Strain
MAPK activation
required PI3K but not AKT ...
PI3K is
required for both
ERK and AKT2 activation, whereas AKT2 is sequentially required for GSK-3beta ...
PI3K is
required for both ERK and
AKT2 activation, whereas AKT2 is sequentially required for GSK-3beta
Eulenfeld et al., J Cell Sci 2009
:
We demonstrate that the presence of
PI3K activity in the cell is not
sufficient for binding
Gab1 to the plasma membrane
Zhang et al., Am J Physiol Cell Physiol 2009
(Diabetes Mellitus...) :
BLX-1002, a novel thiazolidinedione with no PPAR affinity, stimulates AMP activated protein kinase activity, raises cytosolic Ca2+, and enhances glucose stimulated
insulin secretion in a
PI3K dependent manner
Schneider et al., PloS one 2008
:
CTLA-4 ligation
induced PI 3K activation as evidenced by the phosphorylation of PKB/AKT that in turn inactivated GSK-3 ...
CTLA-4 induced
PI 3K and AKT activation also led to phosphorylation of the pro-apoptotic factor BAD as well as the up-regulation of BcL-XL
Zhang et al., Wei Sheng Yan Jiu 2008
:
[
Involvement of EGF receptor and
PI3K in
ICAM-1 expression in human airway epithelial cells exposed to zinc sulfate ] ... The expression of
ICAM-1 mRNA and protein and
activation of epithelial growth factor receptor (EGFR) and
PI3K was determined using PCR and immunoblotting
Martinelli et al., Mol Biol Cell 2009
:
In particular, phosphorylation of
eNOS on S1177 in response to ICAM-1 activation was
regulated by src family protein kinase, rho GTPase, Ca ( 2+ ), CaMKK, and AMPK, but not
Akt/PI3K
Hegner et al., Arterioscler Thromb Vasc Biol 2009
:
We studied
effects of
PI3K/Akt/mTOR signaling on phenotypic modulation of
MSC and VSMC marker expression, including L-type Ca ( 2+ ) channels
Minhajuddin et al., J Biol Chem 2009
:
Stimulation of human vascular endothelial cells with thrombin induced the phosphorylation of
mTOR and its downstream target p70 S6 kinase in a PKC-delta- and
PI3K/Akt dependent manner
Shaw et al., Proc Natl Acad Sci U S A 2008
:
The survival kinase
PI3K/Akt inhibited
Bnip3 expression levels in cells in a manner dependent upon NF-kappaB activation
Szabolcs et al., Am J Pathol 2009
(Disease Progression...) :
Because activation of
PI3K signaling
leads to feedback inhibition of
insulin receptor substrate-2 (IRS2) expression, an upstream activator of PI3K, we therefore anticipated that IRS2 expression would be low in tumors that lack PTEN
Yang et al., Invest Ophthalmol Vis Sci 2009
(Anoxia...) :
Role of
PI3K/Akt and MEK/ERK in mediating hypoxia induced expression of HIF-1alpha and
VEGF in laser induced rat choroidal neovascularization ...
Role of
PI3K/Akt and MEK/ERK in mediating hypoxia induced expression of
HIF-1alpha and VEGF in laser induced rat choroidal neovascularization ... A well established rat model of CNV and cultured human retinal pigment epithelium ( hRPE ) was used to investigate the
role of
PI3K/Akt and MEK/ERK pathways in regulating HIF-1alpha and
VEGF expression in CNV in rat and hRPE under hypoxia by immunohistochemistry, Western blot analysis, real-time PCR, and ELISA ... A well established rat model of CNV and cultured human retinal pigment epithelium ( hRPE ) was used to investigate the
role of
PI3K/Akt and MEK/ERK pathways in regulating
HIF-1alpha and VEGF expression in CNV in rat and hRPE under hypoxia by immunohistochemistry, Western blot analysis, real-time PCR, and ELISA
Yang et al., Microvasc Res 2009
(AIDS Dementia Complex) :
Inhibitors of STAT1, mitogen activated protein kinase kinase ( MEK ) ( PD98059 ), and phosphatidyl inositol 3 kinase
(PI3K) ( LY294002 ),
blocked gp120 induced
STAT1 activation and significantly diminished IL-8-, IL-6-, and gp120 induced monocyte adhesion and migration across in vitro BBB models ... Inhibitors of STAT1, mitogen activated protein kinase kinase ( MEK ) ( PD98059 ), and phosphatidyl inositol 3 kinase
(PI3K) ( LY294002 ), blocked gp120 induced STAT1 activation and significantly
diminished IL-8-,
IL-6- , and gp120 induced monocyte adhesion and migration across in vitro BBB models ... Inhibitors of STAT1, mitogen activated protein kinase kinase ( MEK ) ( PD98059 ), and phosphatidyl inositol 3 kinase
(PI3K) ( LY294002 ), blocked gp120 induced STAT1 activation and significantly
diminished IL-8- , IL-6-, and gp120 induced monocyte adhesion and migration across in vitro BBB models
Brunelli et al., J Steroid Biochem Mol Biol 2009
(Breast Neoplasms) :
These findings suggest that inhibition of
PI(3)K is a novel mechanism which contributes to 8PN activity to inhibit cancer cell survival and
EGF induced proliferation
Plastaras et al., Cancer Biol Ther 2008
(Gastrointestinal Neoplasms) :
PI3K/Akt signaling is
stimulated by
insulin
Brito et al., Atherosclerosis 2009
(Atherosclerosis) :
The activation of
mTOR signaling by oxLDL,
requires the upstream activation of
PI3K and Akt, as assessed by the inhibitory effect of the PI3K inhibitor Ly294002 on mTOR activation and DNA synthesis
Ceschin et al., J Cell Biochem 2009
:
It has been previously demonstrated that
insulin increases the cell surface presentation of LRP1 in adipocytes and hepatocytes, which is mediated by the intracellular
PI(3)K/Akt signaling activation
Binker et al., Biochem Biophys Res Commun 2009
(Neoplasm Invasiveness...) :
Our results also indicate that signaling events downstream of EGF receptor involved
PI3K- and Src dependent
activation of
Rac1 , which mediated the NADPH generated reactive oxygen species responsible for MMP-2 secretion and activation
Yang et al., Proc Natl Acad Sci U S A 2009
:
APC also induced phosphorylation of Ser-9 in
glycogen synthase kinase 3beta ( GSK3beta ), which was
blocked by the
PI3K inhibitor LY294002 ... Thus, we propose that ligation of ApoER2 by APC signals via
Dab1 phosphorylation and subsequent
activation of
PI3K and Akt and inactivation of GSK3beta, thereby contributing to APC 's beneficial effects on cells
Bréchard et al., J Leukoc Biol 2009
:
In contrast to SOCE inhibition, OAG induced
NOX2 activation was
mediated by PKC and
PI3K
Chen et al., Mol Immunol 2009
:
PGN induced
COX-2 expression was
attenuated by a Rac1 dominant negative mutant ( RacN17 ),
PI3K inhibitors ( wortmannin and LY 294002 ), and an Akt inhibitor ( 1L-6-hydroxymethyl-chiro-inositol2- [ ( R ) -2-O-methyl-3-O-octadecylcarbonate ] )
Jutooru et al., Mol Carcinog 2009
(Pancreatic Neoplasms) :
Induction of
NAG-1 in Panc28 cells was p38-MAPK- and
PI3-K dependent but Egr-1 independent, whereas induction in Panc1 cells was associated with activation of p38-MAPK, PI3-K, and p42-MAPK and was only partially Egr-1 dependent
Yamamoto et al., Biomed Res 2008
(Ion Channel Gating) :
These results suggest that the activation of VRAC current requires the presence of intracellular PIP3, that
PI3K mediated increase in
PIP3 level is sufficient to fully activate VRAC current, and that PIP3 alone without osmotic stimulation can not induce VRAC current
Yasuoka et al., Am J Respir Cell Mol Biol 2009
(Fibrosis...) :
Exogenous administration of
IGFBP-5 induced activation of mitogen activated protein kinase ( MAPK ) signaling cascade but not
PI3K in PBMCs. IGFBP-5 induced migration was blocked by the MEK1/2 inhibitor U0126, suggesting that IGFBP-5 induced migration occurs via MAPK activation
Park et al., Biochem Biophys Res Commun 2009
:
HO-1 expression by PGE ( 2 ) was
inhibited by LY294002,
PI3K inhibitor and H89, PKA inhibitor ... HO-1 expression by PGE ( 2 ) was inhibited by LY294002,
PI3K inhibitor and H89,
PKA inhibitor ... Taken together, we conclude that PGE ( 2 )
induces HO-1 protein expression through PKA and
PI3K signaling pathways via EP ( 2 ) receptor in C6 cells
Sly et al., Blood 2009
(Hypothermia) :
Intriguingly, we found, using isoform-specific
PI3K inhibitors, that LPS- or cytosine-phosphate-guanosine induced
interleukin-6 (IL-6) is positively
regulated by p110alpha, -gamma, and -delta but negatively regulated by p110beta ... Intriguingly, we found, using isoform-specific
PI3K inhibitors, that LPS- or cytosine-phosphate-guanosine induced interleukin-6 (IL-6) is positively
regulated by
p110alpha , -gamma, and -delta but negatively regulated by p110beta
Huang et al., Biochem Soc Trans 2009
:
Through negative-feedback mechanisms,
mTORC1 activity
inhibits growth factor stimulation of
PI3K
Liang et al., FEBS J 2009
(Stomach Neoplasms) :
Inhibition of
PI3K/Akt by LY2940002 or Akt siRNA
leads to inhibition of PrP ( C ) -induced drug resistance and
P-gp upregulation in gastric cancer cells, indicating a possible novel mechanism by which PrP ( C ) regulates gastric cancer cell survival
Schulman et al., Curr Hypertens Rep 2009
(Cardiovascular Diseases...) :
In states of insulin resistance,
insulin activation of
PI3K is selectively impaired, whereas the MAPK pathway is spared and activated normally
Balasubramanian et al., Cardiovasc Hematol Agents Med Chem 2009
(Cardiomegaly) :
In pressure overloaded myocardium, adrenergic receptors, growth factor receptors, and integrins are known to activate
mTOR in a
PI3K dependent and/or independent manner with the involvement of specific PKC isoforms
De Santis et al., Oncogene 2009
(Ovarian Neoplasms) :
E-cadherin directly
contributes to
PI3K/AKT activation by engaging the PI3K-p85 regulatory subunit to adherens junctions of ovarian carcinoma cells
Gao et al., Cancer Sci 2009
(Endometrial Neoplasms) :
Leptin induced functional activation of
COX-2 is JAK2/STAT3-, MAPK/ERK-, and
PI3K/AKT dependent , indicating that COX-2 may be a critical factor of endometrial carcinogenesis in obesity
Bouali et al., Cancer Gene Ther 2009
(Prostatic Neoplasms) :
In this study we evaluated whether reintroducing P53 using non-viral gene transfer enhances
PTEN mediated inhibition of
PI3K/AKT signaling by cetuximab in PC3 prostate adenocarcinoma cell line bearing p53 and pten mutations
Berna et al., Cell Signal 2009
(Pancreatic Neoplasms) :
These effects are mediated by
p85 phosphorylation and
activation of
PI3K
Aoki et al., Am J Physiol Endocrinol Metab 2009
:
In the livers of p85alpha-deficient mice, p50alpha played a compensatory role in
insulin stimulated
PI3K activation by binding to insulin receptor substrate (IRS)-1/2 ... In the livers of p85alpha-deficient mice, p50alpha
played a compensatory role in insulin stimulated
PI3K activation by binding to insulin receptor substrate
(IRS)-1/2 ... In the livers of p85alpha-deficient mice, p50alpha
played a compensatory role in insulin stimulated
PI3K activation by binding to insulin receptor substrate
(IRS)-1/2 ...
PI3K activity associated with IRS-1/2 was not
affected by the lack of
p85alpha in the liver ... The absence of an increase in
insulin stimulated
PI3K activation in the liver of p85alpha-deficient mice, unlike the muscles, may be associated with the molecular balance between the regulatory subunit and the catalytic subunit of PI3K
Billottet et al., Cancer Res 2009
(Leukemia, Promyelocytic, Acute) :
In summary, class I
PI3K signaling,
mediated by
p110beta and p110delta, plays an important role in basal and ATRA induced cell survival mechanisms in APL ... In summary, class I
PI3K signaling,
mediated by p110beta and
p110delta , plays an important role in basal and ATRA induced cell survival mechanisms in APL
Fan et al., Science signaling 2009
(Brain Neoplasms...) :
Inhibition of EGFR signaling correlated with decreased abundance of phosphorylated mTOR ( p-mTOR ) and rpS6 ( p-rpS6 ) in cells wild type for the gene encoding
PTEN ( phosphatase and tensin homolog on chromosome 10 ), a negative
regulator of
PI3K
Gayer et al., Am J Physiol Gastrointest Liver Physiol 2009
(Mechanotransduction, Cellular) :
Blocking
PI3K prevented strain stimulated ERK and
p38 phosphorylation ... Blocking
PI3K prevented strain stimulated
ERK and p38 phosphorylation
Kramer et al., Eur J Immunol 2009
:
The limiting
effect of
PI3K on
TNF-alpha production from activated monocytes depended on the decrease of GSK-3beta activity, which significantly reduced the transactivation of NF-kappaB
Méndez-Samperio et al., Cell Immunol 2009
:
Finally, the inhibition of
PI3K affect
NF-kB activation in M. bovis BCG infected cells, indicating that PI3K activity is required for the M. bovis BCG induced activation of NF-kB
Ruhland et al., Exp Parasitol 2009
:
Interestingly, activation of
PI3K/Akt signaling
had differential effects on
ERK and p38 activation ... Interestingly, activation of
PI3K/Akt signaling
had differential effects on ERK and
p38 activation
Kulasekaran et al., Am J Respir Cell Mol Biol 2009
(Idiopathic Pulmonary Fibrosis) :
ET-1 induced activation of
PI3K/AKT is
dependent on
p38 mitogen activated protein kinase ( MAPK ), but not extracellular signal regulated kinase ( ERK ) 1/2, JNK, or transforming growth factor (TGF)-beta1 ... In this study, we show that, although TGF-beta1 induces fibroblast synthesis and secretion of ET-1,
TGF-beta1 activation of
PI3K/AKT is not dependent on ET-1
Alcázar et al., Blood 2009
:
Moreover, deletion of p85beta impaired
CD28 induced intracellular events, including c-CBL and CBL-b down-regulation as well as
PI3K pathway activation
Vagima et al., J Clin Invest 2009
:
Treatment with G-CSF further increased MT1-MMP and decreased
RECK expression in human and murine hematopoietic cells in a
PI3K/Akt dependent manner, resulting in elevated MT1-MMP activity ... Treatment with G-CSF further increased
MT1-MMP and decreased RECK expression in human and murine hematopoietic cells in a
PI3K/Akt dependent manner, resulting in elevated MT1-MMP activity
Nagy et al., J Infect Dis 2009
:
H. pylori enhanced
PI3K-AKT signaling in a Src- and
epidermal growth factor receptor dependent manner, which was also mediated by a functional cag secretion system and peptidoglycan
Sanderson et al., Neurol Res 2009
(Brain Ischemia...) :
Insulin induced
Akt phosphorylation was
suppressed by the
PI3K inhibitor wortmannin ... Insulin induces robust
PI3K dependent phosphorylation of
Akt by 30 minute reperfusion and results in improvement of hippocampal structure and function
Ambesi et al., Mol Cancer Res 2009
:
Both
LPA and S1P
activated PI3K , Ras/ERK, and Rho/Rho kinase pathways, leading to migration, G ( 1 ) -S cell cycle progression, and stress fiber formation, respectively ... Although
LPA and S1P
activated both
PI3K/Akt and Ras/ERK signaling through G ( i ), anastellin inhibited only the Ras/ERK pathway
Hodson et al., Adv Exp Med Biol 2009
:
Although CD40, TLR and cytokines all activate PI3K the
BCR seems especially
dependent upon
PI3K signalling ... Although CD40,
TLR and cytokines all
activate PI3K the BCR seems especially dependent upon PI3K signalling ... The downstream effects of
PI3K may be
mediated to a large extent by activation of
PKB
Ismail et al., Cancer Lett 2009
(Adrenal Cortex Neoplasms...) :
TBX2 was upregulated in a
PI3K dependent manner by growth factors that are tumorigenic for SW13
Takeshima et al., BMC microbiology 2009
(Helicobacter Infections) :
PI3K inhibitor suppressed H. pylori
induced p65 phosphorylation and NF-kappaB transactivation, as well as interleukin-8 expression ...
PI3K inhibitor suppressed H. pylori
induced p65 phosphorylation and NF-kappaB transactivation, as well as
interleukin-8 expression ...
PI3K inhibitor suppressed H. pylori
induced p65 phosphorylation and
NF-kappaB transactivation, as well as interleukin-8 expression
Jerczynska et al., Regul Pept 2009
:
Similarly, CNP and the inhibitors of ERK1/2 ( PD098059 ) and
PI3K ( LY294002 )
attenuated PAI-1 expression induced by TNFalpha
Campos et al., Mol Immunol 2009
:
Endogenous
LTB ( 4 )
contributed to Fc gammaR mediated activation of PKC-alpha, ERK 1/2 and
PI3K , while endogenous cysLTs contributes to activation of PKC-delta, p38 and PI3K
Wang et al., Molecular systems biology 2009
:
We show that, while PI3K signaling is insulated from cross-talk,
PI3K enhances
Erk activation at points both upstream and downstream of Ras
Liu et al., J Cell Biochem 2009
:
A specific
PI3K inhibitor, wortmannin,
blocked Akt phosphorylation and abrogated the beneficial effect of DMOG
Xiao et al., Diabetes Metab Res Rev 2009
:
Taken together, our results demonstrate that
PI3K/Akt mediated upregulation of
DDAH2 expression plays a critical role in visfatin promoted angiogenesis via regulating VEGF dependent pathway
Shineman et al., Biochemistry 2009
:
Since the insulin/IGF-1 signaling pathway is tightly regulated by feedback inhibition pathways, we hypothesized that
myr-Akt overexpression may be
inducing feedback inhibition of
PI3K , resulting in impaired APP trafficking
Koyama et al., Dev Growth Differ 2008
:
However,
FGF7 and FGF10
stimulated phosphorylation of both PLCgamma1 and
PI3K , but elicited only minimal phosphorylation of ERK-1/2
Rotshenker et al., J Mol Neurosci 2009
(Encephalomyelitis, Autoimmune, Experimental...) :
Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging
KRas-GTP dependent
PI3K ( phosphatidylinositol 3-kinase ) activity
Lalioti et al., Proc Natl Acad Sci U S A 2009
:
Insulin activation of
Cdk5 requires
PI3K signaling ...
Insulin activation of Cdk5
requires PI3K signaling
Tamizhselvi et al., J Pharmacol Exp Ther 2009
:
The
PI3K inhibitor LY294002 [ 2- ( 4-morpholinyl ) -8-phenyl-1 ( 4H ) -benzopyran-4-one hydrochloride ] abolished the H ( 2 ) S-mediated activation of AKT and
increases tumor necrosis factor alpha and
interleukin 1beta levels in caerulein treated acinar cells
Hunter et al., J Biol Chem 2009
:
Furthermore, phosphorylation and activation of
PDE3A required the activation of PKC, but not of
PI3K/PKB , mTOR/p70S6K, or ERK/RSK
Uzan et al., PloS one 2009
(MAP Kinase Signaling System) :
In vivo, KGF treatment triggered ductal cell differentiation as revealed by the expression of PDX1 and
Glut2 in a subpopulation of ductal cells via a
PI3K dependent mechanism ... In vivo, KGF treatment triggered ductal cell differentiation as revealed by the expression of
PDX1 and Glut2 in a subpopulation of ductal cells via a
PI3K dependent mechanism
Rubio et al., J Mol Cell Cardiol 2009
(Myocardial Infarction) :
In comparison, overexpression of nuclear targeted
Akt does not
mediate increased translocation of either
PI3K or PDK1 indicating that accumulation of Akt does not drive PI3K or PDK1 into the nuclear compartment
Wheeler et al., Cancer Biol Ther 2009
(Carcinoma, Non-Small-Cell Lung...) :
We now present data that Src family kinases (SFKs) are highly activated in cetuximab-resistant cells and enhance
EGFR activation of HER3 and
PI(3)K/Akt
Kiaer et al., Endocrine 2009
:
In conclusion, it is suggested that albumin may be a survival factor for pancreatic beta cells through scavenging of reactive oxygen species and by
PI3K dependent activation of
Akt
Liu et al., Biochem Biophys Res Commun 2009
(Ovarian Neoplasms) :
We discovered a stem cell factor (SCF) triggered, MEK1 independent, and
PI3K dependent
MAPK activation pathway in the Kit expressing ovarian cancer cell line HEY
Bhattacharjee et al., Biochem Biophys Res Commun 2009
:
These results suggest an important
role of
PI3K/Akt in the regulation of basal
Cx43 expression
Bansal et al., PloS one 2009
:
PIM2 Induced COX-2 and
MMP-9 expression in macrophages
requires PI3K and Notch1 signaling ... PIM2 Induced
COX-2 and MMP-9 expression in macrophages
requires PI3K and Notch1 signaling
Bhaskar et al., Molecular neurodegeneration 2009
:
Finally, our results also demonstrate that Abeta oligomer treated neurons exhibit elevated levels of activated
Akt and mTOR ( mammalian Target Of Rapamycin ) and that
PI3K , Akt or mTOR inhibitors
blocked Abeta oligomer induced neuronal CCEs ... Finally, our results also demonstrate that Abeta oligomer treated neurons exhibit elevated levels of activated Akt and
mTOR ( mammalian Target Of Rapamycin ) and that
PI3K , Akt or mTOR inhibitors
blocked Abeta oligomer induced neuronal CCEs
Kok et al., Trends Biochem Sci 2009
(Neoplasms) :
Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional
regulation of the p110alpha
PI3K gene by FOXO3a, NF-kappaB and
p53 , and of the PI3K regulatory subunits by STAT3, EBNA-2 and SREBP ... Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional
regulation of the p110alpha
PI3K gene by
FOXO3a , NF-kappaB and p53, and of the PI3K regulatory subunits by STAT3, EBNA-2 and SREBP ... Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional
regulation of the p110alpha
PI3K gene by FOXO3a, NF-kappaB and p53, and of the PI3K regulatory subunits by
STAT3 , EBNA-2 and SREBP ... Recently identified mechanisms that control PI3K production include increased gene copy number in cancer, and transcriptional
regulation of the p110alpha
PI3K gene by FOXO3a,
NF-kappaB and p53, and of the PI3K regulatory subunits by STAT3, EBNA-2 and SREBP
Kim et al., Exp Mol Med 2009
:
A chemical inhibitor of MEK1/2 or
PI3K reduced phosphorylation of
ERK or Akt, respectively, and also inhibited CSE mediated MMP-9 induction ... A chemical inhibitor of MEK1/2 or
PI3K reduced phosphorylation of ERK or
Akt , respectively, and also inhibited CSE mediated MMP-9 induction ... A chemical inhibitor of MEK1/2 or
PI3K reduced phosphorylation of ERK or Akt, respectively, and also
inhibited CSE mediated
MMP-9 induction
Yan et al., Biochem Biophys Res Commun 2009
(Carcinoma, Hepatocellular...) :
Hypoxia induced
EMT was
blocked by
PI3K inhibitor LY294002
Fernandez-Vidal et al., Cell cycle (Georgetown, Tex.) 2009
(Lymphoma, Large-Cell, Anaplastic) :
Moreover, similar
PI3K/AKt mediated constitutive expression of
CDC25A takes place down-stream of other hematological oncogenes, including BCR/ABL in Chronic Myeloid Leukemia and FLT3-ITD in Acute Myeloid Leukemia
Rodríguez-Escudero et al., J Biol Chem 2009
:
Phosphatidylinositol 3-kinase dependent activation of mammalian
protein kinase B/Akt in Saccharomyces cerevisiae, an in vivo model for the functional study of Akt mutations ...
Phosphatidylinositol 3-kinase dependent activation of mammalian protein kinase
B/Akt in Saccharomyces cerevisiae, an in vivo model for the functional study of Akt mutations
Gupta et al., Blood 2009
(Lymphoma, Follicular) :
Activation of
PI3K via APRIL results in phosphorylation of
Akt and mammalian target of rapamycin (mTOR) and the mTOR-specific substrates p70S6 kinase and 4E-binding protein 1 in a TACI dependent manner ...
Activation of
PI3K via APRIL results in phosphorylation of Akt and
mammalian target of rapamycin (mTOR) and the mTOR-specific substrates p70S6 kinase and 4E-binding protein 1 in a TACI dependent manner ...
Activation of
PI3K via
APRIL results in phosphorylation of Akt and mammalian target of rapamycin (mTOR) and the mTOR-specific substrates p70S6 kinase and 4E-binding protein 1 in a TACI dependent manner
Cho et al., International journal of molecular sciences 2008
:
This review focuses on the contribution of natural inhibitor or compound in our understanding of the mechanism by which
insulin induces , especially in
PI3K/PDK1/PKB signaling
Watson et al., Arch Dermatol Res 2009
:
PI3K-specific inhibitor LY294002
reduced EGF- and HGF stimulated chemokinesis and chemotaxis on collagen I and fibronectin
Listov-Saabye et al., J Appl Toxicol 2009
(Adenocarcinoma...) :
Also,
PI3K pathway
activation by
insulin was enhanced on a collagen IV surface
García-García et al., J Immunol 2009
:
FcgammaRIIIB induced nuclear phosphorylation of ERK, and of
Elk-1 , was not
affected by Syk,
PI3K , or MEK inhibitors ... FcgammaRIIIB induced nuclear phosphorylation of
ERK , and of Elk-1, was not
affected by Syk,
PI3K , or MEK inhibitors
Miller et al., Cancer Res 2009
(Cell Transformation, Neoplastic...) :
Oncogenic Kras
requires simultaneous
PI3K signaling to induce
ERK activation and transform thyroid epithelial cells in vivo ... Oncogenic
Kras requires simultaneous
PI3K signaling to induce ERK activation and transform thyroid epithelial cells in vivo
Dil et al., Mol Immunol 2009
:
In this study we assess the
role of p110 delta
PI3K in TLR4,
TLR9 , or TLR4+TLR9 mediated B cell responses ... In this study we assess the
role of p110 delta
PI3K in
TLR4 , TLR9, or TLR4+TLR9 mediated B cell responses ... In this study we assess the
role of p110 delta
PI3K in TLR4,
TLR9 , or TLR4+TLR9 mediated B cell responses
Kolliputi et al., Am J Physiol Lung Cell Mol Physiol 2009
(Acute Lung Injury...) :
IL-6 cytoprotection in hyperoxic acute lung injury occurs via
PI3K/Akt mediated
Bax phosphorylation ... Thus IL-6 functions in a cytoprotective manner, in part, by suppressing Bax translocation and dimerization through
PI3K/Akt mediated
Bax phosphorylation
Wu et al., Growth Factors 2008
:
PI3-K blockade downregulated the
CTGF stimulated expressions of phosphorylated
PI3-K , PKB and NF-kappaB but not phosphorylated ERK1/2, partially decreased the expressions of the above chemokines
Utsugi et al., J Immunol 2009
(MAP Kinase Signaling System) :
Knockdown of
PI3K p110alpha by siRNA
reduced LPS induced
IL-12 protein production in both cell types
Isenovic et al., Cell Biol Int 2009
:
Therefore, this investigation used primary cultured rat VSMCs to examine the
role of
PI3K and ERK1/2 in the INS dependent phosphorylation of
cPLA2 and proliferation induced by INS ... Thus, we hypothesized that INS stimulates VSMCs proliferation via a mechanism involving the
PI3K dependent activation of
cPLA2 and release of arachidonic acid ( AA ), which activates ERK1/2 and further amplifies cPLA2 activity
Namkoong et al., Cell Signal 2009
:
Forskolin increases angiogenesis through the coordinated cross-talk of
PKA dependent VEGF expression and Epac mediated
PI3K/Akt/eNOS signaling ... These results suggest that forskolin stimulates angiogenesis through coordinated cross-talk between two distinct pathways,
PKA dependent VEGF expression and Epac dependent ERKactivation and
PI3K/Akt/eNOS/NO signaling
Samarin et al., Journal of cell communication and signaling 2009
:
In endothelial cells
activation of
PI3K -
AKT signaling was inversely related to CCN2 expression
Lee et al., J Cell Physiol 2009
:
Cell adhesion to BM promotes
insulin stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and association of
PI3K with IRS-1, whereas cells cultured on stromal ECM are inefficient in transducing these post-receptor events
Blando et al., Am J Pathol 2009
(Adenocarcinoma...) :
Lesions in both Pten ( +/- ) ; Tsc2 ( +/- ), and Pten ( +/- ) mice exhibited loss of
PTEN expression and
activation of
PI3K signaling
Wee et al., Cancer Res 2009
(Colonic Neoplasms) :
The oncogenic potential of these effector pathways is illustrated by the frequent occurrence of activating mutations in BRAF and PIK3CA as well as loss-of-function mutations in the tumor suppressor
PTEN , a negative
regulator of
PI3K
Gallacher et al., J Physiol 2009
(Influenza, Human) :
This response to virus infection was only partially dependent upon
NS1 mediated activation of
PI3K
Junttila et al., Cancer Cell 2009
(Breast Neoplasms) :
Ligand independent
HER2/HER3/PI3K complex is disrupted by trastuzumab and is effectively
inhibited by the PI3K inhibitor
GDC-0941
Zacharioudaki et al., J Immunol 2009
:
In addition, activation of
PI3K and Akt1 also appeared
necessary for the induction of
IRAK-M by gAd, because treatment of Akt1 ( -/- ) macrophages or pretreatment of macrophages with the PI3K inhibitor wortmannin abolished gAd induced IRAK-M expression
Di Rosa et al., J Cell Biochem 2009
(MAP Kinase Signaling System) :
Prolactin induces chitotriosidase expression in human macrophages through PTK,
PI3-K , and MAPK pathways
Lahusen et al., Breast Cancer Res Treat 2009
(Breast Neoplasms) :
However, AIB1 also affects the growth of hormone independent breast cancer and AIB1 levels are limiting for IGF-1-, EGF- and heregulin stimulated biological responses in breast cancer cells and consequently the
PI3 K/Akt/mTOR and other EGFR/HER2 signaling pathways are
controlled by changes in
AIB1 protein levels
Rudd et al., Immunol Rev 2009
:
We also present recent findings on T-cell receptor interacting molecule ( TRIM ) regulation of CTLA-4 surface expression, and a signaling pathway involving
CTLA-4 activation of
PI3K and protein kinase B (PKB)/AKT by which cell survival is ensured under conditions of anergy induction
Park et al., Cancer Res 2009
(Brain Neoplasms...) :
RIP1 activates
PI3K-Akt via a dual mechanism involving NF-kappaB mediated inhibition of the mTOR-S6K-IRS1 negative feedback loop and down-regulation of PTEN ... Our data suggest that
RIP1 activates
PI3K-Akt using dual mechanisms by removing the two major brakes on PI3K-Akt activity
Mukherjee et al., Cancer Res 2009
(Brain Neoplasms...) :
These in vitro and in vivo data support our hypothesis that EGFRvIII expression promotes
DNA-PKcs activation and DSB repair, perhaps as a
consequence of hyperactivated
PI3K/Akt-1 signaling
Zhang et al., International journal of clinical and experimental medicine 2009
:
The inhibitors of protein tyrosine kinases and
PI3K , genistein and
PI3Kgamma inhibitor II, were used to elucidate the role of protein tyrosine kinase and PI3K in hypoxic modulation of preproET-1 expression
Peairs et al., Clin Exp Immunol 2009
(Lupus Nephritis) :
Mechanistically, AICAR inhibited the
LPS/IFN-gamma stimulated
PI3K/Akt signalling inflammatory cascade but did not affect LPS/IFN-gamma mediated inhibitory kappa B phosphorylation or nuclear factor (NF)-kappaB ( p65 ) nuclear translocation ... Mechanistically, AICAR inhibited the
LPS/IFN-gamma stimulated
PI3K/Akt signalling inflammatory cascade but did not affect LPS/IFN-gamma mediated inhibitory kappa B phosphorylation or nuclear factor (NF)-kappaB ( p65 ) nuclear translocation
San José et al., Free Radic Biol Med 2009
:
Insulin induced O ( 2 ) ( - ) production and
p47(phox) translocation were prevented in the
presence of specific inhibitors of
PI3K and PKC
Wadhone et al., J Immunol 2009
(Leishmaniasis, Visceral) :
Miltefosine induced protein kinase C-dependent and
PI3K dependent
p38MAP kinase phosphorylation and anti-leishmanial function
Jiang et al., J Hepatol 2009
:
The JAK/STAT- and
PI3K/Akt dependent pathways, NF-kappaB activation and expression of the anti-apoptotic proteins
Mcl-1 and A1 were evaluated ... The JAK/STAT- and
PI3K/Akt dependent pathways,
NF-kappaB activation and expression of the anti-apoptotic proteins Mcl-1 and A1 were evaluated ...
PI3K dependent phosphorylation of
Akt depended on NADPH oxidase activity and superoxide production
Li et al., Cancer Lett 2009
(Adenocarcinoma...) :
Arsenic trioxide induces apoptosis and G2/M phase arrest by inducing Cbl to inhibit
PI3K/Akt signaling and thereby
regulate p53 activation
Bellis et al., Arterioscler Thromb Vasc Biol 2009
(Disease Models, Animal...) :
Late ischemic PC protects BAECs against hypoxia through PKA- and
PI3K dependent activation of
Akt
Roesler et al., Peptides 2009
:
These findings provide the first evidence suggesting that
PI3K signaling is
required for
GRPR regulation of CNS function
Kimura et al., Neuroscience 2009
:
Inhibitors of
PI3K ( LY294002 ), Akt ( Akt-I ), and mTOR ( rapamycin )
reduced the GLP-1 induced
GCLc upregulation and its protection against MG-induced PC12 apoptosis
Park et al., Cell Signal 2009
:
In this study, we found that TRAIL inhibited
PI3K/Akt dependent
FoxO phosphorylation and relocated FoxO proteins into the nucleus from the cytosol in activated human hepatic stellate LX-2 cells
O'Neil et al., J Physiol 2009
(Mechanotransduction, Cellular) :
Furthermore, inhibition of
PI3K-PKB activity did not
prevent the activation of
mTOR signalling by ECs, indicating that PI3K-PKB is not part of the upstream regulatory pathway
Petrella et al., Cancer Biol Ther 2009
(Carcinoma, Renal Cell...) :
Activation of
PI3K/Akt/mTOR leads to increased
HIF-1alpha expression in certain cancer cells, supporting the rationale of using mTOR inhibitors as anti-cancer agents
Yamamura et al., Int Arch Allergy Immunol 2009
:
Eotaxin induced production of IL-1beta, IL-6, and
MIP-1beta was significantly
reduced by the MEK inhibitor PD98059, p38 MAPK inhibitor SB203580, or
PI3K inhibitor LY294002 ... Eotaxin induced production of
IL-1beta , IL-6, and MIP-1beta was significantly
reduced by the MEK inhibitor PD98059, p38 MAPK inhibitor SB203580, or
PI3K inhibitor LY294002 ... Eotaxin induced production of IL-1beta,
IL-6 , and MIP-1beta was significantly
reduced by the MEK inhibitor PD98059, p38 MAPK inhibitor SB203580, or
PI3K inhibitor LY294002
Binker et al., Biochem Biophys Res Commun 2009
(Pulmonary Disease, Chronic Obstructive) :
Our results also indicate that signaling events downstream of EGFR involved
PI3K dependent activation of
Rac1 , which mediated the NADPH generated reactive oxygen species responsible for MMP-9 secretion and activation ... Finally, we observed that
EGFR/PI3K/Rac1/NADPH/ROS/MMP-9 regulate
MUC5AC production in LPS challenged NCI-H292 cells
Blalock et al., J Cell Physiol 2009
(Leukemia) :
Increased phosphorylation of
AKT and GSK-3alpha was not
dependent on
PI3K activity ... Increased phosphorylation of AKT and
GSK-3alpha was not
dependent on
PI3K activity ... PKR inhibition augmented levels of p-S473
AKT and p-S21/9 GSK-3alpha/beta in the
presence of the
PI3K inhibitor, LY294002, but was unable to augment GSK-3alpha or beta phosphorylation in the presence of the AKT inhibitor, A443654 ... PKR inhibition augmented levels of p-S473 AKT and p-S21/9
GSK-3alpha/beta in the
presence of the
PI3K inhibitor, LY294002, but was unable to augment GSK-3alpha or beta phosphorylation in the presence of the AKT inhibitor, A443654
Kingham et al., J Cell Sci 2009
:
By comparison, pharmacological inhibition or siRNA mediated knockdown of p110alpha had no effect on mESC self-renewal per se, but instead appeared to reduce proliferation, which was accompanied by inhibition of leukaemia inhibitory factor (LIF) and
insulin induced
PI3K signalling
Yao et al., Clin Cancer Res 2009
(Breast Neoplasms) :
We therefore investigated the combinatorial activity of
GDC-0941 , a novel class I
PI3K inhibitor , with standard-of-care therapies for HER2 amplified breast cancer
Liang et al., J Biol Chem 2009
(Breast Neoplasms) :
Because a substantial percentage of breast tumors have RGS16 mutations and reduced RGS16 protein expression, we investigated the link between
regulation of
PI3K activity by
RGS16 and breast cancer cell growth ... These results suggest that the loss of
RGS16 in some breast tumors
enhances PI3K signaling elicited by growth factors and thereby promotes proliferation and TKI evasion downstream of HER activation
Finkielsztein et al., Biol Cell 2009
:
Altering
PI3K-Akt signalling in zebrafish embryos
affects PTEN phosphorylation and gastrulation
Mortaz et al., Respir Res 2009
:
Moreover,
CSE suppressed
PI3K/Akt signalling in pDC
Baatar et al., Brain Behav Immun 2009
:
Tregs utilize
beta-galactoside binding protein to transiently
inhibit PI3K/p21ras activity of human CD8+ T cells to block their TCR mediated ERK activity and proliferation
Lu et al., Am J Respir Cell Mol Biol 2010
(Neovascularization, Pathologic...) :
Activation of
PI3K/Akt by bleomycin also
led to transcriptional activation and protein expression of hypoxia-inducible factor-1alpha ( HIF-1alpha ) and
vascular endothelial growth factor , which contributed to the fibroproliferative and collagen inducing effects of bleomycin
Zheng et al., J Biol Chem 2009
:
Of particular interest, Klf4 inhibits RAR alpha and PDGFR beta expression while blocking
PI3K and ERK signaling
induced by Am80 and
PDGF-BB , respectively ... The anti-proliferative effects of Klf4 on neointimal formation depend largely on
PDGFR mediated
PI3K signaling without involvement of the RAR alpha activated signaling pathways
Tuo et al., Am J Physiol Cell Physiol 2009
:
Therefore, the possible
involvement of
PI3K in the regulation of cAMP- and cGMP induced duodenal epithelial
CFTR activation was investigated in the present study ... Forskolin and 8-Br-cGMP not only increased the activity of
PI3K but also
induced the phosphorylation of
Akt , a signaling molecule downstream of PI3K, which were again inhibited by wortmannin and LY294002
Shin et al., J Immunol 2009
:
Consistent with this, B. burgdorferi activation of MyD88 or
TLR3/TRIF signaling
resulted in increased activity of
PI3K ... Consistent with this, B. burgdorferi activation of
MyD88 or TLR3/TRIF signaling
resulted in increased activity of
PI3K
Stuart et al., J Clin Endocrinol Metab 2009
:
L6 myoblasts in culture also expressed and translocated GLUT12 in response to insulin, but inhibiting
PI3-K prevented the translocation of GLUT12 and
GLUT4 ... L6 myoblasts in culture also expressed and translocated
GLUT12 in response to insulin, but inhibiting
PI3-K prevented the translocation of GLUT12 and GLUT4 ... Translocation of
GLUT12 in cultured myoblasts was
dependent on activation of
PI3-K
Banerjee et al., Endocrinology 2009
:
Downstream of ERK1/2, CG activates the nuclear
transcription factor , Elk1, also in a
PI3K-MAPK dependent manner
Zhou et al., Cell Mol Immunol 2009
:
PI3K/AKT mediated
p53 down-regulation participates in CpG DNA inhibition of spontaneous B cell apoptosis
Meng et al., Br J Cancer 2009
(Adenocarcinoma...) :
In addition, the
Src inhibitor, PP2,
blocked the phosphorylation of FAK, ERK1/2,
PI3K , and Akt ... The
PI3K inhibitor, LY294002, further
blocked the expression of MMP9 and
RhoA ... The
PI3K inhibitor, LY294002, further
blocked the expression of
MMP9 and RhoA
Fernandes et al., Mol Biol Cell 2009
:
Although Akt is also activated in response to proteasome inactivation, we found that the
PI3K dependent up-regulation of
IL-8 is independent of 3-phosphoinositide dependent protein kinase ( PDK)1 and Akt
Xiao et al., Virology 2009
:
The
PI3K-speci fi c inhibitor, LY294002,
suppressed Akt phosphorylation in a dose dependent manner, suggesting that AcMNPV induced Akt phosphorylation is PI3K dependent
Santos-Sierra et al., EMBO J 2009
:
MyD88 is not
essential for
PI3K activation and Akt phosphorylation ; however, cooperates with Mal for PIP ( 3 ) formation and accumulation at the leading edge
Suzuki et al., J Cell Mol Med 2010
(Endometrial Neoplasms) :
These results indicate cyclin A2 to be involved in the acquisition of aggressive behaviour of tumour cells through the
activation of
PI3K by cyclin A2-induced
periplakin , and to be a promising therapeutic target
Chen et al., Nephron. Experimental nephrology 2009
:
ALD inhibited the activity of
PI3-K/Akt and increased the activation of p38MAPK ...
ALD induces apoptosis in rat podocytes through inhibition of
PI3-K/Akt and stimulation of p38 MAPK signaling pathways
Smith et al., PloS one 2009
(Prostatic Neoplasms) :
Thus, activation of EGFR, GPCRs or
PI3K pathway
leads to
BAD phosphorylation and inhibition of apoptosis
Qin et al., Horm Metab Res 2009
(Disease Models, Animal...) :
Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2,
PI3K and Akt1,
inhibited CD36 , MTTP, and PTEN, and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes ... Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2,
PI3K and Akt1,
inhibited CD36,
MTTP , and PTEN, and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes ... Quantitative real-time PCR assays showed that CE treatment decreased the mRNA expression of IL-1beta, IL-6 and TNF-alpha, improved the mRNA expression of IR, IRS1, IRS2,
PI3K and Akt1,
inhibited CD36, MTTP, and
PTEN , and enhanced the impaired SREBP-1c expression in TNF-alpha treated enterocytes
Jiang et al., Adv Cancer Res 2009
(Neoplasms...) :
PI3K signaling
regulates tumor growth and angiogenesis by activating AKT and other targets, and by inducing HIF-1 and
VEGF expression ...
PI3K signaling
regulates tumor growth and angiogenesis by activating AKT and other targets, and by inducing
HIF-1 and VEGF expression ...
PI3K signaling
regulates tumor growth and angiogenesis by activating
AKT and other targets, and by inducing HIF-1 and VEGF expression
Doan et al., Anticancer Res 2009
(Colorectal Neoplasms) :
Our results identify
TLR4 expression in human CRCs and
activation of
PI3K with LPS treatment
Dai et al., Oncogene 2009
:
Osteopontin induces angiogenesis through activation of
PI3K/AKT and ERK1/2 in endothelial cells ... In turn, OPN induced
VEGF activates
PI3K/AKT and the ERK1/2 pathway as a positive feedback signal
Schild et al., Mol Carcinog 2009
(Carcinoma, Pancreatic Ductal...) :
In this study we demonstrate that
PI3K signaling
controls transcription of the
E2F1 gene and show that E2F1 is essential for S-phase progression of PDAC cells
Yano et al., Biochem J 2009
:
High glucose
induced increases in
PI3K activity, proliferation and
ECM accumulation in mesangial cells
Uranga et al., Toxicological sciences : an official journal of the Society of Toxicology 2009
:
Both
Akt and GSK3beta phosphorylation were
dependent on
PI3K activation ... Both Akt and
GSK3beta phosphorylation were
dependent on
PI3K activation
Bai et al., Int J Cancer 2009
(Cell Transformation, Neoplastic) :
The data further support the conclusion that
NFkappaB activity is
essential for
PI3K- and Akt induced oncogenic transformation
Johnson et al., World J Gastroenterol 2009
(Pancreatic Neoplasms) :
Inhibition of
PI3K with LY294002 suppressed extracellular signal regulated kinase-1 and -2 ( ERK1/2 ) activation in BxPC-3, but
enhanced ERK1/2 activation in PANC-1 cells that express IGFBP-5 ... Inhibition of
PI3K with LY294002
suppressed extracellular signal regulated kinase-1 and -2 ( ERK1/2 ) activation in BxPC-3, but enhanced ERK1/2 activation in PANC-1 cells that express IGFBP-5
Liao et al., Toxicol Lett 2009
:
Cholesterol-3-beta, 5-alpha, 6-beta-triol induced
PI(3)K-Akt-eNOS dependent
cyclooxygenase-2 expression in endothelial cells
Martí-Lliteras et al., Infect Immun 2009
:
Mechanistically, our data showed that
CSE reduced
PI3K signaling activation triggered by NTHI
Uddin et al., Int J Cancer 2010
(Ovarian Neoplasms) :
Cyclooxygenase-2 inhibition
inhibits PI3K/AKT kinase activity in epithelial ovarian cancer
Pan et al., BJU Int 2009
(Urinary Bladder Neoplasms) :
Fibronectin mediated
PI3-K/Akt activation protects T24 cells from MMC induced cell death through inhibition of both caspase-9 and AIF mediated apoptosis and GSK-3beta/cyclin D1 involved G0/G1-phase arrest
Chandras et al., Endocrinology 2009
(MAP Kinase Signaling System) :
ERK1/2 activation results in up-regulation of IL-8 expression, an effect inhibited by the
CRF induced activation of
PI3K/Akt
Li et al., Cancer 2009
(Glioblastoma) :
This stimulation was caused by increased transcription of
ARF6 and by
activation of the MEK/extracellular signal regulated kinase 1 and 2 ( ERK1/2 ) and
PI3K signaling pathways
Kim et al., Am J Chin Med 2009
:
Only LY294002 inhibited Akt activation induced by EGCG, implying that EGCG induced
Akt activation is
PI3K dependent
Elayappan et al., Angiogenesis 2009
:
Of interest, PEDF effectively abrogated
VEGF mediated phosphorylation of
PI3K/Akt
Samaga et al., PLoS Comput Biol 2009
(Liver Neoplasms) :
Our results strongly suggest that the
Rac/Cdc42 induced p38 and JNK cascades are
independent of
PI3K in both primary hepatocytes and HepG2 ... Our results strongly suggest that the
Rac/Cdc42 induced p38 and JNK cascades are
independent of
PI3K in both primary hepatocytes and HepG2
Elsegood et al., Arterioscler Thromb Vasc Biol 2009
:
MEK1/2 and
PI3K activities were also
required for oxLDL induced Bcl-2 and
Bcl-x ( L ) mRNA upregulation ... MEK1/2 and
PI3K activities were also
required for oxLDL induced
Bcl-2 and Bcl-x ( L ) mRNA upregulation
Wu et al., Glia 2010
(Gliosis) :
LPS triggered upregulation of CHL1 expression mediated through translocation of nuclear factor kappaB (NF-kappaB) to the nucleus is blocked by a specific
NF-kappaB inhibitor and by
inhibition of
PI3K , PKCdelta, and ERK1/2 activities, implicating NF-kappaB as a downstream target for upregulation of CHL1 expression ... LPS triggered upregulation of
CHL1 expression mediated through translocation of nuclear factor kappaB (NF-kappaB) to the nucleus is
blocked by a specific NF-kappaB inhibitor and by inhibition of
PI3K , PKCdelta, and ERK1/2 activities, implicating NF-kappaB as a downstream target for upregulation of CHL1 expression
Yu et al., Mol Biol Rep 2010
:
However,
PI3K inhibitor
reduces the increase of phosphorylated
Akt level induced by HGF
Chung et al., FEBS J 2009
:
In addition, the activation of
PI3K significantly
enhanced the 14-3-3 association and cell surface expression of
GPR15 , a G protein coupled receptor which carries an endogenous SWTY-like, C-terminal, 14-3-3 binding sequence and is known to serve as a HIV co-receptor
Ogasawara et al., J Cell Biochem 2009
:
Hemoglobin
induces the expression of
indoleamine 2,3-dioxygenase in dendritic cells through the activation of
PI3K , PKC, and NF-kappaB and the generation of reactive oxygen species
Roman et al., Mol Cell Endocrinol 2010
:
Central
leptin action
requires PI3K activity to modulate glucose homeostasis and peripheral metabolism
Gurunathan et al., Biomaterials 2009
:
To understand the underlying mechanism of Ag-NPs on the inhibitory effect of angiogenesis, we showed that
Ag-NPs could
inhibit the activation of
PI3K/Akt
Kim et al., J Biol Chem 2009
:
In addition, GPVI induced
Akt phosphorylation in the presence of ADP antagonists was completely
inhibited by
PI3K inhibitor LY294002 and PI3Kbeta inhibitor TGX-221 indicating an essential role of PI3Kbeta in Akt activation directly downstream of GPVI
Choi et al., Photochem Photobiol 2009
:
The TE mRNA increase required activation of
Smad4 , shown using Smad4 siRNA, and also
involved the ERK1/2, p38 and JNK MAP kinases but not
PI3K
Cheng et al., J Cell Physiol 2009
:
PI3K/AKT regulates
aggrecan gene expression by modulating Sox9 expression and activity in nucleus pulposus cells of the intervertebral disc ...
PI3K/AKT regulates aggrecan gene expression by modulating
Sox9 expression and activity in nucleus pulposus cells of the intervertebral disc ... Expression of constitutively active ( CA )
-PI3K significantly
induced aggrecan promoter activity ... We observed that PI3K maintained Sox9 gene expression and activity : inhibition of
PI3K/AKT resulted in decreased
Sox9 expression, lowered promoter activity, and mediated a reduction in Sox9 transcriptional activity ... Results of these studies demonstrate for the first time that
PI3K/AKT signaling
controls aggrecan gene expression, in part by modulating Sox9 expression and activity in cells of the nucleus pulposus
Chang et al., Pharmacol Res 2009
:
Moreover, PKC-alpha and
PI3K signal might be
involved in YC-1 induced
Raf-1 activation
Ufer et al., Br J Pharmacol 2009
:
Beta(3)-adrenoceptor treatment activated Akt although
PI3K was not
involved in
beta(3)-adrenoceptor up-regulation
Hubchak et al., American journal of physiology. Renal physiology 2009
(Fibrosis) :
It also partially blocked active Rac1 stimulated collagen promoter activity, suggesting that
PI3K activity
contributes to both TGF-beta activation of
Rac1 and signal propagation downstream of Rac1
Garcia et al., J Immunol 2009
:
In the present study, we demonstrate that
IL-12p70 induces IL-10 production from human memory CD4+ T cells via a
PI3K dependent signaling mechanism ... In the present study, we demonstrate that IL-12p70 induces
IL-10 production from human memory CD4+ T cells via a
PI3K dependent signaling mechanism ... In the present study, we demonstrate that
IL-12p70 induces IL-10 production from human memory CD4+ T cells via a
PI3K dependent signaling mechanism ... Inhibition of
PI3K prevented the inactivation of GSK3beta by IL-12p70, as well as the subsequent ability of IL-12p70 to augment
IL-10 levels by memory CD4+ T cells
Hardy et al., Immunology 2009
:
However,
PKC-alpha phosphorylation was
independent of
PI3K and p38 MAPK, indicating that IFN-gamma induced phosphorylation and nuclear translocation of PKC-alpha are mediated by distinct mechanisms ... In addition, inhibition of
PI3K , but not of p38 MAPK, strongly
impaired IFN-gamma induced
CIITA and MHC II gene expression ... Taken together, our data indicate that PI3K and p38
MAPK modulate IFN-gamma stimulated PKC-alpha nuclear translocation independently of JAK2 activity and that both
PI3K and PKC-alpha are
required for type IV CIITA and MHC II gene expression in IFN-gamma stimulated macrophages ... Taken together, our data indicate that PI3K and p38 MAPK modulate IFN-gamma stimulated PKC-alpha nuclear translocation independently of JAK2 activity and that both
PI3K and PKC-alpha are
required for type IV
CIITA and MHC II gene expression in IFN-gamma stimulated macrophages ... Taken together, our data indicate that PI3K and p38 MAPK modulate
IFN-gamma stimulated PKC-alpha nuclear translocation independently of JAK2 activity and that both
PI3K and PKC-alpha are
required for type IV CIITA and MHC II gene expression in IFN-gamma stimulated macrophages ... Taken together, our data indicate that
PI3K and p38 MAPK modulate IFN-gamma stimulated PKC-alpha nuclear translocation independently of JAK2 activity and that both PI3K and
PKC-alpha are
required for type IV CIITA and MHC II gene expression in IFN-gamma stimulated macrophages
Kuo et al., Mol Nutr Food Res 2009
:
Inotilone also inhibited
LPS induced
activation of
PI3K/Akt and extracellular signal regulated kinase 1/2 and p38 mitogen activated protein kinase
Chang et al., Biochem J 2009
(Ovarian Neoplasms) :
The anti-apoptotic ability was suppressed and the expression of Bcl-2 family in response to mesothelin was altered by inhibiting
PI3K activity, but not by
inhibiting MAPK activity ... Thus mesothelin can inhibit paclitaxel induced cell death mainly by
involving PI3K signalling in the regulation of
Bcl-2 family expression
Westra et al., Ann N Y Acad Sci 2009
(Arthritis, Rheumatoid) :
Protein and mRNA expression of HIF-1alpha and the
effects of inhibitors of the CaMKII-,
PI3K- , and ERK pathway on
VEGF and IL-6 production were analyzed ... Protein and mRNA expression of HIF-1alpha and the
effects of inhibitors of the CaMKII-,
PI3K- , and ERK pathway on VEGF and
IL-6 production were analyzed
Shastry et al., Journal of inflammation (London, England) 2009
:
MIP-2 enhanced leukocyte adhesion to MC and this MIP-2 enhanced leukocyte adhesion was also
dependent on activation of p38 MAPK and
PI3K
Hwang et al., Toxicol Appl Pharmacol 2010
:
Moreover,
Rb1 induced both Nrf2 nuclear translocation, which is upstream of HO-1 expression and
PI3K activation, a pathway that is involved in induced Nrf2 nuclear translocation, HO-1 expression and cytoprotection ... Also, Rb1 mediated increases in
PI3K activation and
HO-1 induction were reversed by co-treatment with ICI 182,780 and pertussis toxin ... Also,
Rb1 mediated
increases in
PI3K activation and HO-1 induction were reversed by co-treatment with ICI 182,780 and pertussis toxin
Kajanne et al., Int J Oncol 2009
(Prostatic Neoplasms) :
Here, we show that constitutive
AP-1 activity in prostate cancer cells is
dependent on the activities of EGF-R and
PI3K ... Together, the findings show that
AP-1 activity in prostate cancer cells
mediates EGF-R and
PI3K signalling, is essential for their proliferation, and confers protection against radiation induced cell death
Frost et al., J Cell Biochem 2009
:
The
PI3K inhibitor LY294002
blocked IGF-I but not Dex induced REDD1
Yin et al., Invest Ophthalmol Vis Sci 2010
:
LL-37 enhanced the closure of a scratch wound in cultured HCECs and partially rescued HG-attenuated wound healing in an EGFR- and a
PI3K dependent manner and restored HG-impaired
EGFR signaling in cultured porcine corneas
Abe et al., PloS one 2009
:
Membrane protein location dependent
regulation by
PI3K ( III ) and rabenosyn-5 in Drosophila wing cells
Matheny et al., Biochem Biophys Res Commun 2009
:
Our results collectively suggest that
mTOR/p70S6K is activated in a
PI3K/Akt dependent manner, but that in the absence of p110alpha or Akt, alternate pathway ( s ) may mediate activation of mTOR/p70S6K in C2C12 myoblasts ... Our results collectively suggest that
mTOR/p70S6K is activated in a
PI3K/Akt dependent manner, but that in the absence of p110alpha or Akt, alternate pathway ( s ) may mediate activation of mTOR/p70S6K in C2C12 myoblasts
Bian et al., Am J Physiol Heart Circ Physiol 2009
(Disease Models, Animal...) :
Inhibition of erbB2,
phosphoinositide 3-kinase (PI3K) , Akt, and mTOR
blocked the protective effects of NRG1 on cTnI and
cTnT in NRVM
Koshikawa et al., J Biol Chem 2009
(Carcinoma, Lewis Lung) :
Stimulation of
HIF-1alpha transcription by the ND6 mutation was
mediated by overproduction of reactive oxygen species ( ROS ) and subsequent activation of phosphatidylinositol 3-kinase
(PI3K)-Akt and protein kinase C ( PKC ) signaling pathways
Hanson et al., Mol Cell Endocrinol 2010
:
The ERK pathway inhibitor, U0126, retarded SS-14 stimulated phosphorylation of ERK 1/2, whereas the
PI3K inhibitor, LY294002,
blocked SS-14 stimulated phosphorylation of
Akt
Mandal et al., Endocrinology 2009
:
Inhibition of
PI3K/Akt signaling
blocked the binding of Smads 1/5 to the CSF-1
BMP-responsive element present in the CSF-1 promoter, resulting in attenuation of Smad dependent CSF-1 transcription ... Inhibition of
PI3K/Akt signaling
blocked the binding of Smads 1/5 to the
CSF-1 BMP-responsive element present in the CSF-1 promoter, resulting in attenuation of Smad dependent CSF-1 transcription ... Together, these data for the first time demonstrate that
PI3K dependent Akt activation
regulates BMP-2 induced
CSF-1 expression and provides a mechanism for osteoblastic cell assisted osteoclast differentiation ... Together, these data for the first time demonstrate that
PI3K dependent
Akt activation regulates BMP-2 induced CSF-1 expression and provides a mechanism for osteoblastic cell assisted osteoclast differentiation
Zhang et al., Int J Gynecol Cancer 2009
(Carcinoma...) :
Interestingly, the mitogen activated protein kinase or extracellular signal regulated kinase inhibitors PD98059 and U0126 actually increased MMP-2 mRNA and protein synthesis, whereas the
PI3-K inhibitors LY294002 and wortmannin further
suppressed the expression of
MMP-2
Biswas et al., Mol Cell Biochem 2010
(Diabetes Mellitus, Experimental...) :
We have isolated mahanine, a carbazole alkaloid, from the leaves of Murraya koenegii that prevented palmitate induced inhibition of
insulin stimulated phosphorylation of IRbeta,
PI3K , PDK1, and Akt in L6 myotubes
Xia et al., Mol Cell Biol 2010
:
Interestingly, the activation of PI3K/Akt appeared to be independent of the activation of PKA, whereas both
PI3K/Akt and PKA signaling inactivated GSK-3 and
increased beta-catenin translocation
Hussain et al., Biochem Biophys Res Commun 2009
(Lymphoma, T-Cell, Peripheral...) :
Phosphatidylinositol-3-kinase dependent phosphorylation of
SLP-76 by the lymphoma associated ITK-SYK fusion-protein
Faber et al., Proc Natl Acad Sci U S A 2009
(Breast Neoplasms...) :
PI3K inhibition
led to down-regulation of
Mcl-1 , and MEK inhibition led to up-regulation of BIM
Yalcin et al., Oncogene 2010
(Neoplasms, Experimental) :
Selective inhibition of
choline kinase simultaneously
attenuates MAPK and
PI3K/AKT signaling
Xing et al., World J Gastroenterol 2009
(Stomach Neoplasms) :
The class I
PI3K inhibitor LY294002 could inhibit the invasiveness of gastric cancer cells by downregulating the expression of MMP-2, MMP-9, and VEGF, and
reducing MVD
Song et al., Cell Signal 2010
:
In this study, we report that Src, c-Cbl, and
PI3K are
involved in the phosphorylation of
Akt during TRAIL treatment
Peng et al., J Gen Virol 2010
(Herpesviridae Infections) :
We found that de novo infection of MHV-68 induced
PI3K dependent
Akt activation and the lytic replication of MHV-68 was enhanced by inhibiting the PI3K-Akt pathway with both chemical inhibitors and RNA interference technology
Udelhoven et al., J Endocrinol 2010
:
Thus, alternative binding of ZBP89 or
SP1 to the described region in the IRS2 promoter regulates neuronal IRS2 expression in a
PI3K dependent manner ... Thus, alternative binding of ZBP89 or SP1 to the described region in the IRS2 promoter regulates neuronal
IRS2 expression in a
PI3K dependent manner
Jackson et al., Virology 2010
:
Surprisingly, given previous reports that
NS1 activates
PI3K to prevent apoptosis, the mutant viruses rUd-Y89F and rUd-P164/7A that fail to activate PI3K did not induce any more apoptosis than wild-type virus in MRC-5 and A549 cells, even though these cells are highly sensitive to inducers of apoptosis
Toy et al., Cell Signal 2010
(MAP Kinase Signaling System) :
EGF induced tyrosine phosphorylation of
Endofin is
dependent on
PI3K activity and proper localization to endosomes
Sonderegger et al., Endocrinology 2010
:
Chemical inhibition of
PI3K abolished Wnt dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not
affect appearance of activated beta-catenin or
Wnt/TCF reporter activity ... Chemical inhibition of
PI3K abolished Wnt dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not
affect appearance of activated beta-catenin or
Wnt/TCF reporter activity ... Chemical inhibition of
PI3K abolished Wnt dependent phosphorylation of AKT and GSK-3beta and trophoblast motility but did not
affect appearance of activated
beta-catenin or Wnt/TCF reporter activity ... The data suggest that
Wnt-3A may
activate canonical Wnt signaling and
PI3K/AKT through distinct receptors
Lee et al., J Biol Chem 2010
:
OSS induced activation of
PI3K/Akt/mTOR/p70S6K and cell proliferation were
inhibited by specific antibodies or small interference RNAs of alpha ( v ) beta ( 3 ) and beta ( 1 ) integrins and by dominant negative mutants of
Shc ( Shc-SH2 ) and focal adhesion kinase ( FAK ) ( FAK ( F397Y ) ) ... OSS also induced sustained activation of ERK, which was inhibited by the specific
PI3K inhibitor LY294002 and was
required for OSS induced activation of
mTOR/p70S6K and proliferation in MG63 cells ... OSS also induced sustained activation of ERK, which was inhibited by the specific
PI3K inhibitor LY294002 and was
required for OSS induced activation of
mTOR/p70S6K and proliferation in MG63 cells
Xia et al., Journal of thrombosis and haemostasis : JTH 2010
:
Subsequently,
PI3K overexpression
activated Rac1 and increased ROS generation ... Protein kinase Czeta mediates
PI3K regulated
NADPH oxidase activation by promoting cellular p47phox translocation
Xie et al., Proc Natl Acad Sci U S A 2009
(Prostatic Neoplasms) :
Gain of function study showed that DAB2IP can suppress the PI3K-Akt pathway and
enhance ASK1 activation leading to cell apoptosis, whereas loss of DAB2IP expression resulted in
PI3K-Akt activation and ASK1-JNK inactivation leading to accelerated PCa growth in vivo ... Gain of function study showed that DAB2IP can suppress the PI3K-Akt pathway and enhance ASK1 activation leading to cell apoptosis, whereas loss of
DAB2IP expression
resulted in
PI3K-Akt activation and ASK1-JNK inactivation leading to accelerated PCa growth in vivo
Wang et al., Cardiovasc Res 2010
(Atherosclerosis) :
Inhibition of either
PI3K or p38 MAPK completely
blocked oxLDL induced
lp-PLA2 expression
Bandara et al., PLoS Comput Biol 2009
:
The experimental approach included the activation of endogenous phosphoinositide 3-kinase (PI3K) by chemically induced recruitment of a regulatory peptide, reversible inhibition of PI3K using a kinase inhibitor, and monitoring of the
PI3K mediated production of
PIP ( 3 ) lipids using the pleckstrin homology (PH) domain of Akt
Bragado et al., J Cell Biochem 2010
:
The
PI3K inhibitor LY294002
increases both spermatozoa motility parameters and the basal
GSK3A phosphorylation, but does not affect either TCM- or 8Br-cAMP stimulated GSK3A phosphorylation
Anggakusuma et al., J Dermatol Sci 2010
(Inflammation) :
These results suggest that macelignan protects skin keratinocytes from UVB induced damage and
inhibits MMP-9 and COX-2 expression by attenuating the activation of MAPKs and
PI3K/Akt ... These results suggest that macelignan protects skin keratinocytes from UVB induced damage and
inhibits MMP-9 and
COX-2 expression by attenuating the activation of MAPKs and
PI3K/Akt
Wenink et al., J Immunol 2009
:
The inhibitory effect of TLR2 on the release of
TNF-alpha but not of IL-12p70 was
mediated by
PI3K ... The inhibitory effect of TLR2 on the release of TNF-alpha but not of
IL-12p70 was
mediated by
PI3K ... The inhibitory effect of TLR2 on the release of TNF-alpha but not of
IL-12p70 was
mediated by
PI3K ... The inhibitory effect of
TLR2 on the release of TNF-alpha but not of IL-12p70 was
mediated by
PI3K
Gigoux et al., Proc Natl Acad Sci U S A 2009
:
Although it is known that
CD28 mediated
PI3K activation is dispensable for GC reaction, the role of ICOS-driven PI3K signaling has not been defined
Salmond et al., J Immunol 2009
:
We show that maximal TCR induced rpS6 phosphorylation in CD8 T cells requires both Lck and
Fyn activity and downstream
activation of
PI3K , mTOR, and MEK/ERK MAPK pathways ... We show that maximal TCR induced rpS6 phosphorylation in CD8 T cells requires both
Lck and Fyn activity and downstream
activation of
PI3K , mTOR, and MEK/ERK MAPK pathways
Levental et al., Cell 2009
(Breast Neoplasms...) :
Consistently, reduction of lysyl oxidase mediated collagen crosslinking prevented
MMTV-Neu induced fibrosis, decreased focal adhesions and
PI3K activity, impeded malignancy, and lowered tumor incidence
Park et al., Haematologica 2010
(Leukemia, Myeloid, Acute) :
Constitutive
PI3K activation is the
result of autocrine
IGF-1/IGF-1R signaling in 70 % of acute myeloid leukemia samples but specific inhibition of this pathway does not induce apoptosis ... However, as mTORC1 activation is independent of
PI3K/AKT in acute myeloid leukemia, dual PI3K and
mTOR inhibitors may
induce apoptosis in blast cells ... However, as
mTORC1 activation is independent of PI3K/AKT in acute myeloid leukemia, dual
PI3K and mTOR inhibitors may
induce apoptosis in blast cells ... However, as mTORC1 activation is independent of
PI3K/AKT in acute myeloid leukemia, dual
PI3K and mTOR inhibitors may
induce apoptosis in blast cells
Beemiller et al., Mol Biol Cell 2010
:
Inhibition of
PI3K resulted in persistently active
Cdc42 and Rac1, but not Rac2, in stalled phagocytic cups ... Inhibition of
PI3K resulted in persistently active Cdc42 and
Rac1 , but not Rac2, in stalled phagocytic cups ... Inhibition of
PI3K resulted in persistently active Cdc42 and Rac1, but not
Rac2 , in stalled phagocytic cups ... Expression of constitutively active Cdc42 ( G12V ) increased 3'PI concentrations in plasma membranes and small phagosomes, indicating a
role for
Cdc42 in
PI3K activation
Hyun et al., Cell 2009
:
USH/FOG2 inhibits
PI3K activity, suppressing cell growth in both flies and humans
Chapuis et al., Haematologica 2010
(Blast Crisis...) :
Autocrine
IGF-1/IGF-1R signaling is
responsible for constitutive
PI3K/Akt activation in acute myeloid leukemia : therapeutic value of neutralizing anti-IGF-1R antibody ... As we previously reported IGF-1 autocriny in acute myeloid leukemia cells, we investigated whether
IGF-1 signaling was
involved in the constitutive activation of
PI3K
Uddin et al., Endocr Relat Cancer 2010
(Carcinoma, Papillary...) :
Inhibition of PI3K activity by its inhibitor LY294002 abrogated
leptin mediated
PI3K/AKT signaling
Sahay et al., PLoS Pathog 2009
(Borrelia Infections...) :
CD14 deficiency
results in increased localization of
PI3K to lipid rafts, hyperphosphorylation of AKT, and reduced activation of p38 ... CD14 deficiency results in increased localization of
PI3K to lipid rafts, hyperphosphorylation of AKT, and reduced
activation of
p38
Maffucci et al., PloS one 2009
:
We further demonstrate that
FGF-2 activates
PI3K , assessed by analysing accumulation of its lipid product phosphatidylinositol-3,4,5-P ( 3 ) using TLC and confocal microscopy analysis ...
PI3K activity is
required for FGF-2 induced
PLCgamma1 activation and the PI3K/PLCgamma1 pathway is involved in FGF-2 dependent cell migration, determined using Transwell assay, and in FGF-2 induced capillary tube formation ( tubulogenesis assays in vitro ) ... Finally we show that
PI3K dependent PLCgamma1 activation
regulates FGF-2 mediated phosphorylation of
Akt at its residue Ser473, determined by Western blotting analysis ... Finally we show that
PI3K dependent
PLCgamma1 activation regulates FGF-2 mediated phosphorylation of Akt at its residue Ser473, determined by Western blotting analysis ... Furthermore these data unveil a novel role for PLCgamma1 as a mediator of
PI3K dependent
Akt activation and as a novel key regulator of different Akt dependent processes
Desai et al., J Biol Chem 2010
:
Expression of constitutively active
PI3K stimulated translocation of
Tiam1 to the membrane, increased Rac1 activity, and increased wound healing of airway epithelial cells ... Expression of constitutively active
PI3K stimulated translocation of Tiam1 to the membrane,
increased Rac1 activity, and increased wound healing of airway epithelial cells
Chetty et al., Int J Cancer 2010
(Lung Neoplasms) :
We also show that MMP-2 suppression disrupted
PI3K dependent
VEGF expression ; ectopic expression of myr-AKT restored VEGF inhibition
Yamashita et al., Journal of ovarian research 2009
:
Areg,
Ereg and Tace/Adam17 gene expressions were not
suppressed by
PI3K inhibitor ( LY294002 ), whereas PKA inhibitor ( H89 ), p38 MAPK inhibitor ( SB203580 ) and MEK inhibitor ( U0126 ) significantly suppressed these gene expressions ...
Areg , Ereg and Tace/Adam17 gene expressions were not
suppressed by
PI3K inhibitor ( LY294002 ), whereas PKA inhibitor ( H89 ), p38 MAPK inhibitor ( SB203580 ) and MEK inhibitor ( U0126 ) significantly suppressed these gene expressions
Bai et al., Life Sci 2010
(Carcinoma, Hepatocellular...) :
The phosphorylation of
EGFR and Akt were elevated in EP1 agonist treated cells, and both EGFR and
PI3K inhibitors
suppressed the upregulation of survivin induced by PGE ( 2 ) or EP1 agonist ... The phosphorylation of EGFR and
Akt were elevated in EP1 agonist treated cells, and both EGFR and
PI3K inhibitors
suppressed the upregulation of survivin induced by PGE ( 2 ) or EP1 agonist
Su et al., Life Sci 2010
(Adenocarcinoma...) :
Immunoblot showed that NFD inhibited
EGFR phosphorylation and the
activation of
PI3K/Akt , downstream molecules of EGFR pathway, in A549 cells
Janas et al., J Exp Med 2010
:
Here, we show that
PI3K signaling from the preTCR
requires p110delta , but not p110gamma ... Here, we show that
PI3K signaling from the preTCR
requires p110delta, but not
p110gamma ... These findings establish a role for
CXCR4 mediated
PI3K signaling that, together with signals from Notch and the preTCR, contributes to continued T cell development beyond beta-selection
Corcione et al., PloS one 2009
:
CX(3)CL1 signalling in germinal centre B cells
involved PI3K , Erk1/2, p38, and Src phosphorylation, as assessed by Western blot experiments
Lim et al., Int J Oncol 2010
(Necrosis) :
In conclusion, these results indicate that
PI3K dependent
HSP27 and p53 induction and PI3K- and ERK1/2 dependent inhibition of the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels by heat play a key role ( s ) in heat shock mediated switch of GD-induced necrosis to apoptosis
Venieratos et al., Cell Signal 2010
:
Inhibition of SOCS-1 expression by SOCS-1-specific small interfering RNA restored
IRS-2/PI3K mediated
Akt phosphorylation suppressed by high glucose
Costa et al., Cancer Res 2010
(Astrocytoma...) :
Reversing
HOXA9 oncogene
activation by
PI3K inhibition : epigenetic mechanism and prognostic significance in human glioblastoma ... Our findings suggest a transcriptional pathway through which
PI3K activates oncogenic
HOXA expression with implications for mTOR or PI3K targeted therapies
Venkatesan et al., Cell Signal 2010
:
Further, WISP1 stimulates
PI3K-Akt dependent GSK3beta phosphorylation and
beta-catenin nuclear translocation ... Further, WISP1 stimulates
PI3K-Akt dependent
GSK3beta phosphorylation and beta-catenin nuclear translocation
Villarreal et al., Regul Pept 2010
:
Role of
IRS-4 in
PI3-K activation by insulin in HepG2 cells, modulation by Angiotensin II ... Role of IRS-4 in
PI3-K activation by
insulin in HepG2 cells, modulation by Angiotensin II ... We report also
Ins induced
PI3-K activation mediated by IRS-4 ... We report also Ins induced
PI3-K activation
mediated by
IRS-4
Krishnaswamy et al., Endocrinology 2010
:
Inhibitors of c-Src ( PP2, 10 microm ) and
PI3K ( LY294002, 25 microm ) produced a significant decrease in OT-induced PGF ( 2 alpha ) production and
reduced COX2 expression ... Thus,
EGFR may simultaneously
activate c-Src and
PI3K to amplify the OT signaling to increase the output of PGF ( 2 alpha ) in bEEL cells
Tseng et al., J Cell Physiol 2010
:
TNF-alpha increased the FAK,
PI3K , and Akt phosphorylation
Kanan et al., J Neurochem 2010
:
In this study, we characterized these two phosphatases in the retina and examined the
role of IR,
PI3K , and Akt signaling on the activity of
PHLPP and PHLPPL ... In this study, we characterized these two phosphatases in the retina and examined the
role of IR,
PI3K , and Akt signaling on the activity of PHLPP and
PHLPPL
Yamada et al., Cytokine 2010
:
These results indicate that human nasal airway fibroblasts strongly
induce BLyS-expression and production by poly ( I:C ) through
PI3-K signaling during airway immune responses
May et al., J Biol Chem 2010
:
Phosphatidylinositol 3-kinase gamma-selective inhibitors
blocked PACAP stimulated
Akt phosphorylation in primary neuronal cultures and in PAC(1)HOP1 overexpressing cell lines ; RNA interference mediated knockdown of the receptor effectors attenuated PACAP mediated Akt activation
Keyes et al., Am J Physiol Heart Circ Physiol 2010
(Disease Models, Animal...) :
Lipid phosphatase and tensin homolog on chromosome 10 ( PTEN ) antagonizes PI3K activity by dephosphorylating Ptdins ( 3,4,5 ) P ( 3 ) ; therefore, the inhibition of
PTEN enhances
PI3K/Akt signaling and could prevent myocardium from ischemia-reperfusion ( I/R ) injury
Kwak et al., J Biol Chem 2010
(Neoplasms) :
This study demonstrates that NEDD4-1 mediated PTEN ubiquitination is crucial in the
regulation of
PI3K/Akt signaling by
PTEN during the neuronal response to zinc, which may represent a common mechanism in neurodegeneration
Iskandar et al., Am J Physiol Endocrinol Metab 2010
(Obesity) :
Both insulin and leptin signaling converge on phosphatidylinositol 3-OH kinase
[PI(3)K ] /3-phosphoinositide
dependent protein kinase-1 ( PDK-1 )
/protein kinase B ( PKB, also known as Akt ) in proopiomelanocortin (POMC) neurons
Wang et al., Clin Neurol Neurosurg 2010
(Brain Neoplasms...) :
To study the expression of
Akt2 and
activation of
PI3K in different grades of human gliomas and correlate the Akt2 expression with the proliferation activity of gliomas
Nencioni et al., PloS one 2010
(Breast Neoplasms...) :
Thus,
Grb7 is
repressed by
PI3K signaling and lapatinib mediated Akt inhibition is responsible for Grb7 de-repression
Liu et al., Int J Oncol 2010
(Prostatic Neoplasms) :
Consistently,
EGF and DHT stimulate Vav3 and AR interaction and
enhance PI3K-Akt signaling
Rafa et al., Int J Oncol 2010
(Colonic Neoplasms...) :
Using pharmacological inhibitors, we showed that
PI3K/Akt , PKAs, PKCs and Rho-like GTPases, but not MAPK, are
involved in
REG4 invasion signals
Yan et al., J Cell Biochem 2010
(Cardiomegaly) :
The inhibitory effect of breviscapine on cardiac hypertrophy is mediated by disrupting
PKC-alpha dependent ERK1/2 and
PI3K/AKT signaling
Jackel-Cram et al., J Gen Virol 2010
:
These results indicate a
role for
PI3K and Akt-2 in increasing
SREBP-1 activity by HCV-3a core protein and provide a mechanism of steatosis caused by HCV
Corey et al., J Neurochem 2010
:
Phosphoinositide 3-kinase (PI3K) activity has been implicated physiologically in olfactory signal transduction, suggesting a potential role for a
G protein coupled receptor activated class I
PI3K
Lawson et al., Proc Natl Acad Sci U S A 2010
(Disease Models, Animal...) :
Stromal induction of FGF signaling, increased expression of the ETS family transcription factor
ERG1 , and constitutive
activation of
PI3K signaling were evaluated ... Stromal induction of
FGF signaling, increased expression of the ETS family transcription factor ERG1, and constitutive
activation of
PI3K signaling were evaluated
Hale et al., Proc Natl Acad Sci U S A 2010
:
Overall, these data suggest that both direct binding of NS1 to
p85beta ( resulting in repositioning of the N-terminal SH2 domain ) and possible NS1 : p110 contacts
contribute to
PI3K activation ... Overall, these data suggest that both direct binding of
NS1 to p85beta ( resulting in repositioning of the N-terminal SH2 domain ) and possible NS1 : p110 contacts
contribute to
PI3K activation
Yang et al., Exp Physiol 2010
(Hypertension) :
These vasorelaxant responses among the three groups became similar after endothelial denudation and pretreatment with the
PI3K inhibitor,
NOS inhibitor or SOD
Small et al., Proc Natl Acad Sci U S A 2010
:
Similarly, we show that
MRTF-A promotes
PI3K/Akt signaling by up-regulating miR-486 expression
Lin et al., Toxicon 2010
(Breast Neoplasms) :
Moreover, the
PI3K inhibitor wortmannin
blocked activation of
STAT3 and Akt without affecting the JAK2 activation, whereas JAK2 inhibitor AG490 suppressed the levels of phospho-STAT3, phospho-Akt, and PI3K, suggesting that PI3K activation occurs after JAK2 phosphorylation, and both PI3K and JAK2 kinases cooperate to mediate STAT3 and Akt phosphorylation ... Moreover, the
PI3K inhibitor wortmannin
blocked activation of STAT3 and
Akt without affecting the JAK2 activation, whereas JAK2 inhibitor AG490 suppressed the levels of phospho-STAT3, phospho-Akt, and PI3K, suggesting that PI3K activation occurs after JAK2 phosphorylation, and both PI3K and JAK2 kinases cooperate to mediate STAT3 and Akt phosphorylation
Kim et al., Neurochem Int 2010
:
Additionally,
NPPB and SITS, another chloride channel blocker,
suppressed NGF induced TrkA phosphorylation and subsequent
PI3K/Akt phosphorylation and Rac1 activation in PC12 cells ... Additionally, NPPB and SITS, another chloride channel blocker, suppressed
NGF induced TrkA phosphorylation and subsequent
PI3K/Akt phosphorylation and Rac1 activation in PC12 cells
Binker et al., Biochem Biophys Res Commun 2010
(Neoplasm Invasiveness...) :
Our results also indicate that signaling events involved in H-R enhanced PANC-1 invasiveness comprehend
PI3K dependent
activation of
Rac1 , which mediated the formation of NADPH generated reactive oxygen species responsible for MMP-2 secretion and activation
Ito et al., Anim Sci J 2010
:
In this study the
effect of a
PI3K inhibitor, LY294002, on the
MAPK and p34 ( cdc2 ) kinase activities of matured porcine oocytes was examined
Tao et al., Journal of molecular signaling 2010
:
Our results showed that 5-aminoimidazole-4-carboxamide-1 ribonucleoside ( AICAR ) greatly
enhanced the ability of insulin to stimulate the insulin receptor substrate-1 (IRS1) associated
PI3K activity in differentiated 3T3-F442a adipocytes, leading to increased Akt phosphorylation at S473, whereas insulin stimulated activation of
mTOR was diminished ... Our results showed that 5-aminoimidazole-4-carboxamide-1 ribonucleoside ( AICAR ) greatly enhanced the ability of
insulin to
stimulate the insulin receptor substrate-1 (IRS1) associated
PI3K activity in differentiated 3T3-F442a adipocytes, leading to increased Akt phosphorylation at S473, whereas insulin stimulated activation of mTOR was diminished ... Our present study demonstrates that AMPK exerts dual effects on the PI3K pathway, stimulating
PI3K/Akt and
inhibiting mTOR/S6K
Li et al., Neuropharmacology 2010
:
These findings suggest that DHEA prevents the Abeta ( 25-35 ) -impaired survival and dendritic growth of newborn neurons through a
sigma(1) receptor mediated modulation of
PI3K-Akt-mTOR-p70S6k signaling
Lee et al., Bone 2010
:
Role of
PI3K on the regulation of BMP2 induced
beta-Catenin activation in human bone marrow stem cells ... In addition, BMP2 induced beta-Catenin activity and
ALP activity were
blocked by
PI3K inhibition ... In addition, BMP2 induced
beta-Catenin activity and ALP activity were
blocked by
PI3K inhibition
Lee et al., Am J Pathol 2010
(Inflammation) :
Furthermore,
LTA could
stimulate TLR2, MyD88,
PI3K , and Rac1 complex formation
Niewiadomska et al., Behav Brain Res 2011
(Alzheimer Disease) :
NGF released from target cells activates TrkA on axon terminals and
triggers activation of
PI3K/Akt , MEK/ERK, and PLC? ( phospholipase C ) signaling pathways
Chan et al., J Immunol 2010
:
PI3K dependent upregulation of
Mcl-1 by human cytomegalovirus is mediated by epidermal growth factor receptor and inhibits apoptosis in short lived monocytes ... Temporal transcriptome and protein analyses revealed
Mcl-1 , a member of the Bcl-2 family, was transiently induced in a
PI3K dependent manner during the early stages of HCMV infection ... Overall, our data indicates that activation of the epidermal growth factor receptor/PI3K signaling pathway, via the
PI3K dependent upregulation of
Mcl-1 , is required to circumvent apoptosis in naturally short lived monocytes during the early stages of HCMV infection, thus ensuring the early steps in the viral persistence strategy
Thimmaiah et al., Cancer Res 2010
(Rhabdomyosarcoma) :
Results indicate that
IGF-I signaling to Bad
requires activation of
PI3K and PKC ( mu, theta, epsilon ) but not mTOR, Ras-extracellular signal regulated kinase 1/2, protein kinase A, or p90 ( RSK )
Bouraïma-Lelong et al., Reprod Fertil Dev 2010
:
Experiments using the specific phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002 revealed that
PI3-K is strongly
involved in FSH induced
aromatase expression in Sertoli cells from both 20- and 30-day-old rats
Shah et al., Am J Physiol Heart Circ Physiol 2010
:
These results suggest that 1 ) ANG- ( 1-7 ) increased ANP secretion at high atrial pacing via the
Mas/PI3K/Akt pathway and the
activation of
Na(+)/H(+) exchanger-1 and CaMKII and 2 ) ANG- ( 1-7 ) decreased cardiac hypertrophy which might be mediated by ANP
Fridell et al., Aging 2009
:
Increased
UCP activity in IPCs
results in decreased steady state Ca ( 2+ ) levels in IPCs as well as decreased
PI3K activity and increased FoxO nuclear localization in periphery
Lin et al., Toxicol In Vitro 2010
(Breast Neoplasms) :
Moreover, the JAK2 inhibitor AG490 blocked JAK2, STAT3, Src, PI3K, and Akt activation, whereas both Src inhibitor PP2 and
PI3K inhibitor wortmannin did not
affect JAK2 activation
Lu et al., Mol Cancer Res 2010
(Carcinoma...) :
These studies show that
PDK1 plays a pivotal role in MAPK and
PI3K signaling in tumor cells
Koutros et al., Cancer Res 2010
(Genetic Predisposition to Disease...) :
In conclusion, we observed a significant association between PIK3C2B and prostate cancer risk, especially for familial, early-onset disease, which may be attributable to
IGF dependent
PI3K signaling
Wang et al., J Bone Miner Res 2010
:
T ( 3 ) activates IGF-1/IGF1R signaling and
IGF-1 dependent
PI3K/Akt/GSK-3beta signaling in growth plate chondrocytes undergoing proliferation and differentiation to prehypertrophy ... T ( 3 ) -mediated
Wnt-4 expression, beta-catenin activation, cell proliferation, and terminal differentiation of growth plate chondrocytes are partially
prevented by the IGF1R inhibitor picropodophyllin as well as by the
PI3K/Akt signaling inhibitors LY294002 and Akti1/2 ... T ( 3 ) -mediated Wnt-4 expression,
beta-catenin activation, cell proliferation, and terminal differentiation of growth plate chondrocytes are partially
prevented by the IGF1R inhibitor picropodophyllin as well as by the
PI3K/Akt signaling inhibitors LY294002 and Akti1/2
Huang et al., Mediators Inflamm 2009
(MAP Kinase Signaling System) :
Upregulation of Salmonella induced
IL-6 production in Caco-2 cells by PJ-34, PARP-1 inhibitor : involvement of
PI3K , p38 MAPK, ERK, JNK, and NF-kappaB
de Araújo et al., J Cancer Res Clin Oncol 2010
(Colorectal Neoplasms) :
Furthermore, we provided evidence that
PI3K inhibition
leads to a decrease in
p-Akt and p-GSK-3ß and increased p-ß-catenin levels, which in turn controlled cell proliferation, motility, and colony formation
Seshadri et al., Proc Natl Acad Sci U S A 2010
:
Receptors ErbB2 and ErbB3, but not
ErbB4 , are responsible for transducing this effect, and
PI3K/Akt signaling is also
required
Ramella et al., J Cell Biochem 2010
:
These results suggest a novel signal transduction pathway for endogenous cationic and amphipathic peptides in endothelial cells : HSPGs interaction and caveolae endocytosis, coupled with a
PI3K dependent
eNOS phosphorylation
Porzia et al., J Immunol 2010
(Mammary Neoplasms, Experimental) :
In conclusion, vaccine induced anti-ErbB2 Abs directly affected the transformed phenotype of rat ErbB2 ( + ) tumors by impairing
ErbB2 mediated
PI3K/Akt signaling
Genc et al., Cell Biochem Funct 2010
:
These results suggest that
Epo induces neural HO-1 expression through the activation of
PI3K , MAPK, and Nrf2 pathways, and this may unveil a novel mechanism which mediates the cytoprotective responses elicited by Epo ... These results suggest that Epo
induces neural
HO-1 expression through the activation of
PI3K , MAPK, and Nrf2 pathways, and this may unveil a novel mechanism which mediates the cytoprotective responses elicited by Epo
Faghiri et al., Exp Eye Res 2010
:
Inhibition of
PI3K or mTOR/p70S6K by wortmannin and rapamycin, respectively, increased apoptosis and
inhibited phosphorylation of
Akt and p70S6K induced by single-dose oxidative stress ... Inhibition of
PI3K or mTOR/p70S6K by wortmannin and rapamycin, respectively, increased apoptosis and
inhibited phosphorylation of Akt and
p70S6K induced by single-dose oxidative stress
Jiang et al., J Biol Chem 2010
(Prostatic Neoplasms) :
Basal tyrosine phosphorylation of p110beta and p110delta could be blocked by
c-Src inhibitors, but this did not
suppress PI3K activity, which was similarly independent of Ras ... Basal PI3K activity was mediated by p110beta in PC3 cells and by both p110beta and p110delta in LNCaP cells, whereas
p110alpha was
required for
PI3K activation in response to RTK stimulation by heregulin-beta1 ... Basal
PI3K activity was
mediated by p110beta in PC3 cells and by both
p110beta and p110delta in LNCaP cells, whereas p110alpha was required for PI3K activation in response to RTK stimulation by heregulin-beta1 ... Basal
PI3K activity was
mediated by p110beta in PC3 cells and by both p110beta and
p110delta in LNCaP cells, whereas p110alpha was required for PI3K activation in response to RTK stimulation by heregulin-beta1 ... These findings show that basal
PI3K activity in PTEN-deficient PCa cells is RTK independent and can be
mediated by
p110beta and p110delta ... These findings show that basal
PI3K activity in PTEN-deficient PCa cells is RTK independent and can be
mediated by p110beta and
p110delta ... Increased
p110beta expression in PCa may be
required for RTK independent
PI3K pathway activation in adult prostate epithelium with genetic or epigenetic PTEN down-regulation
Heger et al., J Cell Physiol 2010
(Cardiomegaly...) :
Specific inhibitors of
PI3K ( 10 microM LY290042 or 10 nM wortmannin ) or ERK ( 10 microM PD98059 ) also
blocked GDF15 induced hypertrophy and
SMAD activation
Kim et al., J Cell Physiol 2010
:
We conclude that NECA stimulated
Cx43 phosphorylation
mediated by
PI3K/Akt , PKC, MAPKs, and NF-kappaB, which subsequently stimulated cell migration and proliferation through Src, integrin beta1, FAK, and paxillin signal pathways
Wang et al., Cancer Lett 2010
(Ovarian Neoplasms) :
Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes ( MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2,
Bcl-xL and XIAP ), as well as
activation of Ras/MEK/ERK and
PI3K/Akt signaling ... Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes (
MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2, Bcl-xL and XIAP ), as well as
activation of Ras/MEK/ERK and
PI3K/Akt signaling ... Meanwhile, the further study demonstrates that the chemoresistance caused by IL-6 is associated with increased expression of both multidrug resistance related genes ( MDR1 and GSTpi ) and apoptosis inhibitory proteins ( Bcl-2, Bcl-xL and
XIAP ), as well as
activation of Ras/MEK/ERK and
PI3K/Akt signaling
Saito et al., American journal of physiology. Renal physiology 2010
:
TNF-alpha caused activation of NF-kappaB, MAP kinases, and
PI3K-Akt in podocytes, whereas blockade of these molecules did not affect inhibition of RAR by TNF-alpha
Jeon et al., Neurochem Int 2010
:
NGF induced
moesin phosphorylation is
mediated by the
PI3K , Rac1 and Akt and required for neurite formation in PC12 cells
Edouard et al., Mol Cell Biol 2010
(LEOPARD Syndrome) :
In conclusion, SHP2 mutations causing LS facilitate
EGF induced
PI3K/AKT/GSK-3beta stimulation through impaired GAB1 dephosphorylation, resulting in deregulation of a novel signaling pathway that could be involved in LS pathology
Preuss et al., Cell Microbiol 2010
:
We show that treatment of HEK293 cells with PMT inhibits staurosporine mediated apoptosis through
PI3K dependent phosphorylation of
Akt and constitutive expression of Pim-1 kinase
Tung et al., J Cell Physiol 2010
(MAP Kinase Signaling System) :
Inhibition of
PI3K by Wortmannin
attenuated EV71 induced Akt and p42/p44
MAPK phosphorylation, but had no effect on PDGFR phosphorylation, suggesting that PDGFR is an upstream and p42/p44 MAPK is a downstream component of PI3K/Akt in these responses ... Inhibition of
PI3K by Wortmannin
attenuated EV71 induced
Akt and p42/p44 MAPK phosphorylation, but had no effect on PDGFR phosphorylation, suggesting that PDGFR is an upstream and p42/p44 MAPK is a downstream component of PI3K/Akt in these responses
Lee et al., J Cell Physiol 2010
(MAP Kinase Signaling System) :
Taken together, these data suggest that in A549 cells, TNF-alpha induces MMP-9 expression via the
TNFR1/TRAF2/PKCalpha dependent JNK1/2/c-Jun and
c-Src/EGFR/PI3K/Akt pathways ... Taken together, these data suggest that in A549 cells, TNF-alpha induces MMP-9 expression via the
TNFR1/TRAF2/PKCalpha dependent JNK1/2/c-Jun and
c-Src/EGFR/PI3K/Akt pathways ... Taken together, these data suggest that in A549 cells, TNF-alpha induces MMP-9 expression via the
TNFR1/TRAF2/PKCalpha dependent JNK1/2/c-Jun and
c-Src/EGFR/PI3K/Akt pathways
Fan et al., J Neurosci 2010
:
Intracerebroventricular E ( 2 ) infusion also increased
PI3K phosphorylation after 15 min, and this effect was
blocked by intrahippocampal PI3K, but not
ERK , inhibition
Huang et al., Journal of thrombosis and haemostasis : JTH 2010
(Thrombosis) :
Western blot analysis showed that
SAA , like the phosphoinositide 3-kinase (PI3K) inhibitors LY294002 and TGX-221, potently
inhibited PI3K , as shown by reduced Akt phosphorylation
Heffron et al., Bioorg Med Chem Lett 2010
:
Identification of
GNE-477 , a potent and efficacious dual
PI3K/mTOR inhibitor ... This discovery led to the identification of
GNE-477 ( 8 ), a potent and efficacious dual
PI3K/mTOR inhibitor
Westra et al., BMC musculoskeletal disorders 2010
(Arthritis...) :
HIF-1 alpha protein expression in LPS stimulated THP-1 macrophages could be
blocked by ERK- and
PI3K-inhibitors , but also by the CaMKII inhibitor KN93 ... THP-1 and SF macrophages produced high levels of VEGF, IL-8, and MMP-9, and
VEGF protein production was significantly
inhibited by
PI3K-inhibitor , and by both CaMKII inhibitors ... THP-1 and SF macrophages produced high levels of VEGF,
IL-8 , and MMP-9, and VEGF protein production was significantly
inhibited by
PI3K-inhibitor , and by both CaMKII inhibitors ... THP-1 and SF macrophages produced high levels of VEGF, IL-8, and
MMP-9 , and VEGF protein production was significantly
inhibited by
PI3K-inhibitor , and by both CaMKII inhibitors
Shen et al., Infect Immun 2010
(Listeriosis) :
Moreover, functional activation of
PI3K and Rac1 was
impaired in
TLR2 ( -/- ) and MyD88 ( -/- ) macrophages ... Moreover, functional activation of
PI3K and Rac1 was
impaired in TLR2 ( -/- ) and
MyD88 ( -/- ) macrophages
Mallon et al., Mol Cancer Ther 2010
:
We are testing whether dual
PI3K/mTOR inhibitors can durably suppress p-Akt,
induce cleaved
PARP , and cause tumor regression in a diverse set of human tumor xenograft models ... We are testing whether dual
PI3K/mTOR inhibitors can durably
suppress p-Akt , induce cleaved PARP, and cause tumor regression in a diverse set of human tumor xenograft models
Liu et al., Oncol Rep 2010
(Breast Neoplasms) :
LY294002, specific inhibitor of
PI3K could
suppress survivin and
P-gp expression, decreased survivin promoter activity and enhanced cell sensitivity to drugs
Lee et al., Mol Biol Cell 2010
:
We further demonstrate that disruption of specific
IQGAP/cortexillin complexes, which also regulate cortical mechanics,
causes extended activation of
PI3K and Akt/PKB but not Ras activation
Chan et al., Molecular vision 2010
:
Furthermore, EGCG is shown to suppress
PDGF-BB induced PDGF-beta receptors, downstream
PI3K/Akt , and MAPK phosphorylation
Kim et al., Matrix Biol 2010
(MAP Kinase Signaling System) :
Results of this study demonstrate that SPP1 binds alphavbeta3 and alpha5beta1 integrins to induce focal adhesion assembly, a prerequisite for adhesion and migration of Tr, through activation of : 1 ) P70S6K via crosstalk between FRAP1/mTOR and MAPK pathways ; 2 ) mTOR,
PI3K , MAPK3/MAPK1 ( Erk1/2 ) and MAPK14 ( p38 ) signaling to stimulate Tr cell migration ; and 3 ) focal adhesion assembly and
myosin II motor activity to
induce migration of Tr cells
Bagchi et al., J Virol 2010
:
In cells either infected with A5-13 or transfected with pcD-NSP1, coimmunoprecipitation of NSP1 with phosphoinositide 3-kinase (PI3K) was observed, indicating that strong activation of
PI3K/Akt could be
due to its interaction with
NSP1
Wang et al., Zhonghua Xin Xue Guan Bing Za Zhi 2010
(Myocardial Reperfusion Injury) :
However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [ the activity of LDH ( 128.47 +/- 7.96 ) U/L vs. ( 223.96 +/- 22.10 ) U/L, P < 0.01, and cardiomyocyte apoptosis rate ( 2.84 +/- 2.56 ) % vs. ( 12.58 +/- 6.69 ) %, P < 0.01, and Caspase-3 activity ( 36,809 +/- 4750 ) RLU vs. ( 57,602 +/- 9161 ) RLU, P < 0.01 ], while LY294002 (
PI3K inhibitor ) and UO126 (
MAPK inhibitor ) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury
Zhao et al., Am J Pathol 2010
(Brain Neoplasms...) :
An EGF receptor (EGFR) kinase inhibitor, a RasN17 dominant negative construct, MEK and
PI3K inhibitors significantly
blocked EGF/EGFR stimulated
MMP-9 , cell invasion, and colony formation in U1242 MG cells, suggesting that MMP-9 is involved in EGFR/Ras/MEK and PI3K/AKT signaling pathway mediated cell invasion and anchorage independent growth in U1242 MG cells
Tawa et al., Circ Res 2010
(Disease Models, Animal...) :
Rap1 regulated the interaction between afadin and phosphatidylinositol 3-kinase (PI3K), recruitment of the
afadin-PI3K complex to the leading edge, and the
activation of
Akt , indicating the involvement of Rap1 and afadin in the PI3K-Akt signaling pathway
Yang et al., Eur J Pharmacol 2010
:
Plumbagin stimulated ERK1/2 activity was attenuated by the MEK1/2 inhibitor PD98059 and Ras inhibitor manumycin A, whereas plumbagin stimulated
Akt activity was
blocked by the
PI3K inhibitor LY294002 ... These results suggest that plumbagin activates
NAD ( P ) H oxidase , Src, and PI3K, and that the activated
PI3K or PDK1 subsequently
stimulate Akt and Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells ... These results suggest that plumbagin activates NAD ( P ) H oxidase, Src, and PI3K, and that the activated
PI3K or PDK1 subsequently
stimulate Akt and
Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells ... These results suggest that plumbagin activates NAD ( P ) H oxidase, Src, and PI3K, and that the activated
PI3K or PDK1 subsequently
stimulate Akt and Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells ... These results suggest that plumbagin activates NAD ( P ) H oxidase, Src, and PI3K, and that the activated
PI3K or PDK1 subsequently
stimulate Akt and
Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells ... These results suggest that plumbagin activates NAD ( P ) H oxidase, Src, and PI3K, and that the activated
PI3K or PDK1 subsequently
stimulate Akt and
Ras-Raf-MEK1/2-ERK1/2 in 3T3-L1 cells
Ko et al., Immunobiology 2011
:
The suppression of
Fgr with PP2 and Fgr siRNA
inhibited activating phosphorylation of PKCd and
PI3K/Akt , but not IL-1 receptor associated kinase (IRAK)1, a well-known MyD88 dependent signaling molecule, and Erk1/2, p38, and JNK ... Rottlerin and PKCd siRNA also inhibited expression of
IL-32a and
activation of
PI3K/Akt , but not of IRAK1 and mitogen activation protein ( MAP ) kinases
Heo et al., J Cell Physiol 2010
:
The inhibition of
PI3K and MAPK
inhibited VEGF induced
MMP-10 expression
Liu et al., Zhonghua Zheng Xing Wai Ke Za Zhi 2010
(Cicatrix, Hypertrophic) :
Ang II increased Akt phosphorylation and
PI3K activity in cultured hypertrophic scar fibroblasts in a dose- and time dependent manner
Han et al., Molecular cancer 2010
(Disease Models, Animal...) :
Co-treatment with
NF-kappaB , STAT3 or/and
PI3K inhibitors led to additive inhibition of iMyc E mu-1 cell proliferation, suggesting that these signaling pathways converge
Zheng et al., J Immunol 2010
:
In addition to promoting both MyD88- and TLR/IL-1 receptor domain containing adaptor protein inducing IFN-beta dependent MAPKs and NF-kappaB activation,
Gab1 enhances
PI3K/Akt activation by directly binding p85 in TLR signaling and VSV infection
Garcia et al., Biochem J 2010
(MAP Kinase Signaling System) :
In the present study, we evaluated the
role of specific
PI3K isoforms alpha, beta, gamma and delta in platelet aggregation, thromboxane A2 generation and
ERK ( extracellular-signal regulated kinase ) activation ... Our results show that loss of the
PI3K signal
impaired the ability of ADP to induce platelet aggregation,
ERK phosphorylation and thromboxane A2 generation
Rotman et al., Reproduction 2010
:
Previously, we reported that short-time activation of protein kinase A ( PRKA, PKA ) leads to
PI3K activation and
protein kinase C(alpha) ( PRKCA, PKC(alpha) )
inhibition ... Moreover, inhibition of
PRKCA causes significant activation of
PI3K
Lakhanpal et al., Blood 2010
(Leukemia, Erythroblastic, Acute) :
In addition, RNA interference ( RNAi ) -mediated suppression of SHIP-1 in erythroleukemia cells activates the phosphatidylinositol 3-kinase (PI 3-K) and extracellular signal regulated kinase/mitogen activated protein kinase ( ERK/MAPK ) pathways, blocks erythroid differentiation, accelerates erythropoietin induced proliferation, and leads to
PI 3-K dependent
Fli-1 up-regulation
Jensen et al., J Pathol 2010
(Thyroid Neoplasms) :
Inhibition of
PI3K/AKT or MAPK/ERK signalling did not
affect the level of
nectin-1 expression but decreased thyroid cancer cell susceptibility to HSV
Su et al., Clin Exp Pharmacol Physiol 2010
:
These observations suggest that
PI3-K is an upstream
activator of
JAK2/STAT3 ... These observations suggest that
PI3-K is an upstream
activator of
JAK2/STAT3
Wang et al., Am J Physiol Cell Physiol 2010
:
Simultaneous inhibition of PKA and
PI3K reduces
IL-6 expression in stimulated chondrocytes well below the basal levels of untreated cells
Dey et al., Cancer Res 2010
(Lung Neoplasms...) :
Targeting
fibroblast growth factor receptors
blocks PI3K/AKT signaling, induces apoptosis, and impairs mammary tumor outgrowth and metastasis
Jia et al., Exp Mol Pathol 2010
:
IGF-1 induced proliferation in both SV and IMA SMCs was
inhibited by a
PI3K inhibitor, wortmannin ... These data demonstrate differential activity of
IGF-1 induced
PI3K-Akt activation , which was quantitatively and temporally greater in SV SMCs than in the IMA
Silva et al., Int J Cancer 2011
(Carcinoid Tumor...) :
The purpose of our study was to : ( i ) assess the expression of VEGFR-2 in the novel human carcinoid cell line BON, ( ii ) to determine the
role of
PI3K/Akt signaling on
VEGFR-2 expression and ( iii ) to assess the effect of VEGFR-2 on BON cell invasion, migration and proliferation
Peng et al., Science signaling 2010
:
TREM2- and
DAP12 dependent
activation of
PI3K requires DAP10 and is inhibited by SHIP1 ... These results demonstrate a previously uncharacterized interaction of SHIP1 with DAP12 that functionally limits TREM2- and DAP12 dependent signaling and identify a mechanism through which
SHIP1 regulates key ITAM containing receptors by directly blocking the binding and activation of
PI3K
Dai et al., Folia Biol (Praha) 2010
:
Importantly,
PI3K/Akt enhanced
GRP78 accumulation through increasing its stability following endoplasmic reticulum stress
Cheung et al., J Cell Biochem 2010
(Colonic Neoplasms) :
The SAA cytotoxicity was blocked by co-incubation with catalase, whereas the SBA cytotoxicity and its subsequent growth arrest were abolished by
N-acetyl-L-cysteine (NAC) , but was not
affected by
PI3K phosphorylation inhibitor LY294002, or catalase, suggesting two separated oxidative stress pathways were mediated by these two ascorbates
Mason et al., IDrugs 2010
(Neoplasms) :
This conference report highlights selected presentations on preclinical data on the novel
pan-PI3K pyrimidine derived inhibitor BKM-120 ( Novartis AG ), the dual
inhibition of
mTOR/PI3K in NSCLC by PF-4691502 ( Pfizer Inc ), the small-molecule PDK-1 inhibitors PF-05177624 and PF-05197281 ( both Pfizer ) and the ability of RO-5323441 ( F Hoffmann-La Roche Ltd/ThromboGenics NV/BioInvent International AB ) to block tumor growth in vivo ... This conference report highlights selected presentations on preclinical data on the novel
pan-PI3K pyrimidine derived inhibitor BKM-120 ( Novartis AG ), the dual
inhibition of
mTOR/PI3K in NSCLC by PF-4691502 ( Pfizer Inc ), the small-molecule PDK-1 inhibitors PF-05177624 and PF-05197281 ( both Pfizer ) and the ability of RO-5323441 ( F Hoffmann-La Roche Ltd/ThromboGenics NV/BioInvent International AB ) to block tumor growth in vivo ... This conference report highlights selected presentations on preclinical data on the novel pan-PI3K pyrimidine derived inhibitor BKM-120 ( Novartis AG ), the dual
inhibition of
mTOR/PI3K in NSCLC by PF-4691502 ( Pfizer Inc ), the small-molecule
PDK-1 inhibitors PF-05177624 and PF-05197281 ( both Pfizer ) and the ability of RO-5323441 ( F Hoffmann-La Roche Ltd/ThromboGenics NV/BioInvent International AB ) to block tumor growth in vivo
Ding et al., J Cell Physiol 2010
:
These results suggest that
FGF-2 mediated
PI3-K signaling may have a direct role in modulating the downstream of Wnt pathway to maintain undifferentiated hESC
Zheng et al., J Cell Biochem 2010
(Stomach Neoplasms) :
FTY720 dramatically increased the expression of Cip1/p21, p27, and BH3-only proteins through the accumulation of p53 by
PTEN mediated inhibition of the
PI3K/Akt/MDM2 signaling
Yang et al., J Cell Physiol 2010
(MAP Kinase Signaling System) :
Results show that overexpression of
FUT4 increases the phosphorylation of ERK1/2, p38 MAPK, and
PI3K/Akt ... Inhibitors of
PI3K ( LY294002 and Wortmannin )
prevented the phosphorylation of ERK1/2, p38
MAPK , and Akt PI3K ) ... Inhibitors of
PI3K ( LY294002 and Wortmannin )
prevented the phosphorylation of
ERK1/2 , p38 MAPK, and Akt PI3K ) ... These data suggested that
FUT4 not only
activates MAPK and
PI3K/Akt signals, but also promotes the crosstalk among these signaling pathways
Ryu et al., Biocell 2010
(Carcinoma, Squamous Cell...) :
Blocking the activation of the PI3K/Akt pathway using LY294002 abolished Akt activation in response to cobalt chloride, suggesting that
Akt phosphorylation by cobalt chloride is
dependent on
PI3K
Faria et al., Naunyn Schmiedebergs Arch Pharmacol 2010
:
Our results show that PKC, MAPK,
PI3K , and cytoskeletal components are
involved in
P2X(7) receptor large-channel formation in 2BH4 cells and peritoneal macrophages
Mohamed et al., Am J Physiol Lung Cell Mol Physiol 2010
:
Interestingly, selective inhibitors of PTK,
PI3K , or MEK1/2
attenuated TGF-beta1 expression through blocking ERK1/2 phosphorylation and TGF-beta1 promoter activity in response to stretch
Liu et al., Ann Hematol 2010
(Leukemia, Myeloid) :
Inactivation of
PI3k/Akt signaling pathway and
activation of
caspase-3 are involved in tanshinone I-induced apoptosis in myeloid leukemia cells in vitro
Wang et al., J Biol Chem 2010
:
Shear induced interleukin-6 synthesis in chondrocytes : roles of E prostanoid ( EP ) 2 and EP3 in cAMP/protein kinase A- and
PI3-K/Akt dependent
NF-kappaB activation ... Selective knockdown of EP2 or ectopic expression of EP3 blocks PKA- and
PI3-K/Akt dependent
p65 activation and markedly diminishes shear induced IL-6 expression
Cohen et al., Antioxid Redox Signal 2011
(Myocardial Infarction...) :
Phosphatidylinositol 3-kinase activation
results in phosphorylation of
Akt promoting activation of nitric oxide synthase and nitric oxide production, which inhibits glycogen synthase kinase-3ß, perhaps the final cytosolic signaling step before inhibition of MPTP formation
Zhang et al., J Cell Mol Med 2011
(Endotoxemia...) :
To determine whether
PI3K regulates
Rac1 activation, cardiomyocytes were treated with LY294002, a PI3K selective inhibitor ... We conclude that
PI3K mediated Rac1 activation is
required for induction of
TNF-a expression in cardiomyocytes and cardiac dysfunction during endotoxemia ... We conclude that
PI3K mediated
Rac1 activation is required for induction of TNF-a expression in cardiomyocytes and cardiac dysfunction during endotoxemia
Choi et al., Korean J Intern Med 2010
(Diabetes Mellitus, Type 2...) :
Although the mechanisms underlying insulin resistance are not completely understood in skeletal muscle, it is thought to result, at least in part, from impaired
insulin dependent
PI3K activation and downstream signaling
Romero et al., J Pineal Res 2010
(Neuroblastoma) :
The neuroprotective effect was prevented by chelerythrine, LY294002, and Sn ( IV ) protoporphyrin IX dichloride ( SnPP ), indicating the participation of the
PKC/PI3K/Akt activation and
induction of the antioxidant enzyme
heme oxygenase-1
Venkatesan et al., J Mol Cell Cardiol 2010
:
EMMPRIN activates multiple transcription factors in cardiomyocytes, and induces interleukin-18 expression via
Rac1 dependent
PI3K/Akt/IKK/NF-kappaB andMKK7/JNK/AP-1 signaling ... We show for the first time that EMMPRIN stimulates the activation of NF-kappaB, AP-1, CREB, and ATF-2 in cardiomyocytes, and induces IL-18 expression via
Rac1 dependent
PI3K/Akt/IKK/NF-kappaB and MKK7/JNK/AP-1 signaling
Liu et al., Acta Biochim Biophys Sin (Shanghai) 2010
:
Results showed that
apelin-13 promoted the expression of
phospho-PI3K and phospho-Akt in dose- and timedependent manner ... PI3K inhibitor LY294002 significantly decreased the expression of
phospho-PI3K , phospho-Akt, phospho-ERK1/2, and cyclin D1
induced by
apelin-13
Zuo et al., Breast Cancer Res 2010
(Breast Neoplasms...) :
To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that mPRalpha, caveolin-1 (Cav-1), and epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed
EMT in MB468 cells can be
blocked by EGFR inhibitor ( AG1478 ) and
PI3K inhibitor ( wortmannin ) ... To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that mPRalpha,
caveolin-1 (Cav-1), and epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed EMT in MB468 cells can be
blocked by EGFR inhibitor ( AG1478 ) and
PI3K inhibitor ( wortmannin ) ... To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that mPRalpha,
caveolin-1 (Cav-1) , and epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed EMT in MB468 cells can be
blocked by EGFR inhibitor ( AG1478 ) and
PI3K inhibitor ( wortmannin ) ... To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that
mPRalpha , caveolin-1 (Cav-1), and epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed EMT in MB468 cells can be
blocked by EGFR inhibitor ( AG1478 ) and
PI3K inhibitor ( wortmannin ) ... To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that mPRalpha, caveolin-1 (Cav-1), and
epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed EMT in MB468 cells can be
blocked by EGFR inhibitor ( AG1478 ) and
PI3K inhibitor ( wortmannin )
Ornelas et al., Int J Dev Neurosci 2010
:
Activation of these pathways by ATP seemed to be independent, since LY294002 and U0126, inhibitors of
PI3K and MEK, did not
block the activation of
ERK and AKT, respectively, although each compound blocked its respective target ... Activation of these pathways by ATP seemed to be independent, since LY294002 and U0126, inhibitors of
PI3K and MEK, did not
block the activation of ERK and
AKT , respectively, although each compound blocked its respective target
Liu et al., J Immunol 2010
(Inflammation) :
Mechanoactivation of VEGFR2 results in its nuclear translocation and elevation of
PI3K dependent
Ser473-Akt phosphorylation
Chen et al., J Biol Chem 2010
(Colorectal Neoplasms) :
rHSP90alpha induced the activities of ERK,
PI3K/Akt , and NF-kappaB p65, but only NF-kappaB activation was
involved in HSP90alpha induced
integrin alpha(V) expression ... rHSP90alpha induced the activities of ERK,
PI3K/Akt , and NF-kappaB p65, but only
NF-kappaB activation was
involved in HSP90alpha induced integrin alpha(V) expression
Luo et al., J Cell Biochem 2010
:
PI3K is
involved in
L-selectin- and PSGL-1 mediated neutrophil rolling on E-selectin via F-actin redistribution and assembly ... Western blot analysis demonstrated that
PI3K activation, peaking within 5 min, was
induced by ligation of
L-selectin and PSGL-1 with E-selectin, and that Vav1 ( the pivotal downstream effector of PI3K signaling pathway involved in cytoskeleton regulation ) was recruited to the membrane and tyrosine phosphorylated, depending on PI3K ... Western blot analysis demonstrated that
PI3K activation, peaking within 5 min, was
induced by ligation of L-selectin and
PSGL-1 with E-selectin, and that Vav1 ( the pivotal downstream effector of PI3K signaling pathway involved in cytoskeleton regulation ) was recruited to the membrane and tyrosine phosphorylated, depending on PI3K
Lee et al., Gastroenterology 2010
(Colitis...) :
Biochemical analyses indicated that
PI3K-Akt signaling
increased nuclear total beta-catenin and
P-beta-catenin ( 552 ) levels and reduced N-terminal beta-catenin phosphorylation, which is associated with degradation ...
PI3K inhibition in interleukin-10 ( -/- ) mice
impaired colitis induced epithelial Akt and
beta-catenin activation, reduced progenitor cell expansion, and prevented dysplasia ...
PI3K inhibition in interleukin-10 ( -/- ) mice
impaired colitis induced epithelial
Akt and beta-catenin activation, reduced progenitor cell expansion, and prevented dysplasia ...
PI3K induced and Akt mediated
beta-catenin signaling are required for progenitor cell activation during the progression from CUC to CAC ; these factors might be used as biomarkers of dysplastic transformation in the colon
Redlak et al., Dig Dis Sci 2011
(Stomach Neoplasms) :
The binding of
HSP90 with pro-survival kinase Akt prevents proteosomal degradation of Akt and
contributes to the functional stabilization of
PI3K/Akt signaling and cell survival
Liu et al., Zhonghua Gan Zang Bing Za Zhi 2010
:
[
Effects of insulin and LY294002 inhibitors of
PI3K on the regulations and expression of
aquaporin 9 in normal liver cells ]
Hinkelmann et al., Eur J Pharm Sci 2010
:
The increased
HO-1 mRNA stability by this compound was
blocked by inhibition of
PI3K/Akt , but not by that of p38 MAPK
Gao et al., Toxicol Appl Pharmacol 2010
:
A constitutive level of
PI3K dependent
Akt phosphorylation remained unchanged by Ni and/or MALP-2 exposure
Merkenschlager et al., J Exp Med 2010
:
These studies therefore explain the negative
regulation of
Foxp3 by
PI3K signaling, and add Foxo proteins to the growing list of nuclear factors capable of modulating Foxp3 expression
Oinuma et al., J Biol Chem 2010
:
Phosphatidylinositol 3-phosphate level is critically
regulated by
PI3K and PTEN ( phosphatase and
tensin homologue deleted chromosome ten )
Kim et al., Biochim Biophys Acta 2010
(Prostatic Neoplasms) :
Collectively, these data in a mouse prostate cell system uncover for the first time a novel and complex relationship between PTEN loss mediated
PI3K/AKT activation and posttranslational
regulation of
MT1-MMP , which may play a role in PC progression ... Collectively, these data in a mouse prostate cell system uncover for the first time a novel and complex relationship between PTEN loss mediated
PI3K/AKT activation and posttranslational
regulation of
MT1-MMP , which may play a role in PC progression
Lee et al., FEBS Lett 2010
:
We demonstrate that reduction in Ca ( 2+ ) by chelating compound BAPTA-AM or by IP ( 3 ) -endoplasmic reticulum blocker 2-APB selectively inhibited
VEGF induced activation of
c-Src-PI3K-Akt but not ERK1/2 in human coronary artery endothelial cells ( HCAEC ) ... We also show that the selective inhibitory effects of NADPH oxidase knockdown on
VEGF mediated
activation of
c-Src-PI3K-Akt signaling and cell proliferation in HCAEC can be reversed by increase in intracellular Ca ( 2+ )
Willox et al., Mol Immunol 2010
(MAP Kinase Signaling System) :
Evidence for
PI3K dependent
CXCR3 agonist induced degranulation of human cord blood derived mast cells
Chi et al., Exp Cell Res 2010
(Lung Neoplasms) :
Inhibitors of various MAPKs,
PI-3K and PKC
attenuated significantly IL-4 stimulated
15-PGDH activity indicating that MAPKs, PI-3K/Akt and PKC pathways participated in IL-4 induced up-regulation of 15-PGDH
Kim et al., Biochem Biophys Res Commun 2010
:
In addition, IBMX induced
PPAR-gamma transcriptional activity was
blocked by
PI3K/Akt , PKA, or Rap1 inhibitors
Zhang et al., J Surg Res 2011
(Aortic Aneurysm, Abdominal...) :
To delineate the underlying molecular mechanism, we showed that
AGE increased phosphorylation of p44/42 ERK, p38, JNK, and
PI3K in macrophages ... Inhibition of ERK ( UO126 ) or p38 ( SB203580 ), but not
PI3K ( LY294002 or wortmannin ),
blocked AGE induced
MMP-9 expression
Jang et al., BMC cancer 2010
(Breast Neoplasms...) :
Inhibition of
PI3K/Akt signaling by ANT2 shRNA
caused down-regulation of membrane-type 1 matrix metalloproteinase ( MT1-MMP ) and
vascular endothelial growth factor ( VEGF ) expression, decreased matrix metalloproteinase 2 (MMP2) and MMP9 activity, and suppressed migration and invasion of breast cancer cells ... Inhibition of
PI3K/Akt signaling by ANT2 shRNA
caused down-regulation of
membrane-type 1 matrix metalloproteinase ( MT1-MMP ) and vascular endothelial growth factor ( VEGF ) expression, decreased matrix metalloproteinase 2 (MMP2) and MMP9 activity, and suppressed migration and invasion of breast cancer cells
Xue et al., PloS one 2010
:
Phosphatidylinositol 3-kinase (PI3K) activity was also
required as indicated by the inhibitory effects of
PI3K inhibitors, wortmannin and LY294002, and a PI3K dominant negative ( DN ) mutant Deltap85alpha
Kim et al., Arch Pharm Res 2010
:
These data suggest that RA-induced
PI3K/Akt activation in the early stage of differentiation is
required for
Nanog expression, which becomes independent of PI3K/Akt signaling once the differentiation is established
Bratton et al., Int J Oncol 2010
(Breast Neoplasms) :
Regulation of ERalpha mediated transcription of
Bcl-2 by
PI3K-AKT crosstalk : implications for breast cancer cell survival
Wang et al., Hepatology 2010
(Carcinoma, Hepatocellular...) :
The role of the Oct4-AKT-ABCG2 axis in cancer cell chemoresistant machinery suggests that
AKT pathway inhibition (
PI3K inhibitors ) not only inhibits cancer cell proliferation, but may also enhance chemosensitivity by target potential chemoresistant cells
Gong et al., Biol Pharm Bull 2010
(Pancreatic Neoplasms) :
Activation of p65
NF-kappaB was
dependent on the phosphorylation of
PI3K/Akt
Kim et al., J Lipid Res 2010
:
The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving
PI3-K/PKB/AMPK dependent
CREB/TORC2 activation ... The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving
PI3-K/PKB/AMPK dependent
CREB/TORC2 activation
Gross et al., J Neurosci 2010
(Disease Models, Animal...) :
In wild type,
gp1 mGluR activation
induces p110beta translation, p110beta protein expression, and
PI3K activity
Lazorchak et al., Mol Cell 2010
:
However, the function and molecular mechanism of
mTOR mediated
PI3K signaling in B cells has not been fully elucidated
Balogh et al., Immunobiology 2011
(Obesity) :
The signal pathway of 50 ng/mL leptin stimulation involves Ca ( 2+ ) signal,
activation of
PI3K , MAPK and
HMG CoA reductase
Van Themsche et al., Molecular cancer 2010
:
Although each TGF-beta isoform decreased PTEN content in a XIAP- and a Smad dependent manner, decrease of
PTEN levels in response to only one isoform, TGF-beta3, was
blocked by
PI3-K inhibitor LY294002
Wu et al., Am J Nephrol 2010
:
LXA ( 4 ) inhibited the expression and activity of
ILK and
activation of Ras, ERK1/2,
PI3-K and Akt in HK-2 cells stimulated by CTGF
Liu et al., Neurotox Res 2011
:
These results suggest that
IL-6 protects neurons against NMDA induced apoptosis, and that the IL-6 neuroprotection is jointly
mediated by JAK-STAT3 and
PI3K-Akt signaling pathways
Zhang et al., Experimental biology and medicine (Maywood, N.J.) 2010
:
These findings demonstrate for the first time that
PI3K/Akt dependent
cyclin D1 activation plays an essential role in HDL induced EPC proliferation, migration and angiogenesis
Knævelsrud et al., Autophagy 2010
(Colonic Neoplasms...) :
One such autophagic inducer is the Beclin 1 binding protein
UVRAG , a positive
regulator of the class III
PI3K/Vps34 complex
Chao et al., Brain Pathol 2011
:
More importantly,
BDNF activation of CK2 is not
affected by co-administration of the ERK1/2 inhibitor, PD98059, and the
PI3-K inhibitor, LY294002
Yan et al., FASEB J 2011
:
The antimitogenic efficacy of PGE ( 2 ) in inhibiting control cultures was associated with greater ability to stimulate sustained
PKA activation and greater
inhibition of late-phase promitogenic p42/p44 and
PI3K activities
Tiwari et al., J Gen Virol 2010
:
We also show that inhibition of
PI3K signalling also
affected RhoA activation required for HSV-1 entry into certain cell types
Zhang et al., Biol Pharm Bull 2010
(Insulin Resistance) :
Moreover, 7-O-MA stimulated the reactivation of insulin mediated phosphorylation of phosphatidylinositol 3-kinase (PI3K) linked protein kinase B ( Akt/PKB ) and adenosine 5'-monophosphate activated protein kinase ( AMPK ) in high glucose induced, insulin-resistant HepG2 cells, and this effect was blocked by either LY294002, a
PI3K inhibitor, or compound C, an
AMPK inhibitor
Wallin et al., Sci Transl Med 2010
(Breast Neoplasms...) :
We used preclinical cancer models to determine the effects of combining the DNA damaging drug doxorubicin with
GDC-0941 , a class I
PI3K inhibitor that is currently being tested in early-stage clinical trials
Moeller et al., Exp Clin Endocrinol Diabetes 2011
(Thyroid Hormone Resistance Syndrome) :
The aim of this study was to examine the
effect of TH, TRß and
PI3K on
stanniocalcin 1 (STC1) expression in human cells
Kim et al., Eur J Immunol 2010
(Airway Remodeling...) :
Moreover, we found that inhibition of the
PI3K p110d isoform (PI3K-d) or HIF-1a
reduced OVA induced
HIF-1a activation in airway epithelial cells
Berna et al., J Biol Chem 2010
:
Akt activation by
CCK and gastrin could be
inhibited by the
PI3K inhibitor wortmannin ...
Akt activation by CCK and gastrin could be
inhibited by the
PI3K inhibitor wortmannin ... Akt activation by CCK and
gastrin could be
inhibited by the
PI3K inhibitor wortmannin
Kim et al., Mediators Inflamm 2010
:
Activation of
CD147 with cyclophilin a
induces the expression of IFITM1 through ERK and
PI3K in THP-1 cells ... Activation of CD147 with cyclophilin a
induces the expression of
IFITM1 through ERK and
PI3K in THP-1 cells ... CD147 induced expression of
IFITM1 was
blocked by inhibitors of ERK,
PI3K , or NF-?B, but not by inhibitors of p38, JNK, or PKC
Lu et al., Journal of molecular signaling 2010
:
Overexpressing the adaptor protein
SH2B1ß enhanced H2O2 induced
PI3K-AKT and MEK-ERK1/2 signaling, reduced nucleus localized FoxOs and the expression of a pro-apoptotic gene, FasL
Sury et al., Neurobiol Dis 2011
(Disease Models, Animal...) :
Protein levels and activity of PTEN, the major antagonist of PI3K, were unaltered by infection, suggesting that the observed decrease in
PIP ( 3 ) and Akt phosphorylation is a
result of decreased
PI3K signaling ... Protein levels and activity of PTEN, the major antagonist of PI3K, were unaltered by infection, suggesting that the observed decrease in PIP ( 3 ) and
Akt phosphorylation is a
result of decreased
PI3K signaling ... These results indicate that the inhibitory effect of bpV ( pic ) on apoptosis was mediated by
PI3K dependent activation of
Akt , strongly suggesting that bpV ( pic ) acted on PTEN
Cui et al., Mol Cell Biochem 2011
:
The aim of this study is to determine whether depletion of
PI3K-C2a affects
ERK or PKB/Akt activity following stimulation with serum and insulin growth factors in Chinese hamster ovary cells expressing human insulin receptors ( CHO-IR ) and human HepG2 liver cells ... The aim of this study is to determine whether depletion of
PI3K-C2a affects ERK or
PKB/Akt activity following stimulation with serum and insulin growth factors in Chinese hamster ovary cells expressing human insulin receptors ( CHO-IR ) and human HepG2 liver cells ... The aim of this study is to determine whether depletion of
PI3K-C2a affects ERK or
PKB/Akt activity following stimulation with serum and insulin growth factors in Chinese hamster ovary cells expressing human insulin receptors ( CHO-IR ) and human HepG2 liver cells ... Insulin- or serum induced stimulation of
ERK was significantly
suppressed by depletion of
PI3K-C2a , whereas phosphorylation of IRS-1 and the stimulation of PKB/Akt by insulin were not affected
Li et al., Biomed Environ Sci 2010
:
Activation of
PI3K/Akt1 pathway and subsequent negative
regulation of
p21 ( WAF1/CIP1 ) and p27 ( KIP1 ) expression might be involved in CagA associated carcinogenesis ... Activation of
PI3K/Akt1 pathway and subsequent negative
regulation of p21 ( WAF1/CIP1 ) and
p27 ( KIP1 ) expression might be involved in CagA associated carcinogenesis
Zhang et al., Biochim Biophys Acta 2011
:
Akt phosphorylation was
inhibited by the
PI3K inhibitor LY294002 ( 10µM ), farnyltranferase inhibitor FTI-276, or transfection with a dominant negative Akt
Wang et al., Am J Physiol Heart Circ Physiol 2010
(Disease Models, Animal...) :
Importantly, inhibition of either
PI3K or eNOS attenuated exercise induced restoration of the dilatation function and
blocked PI3K,
Akt , and eNOS phosphorylation by ACh in the mesenteric arteries ... Importantly, inhibition of either
PI3K or eNOS attenuated exercise induced restoration of the dilatation function and
blocked PI3K, Akt, and
eNOS phosphorylation by ACh in the mesenteric arteries
Byles et al., International journal of biological sciences 2010
:
Aberrant cytoplasm localization and protein stability of
SIRT1 is
regulated by
PI3K/IGF-1R signaling in human cancer cells ... We found this predominant cytoplasmic localization of
SIRT1 is
regulated by elevated mitotic activity and
PI3K/IGF-1R signaling in cancer cells ... We show that aberrant cytoplasmic localization of
SIRT1 is due to increased protein stability and is
regulated by
PI3K/IGF-1R signaling ... Our study represents the first identification that aberrant cytoplasm localization is one of the specific alternations to SIRT1 that occur in cancer cells, and
PI3K/IGF-1R signaling
plays an important role in the regulation of cytoplasmic
SIRT1 stability
Liao et al., J Cell Physiol 2011
(Inflammation) :
MSF-2 suppresses
PI3K activation and phosphatidylinositol ( 3,4,5 ) -trisphosphate ( PIP3 ) production, and consequently inhibits downstream activation of PDK1 and AKT ... In conclusion, MSF-2 opposes fMLP mediated neutrophil activation and inflammation by inhibiting
PI3K activation and subsequent
activation of
AKT and PLC?2 ... In conclusion, MSF-2 opposes fMLP mediated neutrophil activation and inflammation by inhibiting
PI3K activation and subsequent
activation of AKT and
PLC?2
Chiou et al., Eur J Pharmacol 2011
:
Psoralidin inhibits LPS induced iNOS expression via repressing
Syk mediated activation of
PI3K-IKK-I?B signaling pathways
Liu et al., Prostate 2011
(Adenocarcinoma...) :
Androgen induced
PSA expression
requires not only activation of AR but also endogenous IGF-I or
IGF-I/PI3K/Akt signaling in human prostate cancer epithelial cells
Bros et al., Gene 2011
:
Both Cacnb3 isoforms, similar to Fscn1, required JNK and
p38 kinase activity for stimulation associated upregulation, and this process was
inhibited by ERK and
PI(3)K
Georgopoulos et al., PloS one 2010
:
Functional inactivation of E-cadherin interferes with the capacity of NHU cells to form stable calcium mediated contacts, attenuates
E-cadherin mediated
PI3-K/AKT induction and enhances NHU cell proliferation by allowing de-repression of the EGFR/ERK pathway and constitutive activation of ß-catenin-TCF signalling
Gao et al., Br J Pharmacol 2011
:
As NRF1 and NRF2 are under the transcriptional control of peroxisome proliferator activated receptor ? coactivators-1a and -1ß ( PGC-1a and PGC-1ß ), we found that suppressing
PI3K activity selectively
reduced both the mRNA and protein levels of
PGC-1ß but not PGC-1a
de la Monte et al., Journal of population therapeutics and clinical pharmacology = Journal de la thérapeutique des populations et de la pharamcologie clinique 2010
(Insulin Resistance) :
As a result,
insulin activation of
PI3K-Akt , which mediates neuronal survival, motility, energy metabolism, and plasticity, is impaired
Luangdilok et al., Eur J Cancer 2011
(Carcinoma, Squamous Cell...) :
In both cell lines stimulated with endogenous or exogenous ligand, inhibition of MEK1/2 ( with U0126 or PD98059 ) or
PI3K ( with PI-103 or LY294002 )
resulted in a marked reduction of EGFR induced
VEGF-A expression, whereas exogenous EGF induced VEGF-C upregulation was blocked by inhibitors of MEK but not PI3K ... In both cell lines stimulated with endogenous or exogenous ligand, inhibition of MEK1/2 ( with U0126 or PD98059 ) or PI3K ( with PI-103 or LY294002 ) resulted in a marked reduction of EGFR induced VEGF-A expression, whereas exogenous EGF induced
VEGF-C upregulation was
blocked by inhibitors of MEK but not
PI3K
Tan et al., Cancer Cell 2010
(Cell Transformation, Neoplastic...) :
On loss of PPP2R2B,
mTORC1 inhibitor rapamycin
triggers a compensatory Myc phosphorylation in PDK1 dependent, but
PI3K and AKT independent manner, resulting in resistance
Jiang et al., Cancer Res 2011
(Colonic Neoplasms) :
PRL-3 activation
stimulated PI3K/AKT signaling that caused resistance to stress induced apoptosis
Medina et al., J Immunol 2010
(Inflammation...) :
In this study, we demonstrate that the induction of
TNF and IL-6 expression by LVS in mouse bone marrow derived macrophages was markedly
enhanced when
PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002 ... In this study, we demonstrate that the induction of TNF and
IL-6 expression by LVS in mouse bone marrow derived macrophages was markedly
enhanced when
PI3K activity was inhibited by either of the well-known chemical inhibitors, wortmannin or LY294002
Gislette et al., TheScientificWorldJournal 2010
(Neoplasms...) :
IL-17 could
activate Src/PI3K , MAPK, Stat3, and PKC, resulting in carcinogenesis
Li et al., J Biol Chem 2011
(Thrombosis) :
Because of recent reports that arrestins can serve as scaffolds to recruit phosphatidylinositol-3 kinases (PI3K)s to GPCRs, we sought to determine whether arrestins regulate
PI3K dependent
Akt signaling in platelets, with consequences for thrombosis
Su et al., J Steroid Biochem Mol Biol 2011
(Breast Neoplasms) :
Our study reveals that
PI3K/Akt and MAPK inhibitors
suppressed aromatase activity in MCF-7aro cells ... However,
PI3K/Akt pathway inhibitors
stimulated aromatase activity in T47Daro cells
Yu et al., Cancer Chemother Pharmacol 2011
(Carcinoma, Non-Small-Cell Lung...) :
The
PI3 K or ERK inhibitors also
attenuated expression of
VEGF and MMP-9 ... The
PI3 K or ERK inhibitors also
attenuated expression of VEGF and
MMP-9
Leen et al., Endocrinology 2011
:
The
role of
PI3K/Akt in GLP-2 induced
IGF-I mRNA levels in the murine jejunum was also confirmed in vivo
Wang et al., J Immunol 2011
:
JAK1 activity was
required for IFN-ß to activate
PI3K and Akt1 that resulted in repression of glycogen synthase kinase 3 ( GSK3 ) -ß activity ... IFN-ß increased the phosphorylated levels of CREB and
STAT3 but only CREB levels were
affected by
PI3K ... IFN-ß increased the phosphorylated levels of
CREB and STAT3 but only CREB levels were
affected by
PI3K
Eda et al., Cell Biol Int 2011
(Arthritis, Rheumatoid) :
The aim of this study is to investigate whether
PI3K ( phosphatidylinositol-3-kinase ) is
involved in IL-1ß ( interleukin-1ß ) -induced
IL-6 production in A549 ( human lung adenocarcinoma epithelial cell ) and human RASF ( rheumatoid arthritis synovial fibroblast ) ...
PI3K inhibitor, LY294002 significantly
reduced IL-1ß induced
IL-6 production in A549 cells but not in RASF, indicating that IL-1ß induced IL-6 production was partially mediated by PI3Kin A549 cells but not in RASF ... These results indicate that IL-1ß induced
IL-6 production in A549 cells is
mediated by both
PI3K and IRAK4 and suggest that involvement of PI3K in the IL-1 induced IL-6 production is cell type specific
Yingchun et al., Braz J Med Biol Res 2011
:
In the present study, we evaluated whether E3 ubiquitin ligase
Cbl-b , a negative
regulator of
PI3K activation, is involved in the action of ATO
Li et al., J Neuroimmunol 2011
(Chronic Disease...) :
Furthermore, stimulation of
TLR2 by PGN
induces protection from stress induced reduction in the number of splenocytes through
PI3K ... Collectively, our study thus demonstrates that stimulation of
TLR2 mediated
PI3K signaling attenuates splenocyte reduction induced by stress, and that ß-arrestin 2 modulates TLR2 mediated immune response following stress
Wu et al., Zhongguo Ying Yong Sheng Li Xue Za Zhi 2004
:
IGF-1 increases VSM proliferation by increasing
PI3K activity and
inhibiting PTEN activity
Liao et al., J Biol Chem 2011
(Breast Neoplasms) :
PC4 functions are beyond TSA induced phosphatase release,
PI3K mediated
Sp1 phosphorylation, and HDAC1/2/mSin3A co-repressor release indicating its role as linker coactivator of Sp1 and the transcriptional machinery
Bito et al., Journal of skin cancer 2011
:
Furthermore, a
PI3K inhibitor also
suppressed Stat3 activation in HSC-1 cells to some degree ... These data suggest that
Stat3 activation through EGFR and/or
PI3K/Akt activation plays a critical role in the proliferation and survival of human cutaneous SCC
Kim et al., J Neurochem 2011
:
The transcriptional activator
Sox18 was recruited to the MOR promoter in CHX treated cells and this recruitment was also
inhibited by the
PI3-K and p38 MAPK inhibitors, Ly294002 and SB203580, respectively
Martin et al., Cancer Res 2011
(Colorectal Neoplasms) :
Although
AKT activity was elevated in KRAS mutant cells, and
PI3K inhibition did
impair the growth of MEK inhibitor-insensitive CRC cell lines, concurrent treatment with selumetinib did not provide additional antitumor activity
Lee et al., PloS one 2010
(Endotoxemia) :
Furthermore, in vitro cellular studies demonstrated that LPS ( lipopolysaccharide ) activation of
mTORC1-S6K still occurs in the
presence of
PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways ... Furthermore, in vitro cellular studies demonstrated that
LPS ( lipopolysaccharide ) activation of mTORC1-S6K still occurs in the
presence of
PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Bianchi et al., J Biol Chem 2011
(Encephalitis) :
We show here that high S100B stimulates murine microglia migration in Boyden chambers via
RAGE dependent activation of Src kinase, Ras,
PI3K , MEK/ERK1/2, RhoA/ROCK, Rac1/JNK/AP-1, Rac1/NF-?B, and, to a lesser extent, p38 MAPK ... The S100B/RAGE dependent activation of diaphanous-1/Rac1/JNK/AP-1, Ras/Rac1/NF-?B and
Src/Ras/PI3K/RhoA/diaphanous-1 results in the up-regulation of expression of the chemokines, CCL3, CCL5, and CXCL12, whose release and activity are
required for
S100B to stimulate microglia migration ... The
S100B/RAGE dependent activation of diaphanous-1/Rac1/JNK/AP-1, Ras/Rac1/NF-?B and
Src/Ras/PI3K/RhoA/diaphanous-1 results in the up-regulation of expression of the chemokines, CCL3, CCL5, and CXCL12, whose release and activity are required for S100B to stimulate microglia migration
Je et al., Molecular brain 2011
(Synaptic Transmission) :
Previously, we demonstrated that the long-term synaptic modulation requires the endocytosis of
neurotrophin-receptor complex, the
activation of
PI3K and Akt, and mTOR mediated protein synthesis
Banerjee et al., Mol Cancer Ther 2011
(Disease Models, Animal...) :
Third, the incomplete suppression of Nf1-deficient glial cell proliferation in vivo following 5 mg/kg/day rapamycin treatment reflects mTOR mediated AKT activation, such that combined 5 mg/kg/day rapamycin and
PI3-kinase (PI3K) inhibition or dual
PI3K/mTOR inhibition recapitulates the growth suppressive effects of 20 mg/kg/day rapamycin
Ramella et al., Regul Pept 2011
:
Taken together, our data suggest a potential role of TPO as a physiological regulator of CF. By acting on specific receptors present on endothelial cells, TPO may induce
PI3K/Akt dependent
eNOS phosphorylation and NO release
Dutra et al., Br J Pharmacol 2011
(Colitis) :
Importantly, the
PI3K? inhibitor also
up-regulated IL-10 , CD25 and FoxP3 expression ... Importantly, the
PI3K? inhibitor also
up-regulated IL-10,
CD25 and FoxP3 expression ... Importantly, the
PI3K? inhibitor also
up-regulated IL-10, CD25 and
FoxP3 expression
Antoniv et al., Immunology 2011
:
Phosphatidylinositol 3-kinase (PI3K) -mediated signalling regulates inflammatory responses and can
induce IL-10 production, but a role for
PI3K signalling in cellular responses to IL-10 is not known
Sabri et al., Cell Biochem Funct 2011
(MAP Kinase Signaling System) :
In this study, we investigated the
effects of
PI3K/AKT , ERK1/2, P38 and JNK on
EGF signalling in hMSCs ... The
effects of
EGF on MAPKs and
PI3K/AKT crosstalk were investigated by immunoblotting ; cyclooxygenase-2 (COX-2) expression was studied by real-time RT-PCR ; and cell proliferation was evaluated by methylthiazolyl tetrazolium bromide assay
Lin et al., J Biol Chem 2011
:
Thrombin induced IL-8/CXCL8 release and
IL-8/CXCL8-luciferase activity were
attenuated by a
PI3K inhibitor ( LY294002 ), an Akt inhibitor ( 1-L-6-hydroxymethyl-chiro-inositol-2- ( ( R ) -2-O-methyl-3-O-octadecylcarbonate ) ), and the dominant negative mutants of Rac1 ( RacN17 ) and Akt ( AktDN ) ... Thrombin induced IL-8/CXCL8 release and
IL-8/CXCL8-luciferase activity were
attenuated by a
PI3K inhibitor ( LY294002 ), an Akt inhibitor ( 1-L-6-hydroxymethyl-chiro-inositol-2- ( ( R ) -2-O-methyl-3-O-octadecylcarbonate ) ), and the dominant negative mutants of Rac1 ( RacN17 ) and Akt ( AktDN )
Heldsinger et al., J Biol Chem 2011
(Ion Channel Gating) :
Synergistic interaction between leptin and
cholecystokinin in the rat nodose ganglia is
mediated by
PI3K and STAT3 signaling pathways : implications for leptin as a regulator of short term satiety ... Synergistic interaction between
leptin and cholecystokinin in the rat nodose ganglia is
mediated by
PI3K and STAT3 signaling pathways : implications for leptin as a regulator of short term satiety
Belo et al., Am J Physiol Gastrointest Liver Physiol 2011
(Colonic Neoplasms...) :
Collectively, these findings indicate that ACh induced cell migration is mediated by
MMP7 mediated release of HBEGF, an ERBB ligand that activates ERBB1 and downstream ERK and
PI3K signaling
Bhattacharyya et al., J Biol Chem 2011
(Cystic Fibrosis...) :
However, overexpressing SHIP1 or inhibition of
PI3K in CF cells
suppressed IL-8 expression
Han et al., Invest Ophthalmol Vis Sci 2011
(Glaucoma, Open-Angle) :
PI3K inhibition with LY294002
reduced a-SMA expression
Voskas et al., F1000 biology reports 2010
:
Does GSK-3 provide a shortcut for
PI3K activation of
Wnt signalling ?
Wang et al., PloS one 2011
(Adenocarcinoma...) :
Several compounds in the categories of
HSP90 inhibitor, HDAC inhibitor, PPAR agonist,
PI3K inhibitor , passed our screening to be the leading candidates
Yoshimi et al., Blood 2011
(Leukemia) :
Evi1 represses PTEN expression and
activates PI3K/AKT/mTOR via interactions with polycomb proteins
Lau et al., Oncogene 2011
(Ovarian Neoplasms) :
E-cadherin inhibits tumor cell growth by
suppressing PI3K/Akt signaling via ß-catenin-Egr1 mediated PTEN expression ... Thus, the loss of
E-cadherin itself may
contribute to dysregulated
PI3K/Akt signaling through its effects on PTEN, or it may exacerbate the frequent activation of PI3K/Akt signaling that occurs as a result of overexpression, mutation and/or amplification
Gamell et al., PloS one 2011
:
In our earlier report we showed that activation of
LIMK1 also
requires the activation of PAKs through Cdc42 and
PI3K
Liu et al., Prostate 2011
(Prostatic Neoplasms) :
G-protein alpha-s and -12 subunits are involved in androgen stimulated
PI3K activation and
androgen receptor transactivation in prostate cancer cells
Gan et al., J Biol Chem 2011
:
In HEK293T cells, insulin and constitutively active mutants of small GTPase H-Ras and PI3K could induce HM phosphorylation of both
AKT mutants, which was
blocked by the
PI3K inhibitor LY294002
Zeidan et al., Mol Cell Biochem 2011
:
Our results demonstrate a critical
role for
PI3K/mTOR/p70 ( S6K ) in leptin induced
RhoA activation resulting in cardiomyocyte hypertrophy associated with GATA4 stimulation
Di Santo et al., Journal of thrombosis and haemostasis : JTH 2011
(Thrombosis) :
The results demonstrated that, in MN interacting with activated PLT : ( i ) TF activity, antigen and mRNA were low until 8-10 h and dramatically increased thereafter, up to 24 h ; ( ii ) according to the kinetics of TF expression in MN, GSK3ß undergoes phosphorylation on serine 9, a process associated with down-regulation of enzyme activity ; ( iii ) pharmacological blockade of GSK3 further increased TF expression and was accompanied by increased accumulation of NF-kB, in the nucleus ; ( iv ) blockade of phosphoinositide-3 kinase ( PI(3)K ) by wortmannin inhibited PLT induced TF expression ; and ( v ) according to the established role of the GSK3 downstream insulin receptor,
insulin increased PLT induced TF expression in a
PI(3)K dependent manner ... The results demonstrated that, in MN interacting with activated PLT : ( i ) TF activity, antigen and mRNA were low until 8-10 h and dramatically increased thereafter, up to 24 h ; ( ii ) according to the kinetics of TF expression in MN, GSK3ß undergoes phosphorylation on serine 9, a process associated with down-regulation of enzyme activity ; ( iii ) pharmacological blockade of GSK3 further increased TF expression and was accompanied by increased accumulation of
NF-kB , in the nucleus ; ( iv ) blockade of phosphoinositide-3 kinase ( PI(3)K ) by wortmannin inhibited PLT induced TF expression ; and ( v ) according to the established role of the GSK3 downstream insulin receptor, insulin increased PLT induced TF expression in a
PI(3)K dependent manner
Park et al., J Cell Physiol 2011
:
In addition, laminin-111 induced
Akt phosphorylation was
inhibited by integrin ß1 small interfering RNA ( siRNA ) and
PI3K inhibitors ( LY294002 and wortmannin )
Tramentozzi et al., J Cell Mol Med 2011
:
Results reveal a fundamental
role of
HSP90 in the
PI3K/Akt pathway mediated angiogenic-like effect of Grp94-IgG, also questioning the capacity of CTT to serve as an effective inhibitor of the angiogenic effect
Metlakunta et al., Am J Physiol Regul Integr Comp Physiol 2011
(Obesity...) :
In food restricted WT mice with reduced body weight,
leptin increased hypothalamic
PI3K activity only at 30 min, and p-STAT3 levels at 30-120 min postinjection ... In the next experiment with a clonal hypothalamic neuronal cell line expressing proopiomelanocortin, we observed that whereas
leptin significantly
increased IRS1 associated
PI3K activity and p-JAK2 levels in cells transfected with control vector, it failed to do so in SOCS3 overexpressed cells
Yin et al., J Mol Med (Berl) 2011
(Disease Models, Animal...) :
Our results demonstrated that administration of Rg1 increased VEGF expression levels, activated
PI3K/Akt , and
inhibited p38
MAPK in vitro and in vivo ...
PI3K inhibitor LY294002 significantly
attenuated Rg1 enhanced
VEGF expression and capillary density ... Rg1 induced activation of
PI3K/Akt also
contributed to the downregulation of p38
MAPK ...
Rg1 induced
activation of
PI3K/Akt also contributed to the downregulation of p38 MAPK
Feng et al., J Cell Biochem 2011
:
PI3K and ERK/Nrf2 pathways are
involved in oleanolic acid induced
heme oxygenase-1 expression in rat vascular smooth muscle cells
Brown et al., Infect Immun 2011
(Colitis...) :
We show that the inhibition of
PI3K signaling
attenuates epithelial
Akt activation, the Ser552 phosphorylation and activation of ß-catenin, and epithelial cell proliferative responses during C. rodentium infection
Wang et al., World J Gastroenterol 2011
(Colonic Neoplasms) :
SDF-1 induced significant phosphorylation of
PI3K/AKT and ß-catenin
Weigelt et al., Oncogene 2011
(Breast Neoplasms) :
PI3K pathway activation
leads to stimulation of the key growth and proliferation regulatory kinase
mammalian target of rapamycin (mTOR) , which can be inhibited by rapamycin analogues and by kinase inhibitors ; the effectiveness of these drugs in breast cancer treatment is currently being tested in clinical trials
Hsu et al., Cancer Res 2011
(Colorectal Neoplasms...) :
Taken together, the results indicate that stimulation of the
TLR4/MD2 complex by LPS
activates PI3K/AKT signaling and promotes downstream ß1 integrin function, thereby increasing the adhesiveness and metastatic capacity of CRC cells ... Taken together, the results indicate that stimulation of the TLR4/MD2 complex by
LPS activates
PI3K/AKT signaling and promotes downstream ß1 integrin function, thereby increasing the adhesiveness and metastatic capacity of CRC cells
Xiang et al., Cell Biochem Funct 2011
:
The inhibitory effect of ghrelin on
caspase-3 activity was
attenuated by inhibitors of ERK1/2 ( PD98059 ),
PI3K/Akt ( LY294002 ) and growth hormone secretagogue receptor ( GHSR ) -1a ( D-Lys ( 3 ) -growth hormone releasing peptide-6 )
Suzuki et al., J Biol Chem 2011
(Cell Transformation, Neoplastic...) :
The levels of Cbp expression were inversely correlated with the activity of MEK and Akt, and
Cbp down-regulation was
suppressed by inhibiting MEK and
PI3K
Wilson et al., J Biol Chem 2011
:
Interestingly, we also show that
PDE3B binds directly to p84, a PI3K? regulatory subunit, and that this interaction
allows PI3K? recruitment to the PDE3B-EPAC1 complex ... Of potential cardiovascular importance, we demonstrate that PDE3B tethered
EPAC1 regulates HAEC
PI3K? activity and that this allows dynamic cAMP dependent regulation of HAEC adhesion, spreading, and tubule formation
Zhang et al., J Cell Physiol 2012
(Carcinoma, Non-Small-Cell Lung...) :
EGF stimulated IL-8 production, phosphorylation of Akt and
Erk , and cell proliferation and movement could be
inhibited by EGFR inhibitor ( Erlotinib ),
PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 ) ... EGF stimulated IL-8 production, phosphorylation of
Akt and Erk, and cell proliferation and movement could be
inhibited by EGFR inhibitor ( Erlotinib ),
PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 ) ... EGF stimulated
IL-8 production, phosphorylation of Akt and Erk, and cell proliferation and movement could be
inhibited by EGFR inhibitor ( Erlotinib ),
PI3K inhibitor ( GDC-0941 BEZ-235 and SHBM1009 ), and ERK1/2 inhibitor ( PD98059 )
Vasudevan et al., Mol Cell 2011
:
We show here that
PI3K? inhibits protein
phosphatase 2A (PP2A) at the ß-adrenergic receptor ( ßAR, a GPCR ) complex altering G protein coupling ... Mechanistically,
PI3K? inhibits
PP2A activity at the ßAR complex by phosphorylating an intracellular inhibitor of PP2A ( I2PP2A ) on serine residues 9 and 93, resulting in enhanced binding to PP2A ... Our study provides the underpinnings of a
PI3K? mediated regulation of
PP2A activity that has significant consequences on receptor function with broad implications in cellular signaling
WEI et al., Nan Fang Yi Ke Da Xue Xue Bao 2011
:
TSA dose-dependently inhibited the transcription and protein expression of CD28 in CD(4) ( + ) T cells and
reduced the expression of
PI3K protein in activated CD(4) ( + ) T cells, without showing significant effect on the expression of ZAP70
Li et al., Zhongguo Dang Dai Er Ke Za Zhi 2011
(Neuroblastoma) :
The synthesis and secretion of
VEGF can be
inhibited by blocking TrkB-BDNF signal pathway with K252a or blocking the TrkB-BDNF downstream signal pathway
PI3K/Akt with LY294002
Oh et al., Int Immunopharmacol 2011
:
CKD712, ( S ) -1- ( a-naphthylmethyl ) -6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline,
inhibits the lipopolysaccharide stimulated secretion of
HMGB1 by inhibiting
PI3K and classical protein kinase C
Toubiana et al., J Biol Chem 2011
:
We report here that IMPDHII
plays an important role in the negative regulation of
TLR2 signaling by modulating
PI3K activity
Noh et al., Mol Med Report 2011
(Breast Neoplasms) :
Inhibition of
PI3K with an inhibitor, wortmannin,
increased the level of
PTEN protein in ERa positive MCF-7 cells, while levels in ERa negative MDA-MB 231 cells were not altered
Fortin et al., Eur J Immunol 2011
:
Finally, we show that in
LPS- and TNF activated neutrophils,
PI3K acts downstream of the kinases p38 MAPK and TAK1
Weisser et al., Eur J Immunol 2011
(Neoplasms) :
STAT6 transcription was
inhibited by
PI3K inhibitors and enhanced when SHIP was reduced using siRNA
Liu et al., Mol Med Report 2010
:
Further investigation revealed that
TRAIL engagement
led to the activation of
PI3K/Akt as well as of NF-?B ... Our data demonstrated that the
activation of
PI3K/Akt and NF-?B by
TRAIL is responsible for resistance to TRAIL in human gastric cancer cells
Suzuki et al., Mol Med Report 2008
:
In addition, our study revealed that neither the
PI3K/Akt nor the p53 signaling pathway is
required for Zeb induced
HIF-1a degradation
Yadav et al., Mol Carcinog 2011
:
Fyn is
induced by
Ras/PI3K/Akt signaling and is required for enhanced invasion/migration ... In addition, expression of
Fyn in MDA-MB-231 breast cancer cells was
dependent on
PI3K activity and was involved in their invasive phenotype
Chung et al., Endocr J 2011
:
In addition, phospho-Akt was translocated to the nucleus in response to ghrelin and
PI3K inhibition by LY294002
prevented ghrelin induced effect on
phospho-Akt localization
Voloshenyuk et al., Cytokine 2011
(MAP Kinase Signaling System) :
Induction of cardiac fibroblast
lysyl oxidase by TGF-ß1
requires PI3K/Akt , Smad3, and MAPK signaling ... The increase of
LOX protein in response to TGF-ß1 was
prevented by inhibitors of
PI3K , Smad3, p38-MAPK, JNK and ERK1/2
Ketschek et al., Communicative & integrative biology 2011
:
Thus,
NGF increases formation of axonal filopodia through localized
PI3K signaling that promotes the initiation of actin patch precursors to the formation of axonal filopodia
Chern et al., Planta Med 2011
(Cerebral Infarction...) :
Andrographolide inhibits
PI3K/AKT dependent
NOX2 and iNOS expression protecting mice against hypoxia/ischemia induced oxidative brain injury ... Andrographolide inhibits
PI3K/AKT dependent NOX2 and
iNOS expression protecting mice against hypoxia/ischemia induced oxidative brain injury ... Our results indicate that andrographolide reduces NOX2 and iNOS expression possibly by impairing
PI3K/AKT dependent NF- ?B and
HIF-1 a activation
Shen et al., Physiol Behav 2011
:
To determine whether the
activation of
PI3K by
apoE is required for the ability of apoE to reduce food intake, LY294002 ( 1 nmol ) was infused into the 3rd-cerebral ventricle before injection of an anorectic dose of apoE
Makarova et al., J Biol Chem 2011
(Acute Lung Injury...) :
uPA induced phosphorylation of eNOS was also inhibited by the
protein kinase A (PKA) inhibitor, myristoylated PKI, but was not
dependent on
PI3K-Akt signaling ... uPA induced phosphorylation of
eNOS was also inhibited by the protein kinase A (PKA) inhibitor, myristoylated PKI, but was not
dependent on
PI3K-Akt signaling
Wang et al., J Cell Mol Med 2012
(Carcinoma, Hepatocellular...) :
Tumour necrosis factor-a (TNF-a) significantly induced phosphorylation of p38 MAPK, ERK, Akt and production of IL-8 from HCC cells, which were prevented by SB203580 (
p38 MAPK inhibitor ), PD98059 ( ERK inhibitor ), LY294002 and Wortmannin (
PI3K inhibitor ) and SB328437 ( CCR3 inhibitor ) ... Tumour necrosis factor-a (TNF-a) significantly induced phosphorylation of p38 MAPK, ERK, Akt and production of IL-8 from HCC cells, which were prevented by SB203580 ( p38
MAPK inhibitor ), PD98059 ( ERK inhibitor ), LY294002 and Wortmannin (
PI3K inhibitor ) and SB328437 ( CCR3 inhibitor )
Saito et al., Hum Reprod 2011
(Endometriosis...) :
The TGF-ß1 induced increase in
PAR2 gene expression was
repressed by inhibition of p38 MAPK, p42/44 MAPK or
PI3K , but not by knockdown of Smad4 expression
Jin et al., Stroke 2011
(Infarction, Middle Cerebral Artery...) :
PI3K? deficiency
suppressed ischemia/reperfusion induced nuclear factor-?B p65 ( Ser536 ) phosphorylation and the expression of the pro-oxidant enzyme NADPH oxidase ( Nox1, Nox2, and Nox4 ) and proinflammatory adhesion molecules ( E- and
P-selectin , intercellular adhesion molecule-1 ) at different time points ...
PI3K? deficiency
suppressed ischemia/reperfusion induced nuclear factor-?B
p65 ( Ser536 ) phosphorylation and the expression of the pro-oxidant enzyme NADPH oxidase ( Nox1, Nox2, and Nox4 ) and proinflammatory adhesion molecules ( E- and P-selectin, intercellular adhesion molecule-1 ) at different time points ...
PI3K? deficiency
suppressed ischemia/reperfusion induced nuclear factor-?B p65 ( Ser536 ) phosphorylation and the expression of the pro-oxidant enzyme
NADPH oxidase ( Nox1, Nox2, and Nox4 ) and proinflammatory adhesion molecules ( E- and P-selectin, intercellular adhesion molecule-1 ) at different time points
Ferretti et al., Leukemia 2011
(Leukemia, Lymphocytic, Chronic, B-Cell) :
CX(3)CL1 induced phosphorylation of
PI3K , Erk1/2, p38, Akt and Src was involved in induction of CLL chemotaxis
Li et al., Cancer Res 2011
(Neoplasms) :
Finally, ErbB2 potentiated RNA
Pol I transcription could be stimulated by ligand and was not substantially
repressed by inhibition of
PI3-K and MEK/ERK ( extracellular signal regulated kinase ), the main ErbB2 effector signaling pathways
Chen et al., EMBO J 2011
(Prostatic Neoplasms) :
Importantly, we find that the molecular mechanism underlying MED1 mediated chromatin looping involves
PI3K/AKT phosphorylated MED1
mediated recruitment of FoxA1, RNA polymerase II and TATA binding protein and their subsequent interactions at the
UBE2C locus
Zhu et al., DNA Cell Biol 2011
:
Salidroside increased the intracellular mRNA expression and activities of
catalase and Mn-superoxide dismutases in a
PI3K dependent manner
Wen et al., FASEB J 2011
:
Overall, using biochemical, cellular, genetic, and physiological approaches, our findings reveal that adenosine is a novel molecule signaling via A ( 2B ) R activation, contributing to penile erection via
PI3K/AKT dependent
eNOS activation
Lee et al., Mol Cells 2011
(Breast Neoplasms) :
Moreover, the higher production of
vascular endothelial growth factor ( VEGF ) in TAMR-MCF-7 cells was significantly
diminished by suppression of
PI3K or p38 kinase
Sévère et al., J Biol Chem 2011
:
Analysis of molecular mechanisms revealed that the
Cbl mutant
increased PDGF receptor a and FGF receptor 2 but not EGF receptor expression in hMSCs, resulting in increased ERK1/2 and
PI3K signaling
Xu et al., Eur Rev Med Pharmacol Sci 2011
(Diabetes Mellitus, Experimental) :
Effect of insulin in combination with selenium on blood glucose and
PI3K mediated
GLUT4 expression in skeletal muscle of streptozotocin induced diabetic rats
Zhang et al., Front Biosci (Elite Ed) 2011
:
Taken together, the present study demonstrates that T3 potentiates the cell survival action of FSH through Src- and
PI3K mediated Xiap up-regulation and decreased
Fas and FasL expression ... Taken together, the present study demonstrates that T3 potentiates the cell survival action of FSH through Src- and
PI3K mediated Xiap up-regulation and decreased Fas and
FasL expression ... Taken together, the present study demonstrates that T3 potentiates the cell survival action of FSH through Src- and
PI3K mediated
Xiap up-regulation and decreased Fas and FasL expression
Xu et al., Yao Xue Xue Bao 2011
(Diabetes Mellitus, Experimental) :
The result showed that
insulin in combination with selenium could significantly lower blood glucose and blood lipid levels and markedly
restored the
PI3K and GLUT4 levels in cardiac muscle
Ito et al., J Lipid Res 2011
(Obesity) :
Furthermore,
insulin increased both Akt and JNK phosphorylation, which was abrogated by the
PI3K inhibitors
Kim et al., Immune network 2011
:
Both
TNF-a and IL-6 production by HBHA was
regulated by the NF-?B,
PI3-K , and MAPK pathways ... Both TNF-a and
IL-6 production by HBHA was
regulated by the NF-?B,
PI3-K , and MAPK pathways ... Furthermore,
PI3-K activity was
required for the HBHA induced activation of ERK1/2 and p38
MAPK , but not JNK, pathways ... Furthermore,
PI3-K activity was
required for the HBHA induced activation of
ERK1/2 and p38 MAPK, but not JNK, pathways
Klöckener et al., Nat Neurosci 2011
(Body Weight...) :
Collectively, our experiments reveal that high-fat diet induced,
insulin dependent
PI3K activation in VMH neurons contributes to obesity development
Wang et al., J Cell Physiol 2011
:
Taken together, these results suggested that in astrocytes, activation of NF-?B by ET ( B ) -dependent c-Src,
PI3K/Akt , and p42/p44 MAPK signalings is
necessary for ET-1 induced
iNOS gene up-regulation
Schmid et al., Cancer Cell 2011
(Disease Progression...) :
Receptor tyrosine kinases and
TLR/IL1Rs unexpectedly
activate myeloid cell
PI3k? , a single convergent point promoting tumor inflammation and progression ... Receptor tyrosine kinases and
TLR/IL1Rs unexpectedly
activate myeloid cell
PI3k? , a single convergent point promoting tumor inflammation and progression
Karst et al., Gynecol Oncol 2011
(Cystadenocarcinoma, Serous...) :
Stathmin 1, a marker of
PI3K pathway
activation and
regulator of microtubule dynamics , is expressed in early pelvic serous carcinomas
Margolis et al., J Physiol 2011
:
Using a variety of blockers we determined that the augmentation is probably due to insertion of GABA ( A ) Rs into the synapse by a mechanism that is G-protein independent and mediated by
activation of
Akt via
PI3K
Lasala et al., Am J Physiol Endocrinol Metab 2011
:
Blocking PKA abolished the effect of cAMP on Sox9, Sf1, and Gata4 expression, inhibiting
PI3K/PKB impaired the effect on
Sf1 and Gata4, and reducing MEK1/2 and p38 MAPK activities curtailed Gata4 increase ... Blocking PKA abolished the effect of cAMP on Sox9, Sf1, and Gata4 expression, inhibiting
PI3K/PKB impaired the effect on Sf1 and Gata4, and
reducing MEK1/2 and p38
MAPK activities curtailed Gata4 increase ... Blocking PKA abolished the effect of cAMP on Sox9, Sf1, and Gata4 expression, inhibiting
PI3K/PKB impaired the effect on Sf1 and
Gata4 , and reducing MEK1/2 and p38 MAPK activities curtailed Gata4 increase ... Blocking PKA abolished the effect of cAMP on Sox9, Sf1, and Gata4 expression, inhibiting
PI3K/PKB impaired the effect on Sf1 and Gata4, and
reducing MEK1/2 and p38 MAPK activities curtailed Gata4 increase
Yang et al., Mol Biol Rep 2012
(Coronary Restenosis...) :
High mobility group box-1 induces migration of vascular smooth muscle cells via
TLR4 dependent
PI3K/Akt pathway
activation ... We also found pretreated cells with TLR4 siRNA or the PI3 K inhibitor LY294002 could markedly block
PI3K/Akt pathway activation and VSMCs migration
mediated by
HMGB1 ( P both < 0.05 )
Kazlauskas et al., EMBO J 1990
:
Binding is rapid, saturable and
requires phosphorylation of the
PDGFR at Y751, but does not require PDGF dependent phosphorylation of
PI3K
Lu et al., J Immunol 2011
(Infarction, Middle Cerebral Artery...) :
More significantly, either
TLR2 deficiency or
PI3K inhibition with LY29004 abolished the protection by Pam3CSK4
Alvin et al., Med Sci Monit 2011
(Cardiomegaly) :
However in the absence of angiotensin converting enzyme inhibition, ANG II increased both IK and
IK1 in a
PI3-K dependent manner in hypertrophied cardiomyocytes ... Thus, captopril treatment reveals a negative effect of ANG II on IK and IK1, which is PI3-K independent, whereas in the absence of angiotensin converting enzyme inhibition IK and
IK1 regulation is
dependent upon
PI3-K
Lai et al., International journal of biological sciences 2011
:
Moreover, we demonstrated that
IL-8 activated
PI3K following the same kinetics observed from IL-8 induction of cytoskeletal rearrangement, suggesting the participation of PI3K in these processes
Weidinger et al., J Clin Endocrinol Metab 2011
(Carcinoma...) :
FOXO3 is
inhibited by oncogenic
PI3K/Akt signaling but can be reactivated by the NSAID sulindac sulfide
Ke et al., J Hepatol 2012
(Disease Models, Animal...) :
These findings underscore the
role of
HO-1 induced STAT3 in modulating
PI3K/PTEN in liver IRI cascade
Kim et al., J Mol Biol 2011
:
Both
P-TEFb recruitment to the HIV long terminal repeat and enhanced HIV processivity were
blocked by the ERK ( extracellular-signal regulated kinase ) inhibitor U0126, but not by AKT ( serine/threonine protein kinase Akt ) and
PI3K ( phosphatidylinositol 3-kinase ) inhibitors
Hagiwara et al., J Cell Physiol 2012
(Liver Neoplasms) :
Our findings suggest that BCAA supplementation may be useful to suppress liver cancer progression by inhibiting
insulin induced
PI3K/Akt and subsequent anti-apoptotic pathway, indicating the importance of BCAA supplementation to the obese patients with advanced liver disease
Schmid et al., Carcinogenesis 2011
(Breast Neoplasms...) :
In summary, we characterized
PI3K-mTOR dependent proteasome mediated
Pdcd4 degradation in tumor cells in the inflammatory tumor microenvironment
Yang et al., Cancer Res 2011
(Carcinoma, Non-Small-Cell Lung...) :
This approach also determined the molecular mechanisms and adaptors required for
PI3K activation following inhibition of the mTOR kinase
TORC1
Elgort et al., Genes & cancer 2010
:
Mechanistically, Ras-MAPK and
PI3K/Akt signaling
inhibit TXNIP translation and MondoA dependent
TXNIP transcription, respectively
Pangon et al., Genes & cancer 2010
:
In addition, exposure to ultraviolet radiation ( UV ), but not phleomycin, caused
PI3K dependent phosphorylation of
MCC and its nuclear localization
Dennis et al., J Steroid Biochem Mol Biol 2011
:
G36 selectively inhibits estrogen mediated
activation of
PI3K by
GPER but not ERa
Singhal et al., J Biol Chem 2011
:
Notably,
Btk activation is
necessary for HGF induced association of c-Src and
PI3K with c-MET ... Notably, Btk activation is necessary for
HGF induced association of c-Src and
PI3K with c-MET
Hart et al., Proc Natl Acad Sci U S A 2011
(Cell Transformation, Neoplastic) :
GDC-0941, a specific inhibitor of
PI3K reduces the level of
Stat3 phosphorylation ... The
effect of
PI3K on
Stat3 appears to be mediated by a member of the Tec kinase family ... In some human tumor cell lines, the enhanced phosphorylation of
Stat3 is
inhibited by both
PI3K and by Tec kinase inhibitors, suggesting that the link between PI3K and Stat3 is significant in human cancer
Ma et al., Blood 2011
:
Conversely, loss of
PI3K activation reduces the maturation of mast cells by inhibiting the activation of AKT, leading to reduced Mitf but
enhanced Gata-2 expression and accumulation of Gr1 ( + ) Mac1 ( + ) myeloid cells as opposed to mast cells
Wong et al., Biochem Pharmacol 2011
(Glucose Intolerance...) :
In corresponding Ang-IV treated animals,
insulin induced IRAP and
PI3K interaction, activation of pAkt and GLUT4 translocation, but no corresponding activation of IR, IRS-1 and IRS-1-PI3K coupling were observed
Subramaniam et al., Arch Pathol Lab Med 2011
(Sarcoma, Synovial) :
In monophasic fibrous tumors, increased expression of Snail ( 17 of 27 ; 63 % ),
Slug ( 18 of 27 ; 67 % ), and dysadherin ( 14 of 27 ; 52 % ) and
activation of Wnt ( nucleocytoplasmic ß-catenin accumulation in 63 % ; n = 27 ; and positive expression of GSK3 and pGSK3 in 24 of 27 [ 89 % ] and 21 of 27 [ 78 % ], respectively ) and
PI3K/Akt ( Akt : 22 of 27 [ 81 % ] ; pAkt : 25 of 27 [ 93 % ] ; and PI3K : 20 of 27 [ 74 % ] ) signaling correlated significantly with inactivated E-cadherin expression ( 1 of 27 ; 4 % ) ... In monophasic fibrous tumors, increased expression of Snail ( 17 of 27 ; 63 % ), Slug ( 18 of 27 ; 67 % ), and
dysadherin ( 14 of 27 ; 52 % ) and
activation of Wnt ( nucleocytoplasmic ß-catenin accumulation in 63 % ; n = 27 ; and positive expression of GSK3 and pGSK3 in 24 of 27 [ 89 % ] and 21 of 27 [ 78 % ], respectively ) and
PI3K/Akt ( Akt : 22 of 27 [ 81 % ] ; pAkt : 25 of 27 [ 93 % ] ; and PI3K : 20 of 27 [ 74 % ] ) signaling correlated significantly with inactivated E-cadherin expression ( 1 of 27 ; 4 % )
Liu et al., Cell Mol Neurobiol 2012
:
Activation of ERK1/2 and
PI3K/Akt by
IGF-1 on GAP-43 expression in DRG neurons with excitotoxicity induced by glutamate in vitro
Welsch et al., PloS one 2011
(Carcinoma, Pancreatic Ductal...) :
Epo could
initiate PI3K/Akt signaling via EpoR in PDAC cells but failed to alter their functions, probably due to co-expression of the soluble EpoR isoform, known to antagonize Epo
Amente et al., Nucleic Acids Res 2011
:
Myc and
PI3K/AKT signaling cooperatively
repress FOXO3a dependent PUMA and
GADD45a gene expression
Park et al., Int Immunopharmacol 2011
:
Schisandra chinensis a-iso-cubebenol
induces heme oxygenase-1 expression through
PI3K/Akt and Nrf2 signaling and has anti-inflammatory activity in Porphyromonas gingivalis lipopolysaccharide stimulated macrophages
Gopinath et al., Mol Oncol 2011
(Glioma) :
uPAR and cathepsin B downregulation was recently shown to
induce p27 expression through
PI3K/Akt/FOXO3a signaling
Lei et al., Am J Physiol Lung Cell Mol Physiol 2011
:
In the present study, we assessed the
role of
Akt in Na-K-ATPase activity and the interaction between the
PI3K and MAPK in response to T3 by using MP48 cells, inhibitors, and constitutively active mutants in the MP48 ( alveolar type II-like ) cell line ... Inhibitors of Src kinase ( PP1 ),
PI3K ( wortmannin ), and ERK1/2 ( U0126 ) all
blocked the T3-induced
Na-K-ATPase activity ...
PP1 blocked the activation of
PI3K and also ERK1/2 by T3, whereas U0126 did not prevent T3 activation of Src kinase or PI3K activity ... In summary, in adult rat AECs T3-stimulated
Src kinase activity can
activate both
PI3K/Akt and MAPK/ERK1/2, and activation of Akt is necessary for T3-induced Na-K-ATPase activity
Wen et al., Oncogene 2012
(Helicobacter Infections...) :
These results show that H. pylori infection induces
AKT/PI3K mediated phosphorylation of
p27 at T157 and T198 to cause cytoplasmic p27 mislocalization in gastric cancer, and that p27 mislocalization is an adverse prognostic feature in gastric cancer
Xia et al., Mol Cell Biochem 2012
(Asthma...) :
We investigated the
effects of
PI3K inhibitor wortmannin on iNOS expression in bronchiole epithelial cells and NO,
IL-4 and IFN-? levels in lung tissues of asthmatic rat model, which was prepared by 10 % OVA solution sensitization and 1 % OVA aerosol challenge ... We investigated the
effects of
PI3K inhibitor wortmannin on
iNOS expression in bronchiole epithelial cells and NO, IL-4 and IFN-? levels in lung tissues of asthmatic rat model, which was prepared by 10 % OVA solution sensitization and 1 % OVA aerosol challenge ...
PI3K inhibitor wortmannin could
lead to reduced
iNOS expression and NO production, therefore inhibiting airway inflammatory responses
Ishikawa et al., Nihon Arukoru Yakubutsu Igakkai Zasshi 2011
:
Alternatively, cytokine signaling studies indicate that
IL-12 production by DCs is negatively
regulated by
PI3K and GSK-3, but positively regulated by p38 MAPK, mTOR, and NF-kappa B
Yohn et al., BMC urology 2011
(Carcinoma, Transitional Cell...) :
Phosphatidylinositol 3'-kinase , mTOR, and glycogen synthase kinase-3ß
mediated regulation of
p21 in human urothelial carcinoma cells
Goertz et al., J Clin Invest 2011
(Infertility, Male) :
By conditional inactivation of 3-phosphoinositide dependent protein kinase 1 ( Pdk1 ) and phosphatase and tensin homolog (Pten) in the male germ line, we found that
PI3K signaling
regulates Foxo1 stability and subcellular localization, revealing that the Foxos are pivotal effectors of PI3K-Akt signaling in SSCs
Xiao et al., Cell Physiol Biochem 2011
:
Specific inhibitors of
PI3K suppressed stretch -induced
CTGF expression in a time dependent manner
de la Torre et al., Pharmacol Res 2012
:
However, neither of the CDK inhibitors nor SB415286 prevented the increase in
c-Jun phosphorylation
induced by
PI3K inhibition
Hwang et al., Toxicol Appl Pharmacol 2011
:
These results indicate that puerarin stimulates eNOS phosphorylation and NO production via activation of an
estrogen receptor mediated
PI3K/Akt- and CaMKII/AMPK dependent pathway
Wertheimer et al., Cell Signal 2012
(Breast Neoplasms...) :
P-Rex1 is
activated by the
PI3K product PIP3 and Gß? subunits, and integrates signals from ErbB receptors and GPCRs
Visser et al., PloS one 2011
:
We used Rac1 dominant negative transfection and chemical inhibition of phosphatidylinositol-3 kinase (PI3K) to show that even though
Rac1 activation was
PI3K dependent , neither was required for Msp induced actin rearrangement
Fox et al., Cancer Res 2011
(Adenocarcinoma...) :
Inhibition of InsR and
IGF-IR with the dual tyrosine kinase inhibitor OSI-906 prevented the emergence of hormone independent cells and tumors in vivo,
inhibited parental and LTED cell growth and
PI3K/AKT signaling, and suppressed growth of established MCF-7 xenografts in ovariectomized mice, whereas treatment with the neutralizing IGF-IR monoclonal antibody MAB391 was ineffective ... Inhibition of
InsR and IGF-IR with the dual tyrosine kinase inhibitor OSI-906 prevented the emergence of hormone independent cells and tumors in vivo,
inhibited parental and LTED cell growth and
PI3K/AKT signaling, and suppressed growth of established MCF-7 xenografts in ovariectomized mice, whereas treatment with the neutralizing IGF-IR monoclonal antibody MAB391 was ineffective
Guo et al., J Biol Chem 2011
(Breast Neoplasms...) :
IKBKE activation of Akt was not
affected by inhibition of
PI3K , knockdown of PDK1 or mTORC2 complex ... IKBKE activation of
Akt was not
affected by inhibition of
PI3K , knockdown of PDK1 or mTORC2 complex
Williams et al., J Neurosci 2011
:
The acute effects of
leptin require
PI3K signaling in the hypothalamic ventral premammillary nucleus
Dai et al., Int J Cancer 2012
:
We found that KSHV activation of
emmprin induces
PI3K/Akt- and mitogen activated protein kinase ( MAPK ) -dependent secretion of vascular endothelial growth factor ( VEGF ) ... Functionally, EC invasion following de novo infection is induced by
emmprin dependent
PI3K/Akt and MAPK activation of VEGF
Janas et al., J Immunol 2011
:
Mice with a mutant allele of p110? unable to bind active Ras revealed that
CXCR4 mediated
PI3K activation is Ras dependent
Xu et al., Hepatogastroenterology 2011
(Fatty Liver) :
Leptin may be involved in NAFLD pathogenesis by activating the PI3-K/Akt kinase pathway via OB-R and the defective
leptin activation of
PI3-K is a novel mechanism of leptin resistance in NAFLD
Mantuano et al., J Neurosci 2011
:
In cultured SCs, the PKR-like ER kinase target eIF2a was phosphorylated and
CHOP was
induced by ( 1 ) inhibiting
PI3K , ( 2 ) treating the cells with tumor necrosis factor-a (TNF-a), or ( 3 ) genetic silencing of LRP1
Yen et al., J Biol Chem 2011
(MAP Kinase Signaling System) :
We show that PGE2 induced MMP-9 expression is mediated primarily through the EP2/EP4 cAMP protein kinase A
(PKA)/PI3K ERK signaling pathway, leading to c-Fos expression, and through JNK mediated
activation of
c-Jun in a PKA/PI3K/ERK independent manner ... PKA,
PI3K , and ERK inhibitors abolished PGE2- and cAMP induced c-Fos and MMP-9 up-regulation, and ERK activation was
required for the binding of activator protein 1 (AP-1)
transcription factor to the MMP-9 promoter ... PKA,
PI3K , and ERK inhibitors abolished PGE2- and cAMP induced c-Fos and MMP-9 up-regulation, and
ERK activation was
required for the binding of activator protein 1 (AP-1) transcription factor to the MMP-9 promoter ... PKA,
PI3K , and ERK inhibitors abolished PGE2- and cAMP induced c-Fos and MMP-9 up-regulation, and ERK activation was
required for the binding of activator protein 1 (AP-1) transcription factor to the
MMP-9 promoter
Hien et al., Mol Pharmacol 2011
:
Moreover, AMPK inhibition significantly reversed the activation of ER-dependent transcription and
PI3K activation in response to nectandrin B. Nectandrin B evoked endothelium dependent relaxation in rat aortic rings, and this was
blocked by inhibition of
AMPK , ER, or PI3K
Xiong et al., Genome Res 2012
(Crohn Disease...) :
The analysis of two human diseases, glioblastoma and Crohn 's disease, detected abnormalities in previously identified disease associated pathways, such as pathways related to
PI3K signaling, DNA damage response, and the
activation of
NFKB
Makrodouli et al., Molecular cancer 2011
(Colonic Neoplasms...) :
In parallel, KRASG12V enhances the ability of colon adenocarcinoma cells Caco-2 to migrate and invade through filopodia formation and
PI3K dependent
Cdc42 activation
Kent et al., Mol Cell Biol 2011
:
Nuclear
FOSL1 increased during trophoblast cell differentiation in a
PI3K/AKT dependent manner
Urtasun et al., Hepatology 2012
(Liver Cirrhosis) :
Likewise, inhibition of
PI3K and NF?B
blocked the OPN mediated
Collagen-I increase
Manna et al., J Biol Chem 2011
:
The PIP3 increase is mediated by
PI3K activation and
inhibition of PTEN but not of
SHIP2 ... The PIP3 increase is mediated by
PI3K activation and
inhibition of
PTEN but not of SHIP2 ... The
PIP3 increase is
mediated by
PI3K activation and inhibition of PTEN but not of SHIP2
Lin et al., Science signaling 2011
:
These phosphorylation events enabled direct binding of GIV to the amino- and carboxyl-terminal
Src homology 2 domains of p85a, a regulatory subunit of PI3K ; stabilized receptor association with PI3K ; and enhanced
PI3K activity at the plasma membrane to
trigger cell migration ... These phosphorylation events enabled direct binding of
GIV to the amino- and carboxyl-terminal Src homology 2 domains of p85a, a regulatory subunit of PI3K ; stabilized receptor association with PI3K ; and enhanced
PI3K activity at the plasma membrane to
trigger cell migration
Ueno et al., Dev Growth Differ 2011
:
In contrast, the
activation of
PI3K-TOR by
Rheb-S16H expression delayed the initiation of cell cycle elongation
Chen et al., J Biol Chem 2011
:
The
PI3K dependent signaling kinase complex
mTORC2 ( mammalian target of rapamycin complex 2 ) has been defined as the regulatory Ser-473 kinase of Akt
Tokuyama et al., PLoS Pathog 2011
(Cell Transformation, Viral...) :
Similarly, inhibition of p110a
PI3K reduces cell surface expression of
RAE-1 on transformed cells
Rowland et al., Mol Cell Biol 2011
:
Insulin increased 14-3-3 binding to RhoGAP22 fourfold, and this effect was
PI3K dependent
Du et al., PloS one 2011
(Breast Neoplasms) :
Both
PI3K inhibitor LY294002 and ERK inhibitor U0126
suppressed hypoxia induced Rac1 activation as well as
HIF-1a expression ... Both
PI3K inhibitor LY294002 and ERK inhibitor U0126
suppressed hypoxia induced
Rac1 activation as well as HIF-1a expression ... Taken together, our study demonstrated that hypoxia induced HIF-1a expression involves a cascade of signaling events including ROS generation, activation of
PI3K and ERK signaling, and subsequent
activation of
Rac1
Beaulieu et al., PloS one 2011
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
The effect of a-linolenic acids seemed to be due to
PI3K pathway and
Bcl-2 inhibition
Kim et al., The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2011
:
Thrombin induced Migration and
Matrix Metalloproteinase-9 Expression Are
Regulated by MAPK and
PI3K Pathways in C6 Glioma Cells
Wang et al., Oncogene 2012
(Ovarian Neoplasms) :
LY294002 and GDC-0941, inhibitors of
PI3K , or Rapamycin, an
inhibitor of PI3K downstream target
mTOR , can reverse the effects of Gab2 on migration and invasion
Chatterjee et al., Am J Physiol Heart Circ Physiol 2012
(Ischemia) :
Activation of
NOX2 was greatly
diminished by wortmannin, knockout of Akt1, or dominant negative
PI3K , whereas membrane depolarization was unaffected
Bhattacharyya et al., Diabetologia 2012
(Glucose Intolerance...) :
Carrageenan exposure completely inhibited
insulin induced increases in phospho- ( Ser473 ) -Akt and
PI3K activity in vivo in mouse liver and in human HepG2 cells
Deng et al., Dev Cell 2011
(Agammaglobulinemia...) :
Noninvasive live imaging of Rac2 morphants or Rac2D57N zebrafish larvae demonstrates an essential
role for
Rac2 in regulating 3D motility and the polarization of F-actin dynamics and
PI(3)K signaling in vivo
Díaz et al., Cell Signal 2012
:
Considering the relevance of the PI3K-Akt signaling in cell survival and in the pathogenesis of cancer, and that GH was reported to modulate EGFR expression and signaling, the objective of this study was to analyze the effects of increased GH levels on
EGF induced
PI3K-Akt signaling
Lee et al., Food Chem Toxicol 2012
(Mesothelioma) :
Reactive oxygen species and
PI3K/Akt signaling
play key roles in the induction of Nrf2-driven
heme oxygenase-1 expression in sulforaphane treated human mesothelioma MSTO-211H cells ... Overall, our results indicate that ROS generation and/or activation of
PI3K/Akt signaling
regulate cell survival and Nrf2-driven
HO-1 expression in sulforaphane treated MSTO-211H cells
Li et al., J Immunol 2011
(HIV Infections...) :
In this study we assessed in these macrophages if the blunted increase in TLR-4 mediated TNF-a release induced by lipid A ( LA ) is associated with
PI3K induced upregulation of
mammalian target of rapamycin (mTOR) activity
Alam et al., J Biol Chem 2011
(Inflammation) :
Importantly,
HDAC3 was
essential for the constitutive transcription of
PI3K and IRF3, which might be responsible for the basal level of galectin-9 expression ... Importantly,
HDAC3 was
essential for the constitutive transcription of
PI3K and IRF3, which might be responsible for the basal level of galectin-9 expression
Zhang et al., PloS one 2011
:
In adult C57BL/6 mice, acute ßAR stimulation induced significant increases in
PI3K activity and
activation of Akt and
ERK1/2 in the heart, but not in lungs or livers ... In adult C57BL/6 mice, acute ßAR stimulation induced significant increases in
PI3K activity and
activation of
Akt and ERK1/2 in the heart, but not in lungs or livers
Uttarwar et al., American journal of physiology. Renal physiology 2012
(Diabetes Mellitus, Experimental...) :
Thus HG-induced
SREBP-1 activation
requires EGFR/PI3K/RhoA signaling and SCAP mediated transport to the Golgi for its proteolytic cleavage
Gallagher et al., Oncogene 2012
(Cell Transformation, Neoplastic...) :
We also investigated the
effect of targeted
PI3K/mTOR inhibition on
PI3K/Akt/mTOR and Erk1/2 signaling, and the potential effects on glycemia ... We also investigated the
effect of targeted
PI3K/mTOR inhibition on
PI3K/Akt/mTOR and Erk1/2 signaling, and the potential effects on glycemia ... We also investigated the
effect of targeted
PI3K/mTOR inhibition on PI3K/Akt/mTOR and
Erk1/2 signaling, and the potential effects on glycemia ... We also investigated the
effect of targeted
PI3K/mTOR inhibition on PI3K/Akt/mTOR and
Erk1/2 signaling, and the potential effects on glycemia
Chin et al., Am J Physiol Gastrointest Liver Physiol 2012
(Crohn Disease...) :
Secretion was also inhibited by H-89 ( PKA inhibitor ) while Tph1 and
VMAT1 transcription was
regulated by PKA/MAPK and
PI3K mediated signaling ... Secretion was also inhibited by H-89 ( PKA inhibitor ) while
Tph1 and VMAT1 transcription was
regulated by PKA/MAPK and
PI3K mediated signaling
Guo et al., Cancer Discov 2011
(Brain Neoplasms...) :
These results show that EGFRvIII can promote tumor survival through
PI3K/SREBP-1 dependent upregulation of
LDLR and suggest a role for LXR agonists in the treatment of GBM patients
Bechard et al., Mol Cell Biol 2012
:
These findings provide new links between
PI3K/Akt signaling and
regulation of Gsk3ß activity by
Frat , an oncogene previously shown to cooperate with Myc in tumorigenesis
Sun et al., J Biol Chem 2011
:
Suppression of
WDR26 by siRNAs selectively
inhibited Gß? dependent phospholipase Cß and
PI3K activation, and attenuated chemotaxis in Jurkat T cells and differentiated HL60 cells in vitro and Jurkat T cell homing to lymphoid tissues in scid mice
Perron et al., Neural development 2011
:
BMP6 , which evokes neural induction but does not have orienting activity, activates Smad signaling but does not
stimulate PI3K
Dubé et al., Biochem Cell Biol 2011
:
MTF-1 activation was
inhibited by PKC, JNK, and
PI3K inhibitors and by the electron transport chain inhibitors rotenone and myxothiazol, but not by the antioxidant N-acetylcysteine
Darido et al., Cancer Cell 2011
(Carcinoma, Squamous Cell...) :
Deletion of Grhl3 in adult epidermis evokes loss of expression of PTEN, a direct GRHL3 target, resulting in aggressive
SCC induced by activation of
PI3K/AKT/mTOR signaling
Buitrago et al., J Cell Biochem 2012
:
Of relevance, Src and
PI3K are
involved in
Akt activation and in MHC and myogenin increased expression by 1a,25 ( OH ) ( 2 ) D ( 3 ) ... Of relevance, Src and
PI3K are
involved in Akt activation and in MHC and
myogenin increased expression by 1a,25 ( OH ) ( 2 ) D ( 3 )
Nawroth et al., PloS one 2011
(Carcinoma, Transitional Cell...) :
Instead, we provide evidence for an alternative mTOR independent but
PI3K dependent regulation of
4E-BP1
He et al., Ann Oncol 2012
(Breast Neoplasms...) :
Human
epidermal growth factor receptor ( HER2 ), insulin receptor and IGF-I receptor
involve the same
PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer ... Human epidermal growth factor receptor ( HER2 ), insulin receptor and
IGF-I receptor involve the same
PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer ... Human epidermal growth factor receptor ( HER2 ),
insulin receptor and IGF-I receptor
involve the same
PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer ... Human epidermal growth factor receptor ( HER2 ),
insulin receptor and IGF-I receptor
involve the same
PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer
Miller et al., Breast Cancer Res 2011
(Breast Neoplasms...) :
PI3K activates AKT,
serum/glucocorticoid regulated kinase ( SGK ), phosphoinositide dependent kinase 1 ( PDK1 ), mammalian target of rapamycin (mTOR), and several other molecules involved in cell cycle progression and survival ...
PI3K activates
AKT , serum/glucocorticoid regulated kinase ( SGK ), phosphoinositide dependent kinase 1 ( PDK1 ), mammalian target of rapamycin (mTOR), and several other molecules involved in cell cycle progression and survival ...
PI3K activates AKT, serum/glucocorticoid regulated kinase ( SGK ), phosphoinositide dependent kinase 1 ( PDK1 ),
mammalian target of rapamycin (mTOR) , and several other molecules involved in cell cycle progression and survival
Erlich et al., Br J Cancer 2012
(Carcinoma, Squamous Cell...) :
Importantly, we observed intratumoural
HDAC inhibition and
PI3K inhibition as assessed by histone H3 acetylation status and phospho-AKT staining, respectively
Loh et al., Diabetologia 2012
(Diabetes Mellitus, Type 2...) :
Blood glucose and insulin levels, insulin and glucose tolerance, and
insulin induced muscle insulin receptor
activation and downstream
PI3K/Akt signalling remained unaltered in chow fed Mck-Cre ; Ptpn2 ( lox/lox ) versus Ptpn2 ( lox/lox ) mice
Li et al., Methods Mol Biol 2012
(Disease Models, Animal...) :
It is hoped that these inhibitors will have widespread clinical impact in oncology because
mTOR is a major downstream
effector of
PI3K signaling, one of the most frequently activated pathways in cancer
Cai et al., Proc Natl Acad Sci U S A 2011
(Ion Channel Gating) :
Tripartite motif containing protein 27 negatively regulates CD4 T cells by ubiquitinating and
inhibiting the class II
PI3K-C2ß
Willems et al., Leukemia 2012
(Leukemia, Myeloid, Acute) :
In addition, the
mTORC1 dependent
PI3K/Akt feedback
activation was fully abrogated in AZD8055 treated AML cells
Warne et al., Cell Metab 2011
(Fatty Liver) :
Impairment of central
leptin mediated
PI3K signaling manifested as hepatic steatosis independent of hyperphagia and obesity ... Attenuation of
leptin induced
PI3K signaling, brought about by transgenic expression of phosphatase and tensin homolog (PTEN) in leptin receptor neurons, leads to decreased hepatic sympathetic tone and increased triglyceride levels without affecting adiposity or hepatic insulin signaling
Maeno et al., J Biol Chem 2012
(Metabolic Diseases) :
In this study, it was observed that PKC activation differentially inhibited insulin receptor substrate 1/2 ( IRS1/2 ) signaling of
insulin 's
activation of
PI3K/eNOS by decreasing only tyrosine phosphorylation of IRS2 ... Thus, PKC and angiotensin induced phosphorylation of Thr-86 of
p85/PI3K may partially
inhibit the activation of
PI3K/eNOS by multiple cytokines and contribute to endothelial dysfunction in metabolic disorders ... Thus, PKC and angiotensin induced phosphorylation of Thr-86 of
p85/PI3K may partially
inhibit the activation of
PI3K/eNOS by multiple cytokines and contribute to endothelial dysfunction in metabolic disorders
Zhuang et al., Ann Clin Lab Sci 2011
(Subarachnoid Hemorrhage) :
Rats were randomly divided into 6 groups : control group, SAH group, SAH+ saline group, SAH+ vehicle group, SAH+ Insulin-like Growth Factor 1 (IGF-1) group, and
SAH+Ly294002 (
PI3K pathway
inhibitor ) group
Lee et al., J Cell Biochem 2012
(Chondrosarcoma) :
The phosphatidylinositol 3-kinase (PI3K),
Akt , and NF-?B pathways were activated by MIF treatment, and the MIF induced expression of integrin and migration activity were
inhibited by the specific inhibitors and mutant forms of
PI3K , Akt, and NF-?B cascades ... The
phosphatidylinositol 3-kinase (PI3K) , Akt, and NF-?B pathways were activated by MIF treatment, and the MIF induced expression of integrin and migration activity were
inhibited by the specific inhibitors and mutant forms of
PI3K , Akt, and NF-?B cascades
Zheng et al., PloS one 2011
:
Surprisingly, the activation of
CaRF , a previously identified transcription factor for CaRE1, was stimulated via L-VGCC but not NMDAR, and
required MEK,
PI3K and CaMKII activity
Meira et al., Molecular cancer 2011
:
The combination of PD98059 and matuzumab did not show the same effect suggesting that
PI3K is an important
effector of
EGFR signaling in matuzumab treated cells
Úriz et al., PloS one 2011
(Choledochal Cyst...) :
Experiments with inhibitors and Ca ( 2+ ) -chelator confirmed that the synergistic
effect of
secretin plus TUDCA involves microtubules, intracellular Ca ( 2+ ), PKCa,
PI3K , PKA and MEK pathways ... UDCA is conjugated in order to promote
secretin stimulated hydrocholeresis in rats through Ae2, microtubules, intracellular Ca ( 2+ ), PKCa,
PI3K , PKA, and MEK
Kim et al., J Clin Immunol 2012
(Acute Lung Injury) :
Additionally, infiltration of dendritic cells (DCs) and expression of
toll-like receptor 4 (TLR4) were significantly increased in the lung of LPS treated mice, and inhibition of
PI3K-? reduced the infiltration of DCs and TLR4 expression in the lung
Shimizu et al., Biochem Biophys Res Commun 2012
:
LY294002 (
PI3K inhibitor ) or
UCN-01 ( PDK-1 inhibitor ) increased the percentage of apoptotic cells in the granulosa cells treated with BMP-4 or BMP-7
Takahashi et al., Aging Cell 2012
:
Finally, small interfering RNA ( siRNA ) -mediated knockdown of p85a expression in acinar cells from young mice resulted in markedly attenuated activation of
PI3K/Akt downstream signaling in
response to
IGF-1
de Oliveira et al., Journal of neuroinflammation 2012
:
Interestingly, NVP-BEZ235, a dual
PI3K/mTOR inhibitor,
enhanced COX-2 and reduced
mPGES-1 immunoreactivity, albeit PGE2 and PGD2 levels were enhanced in LPS stimulated microglia ... Interestingly, NVP-BEZ235, a dual
PI3K/mTOR inhibitor,
enhanced COX-2 and reduced mPGES-1 immunoreactivity, albeit PGE2 and PGD2 levels were enhanced in LPS stimulated microglia ... Taken together, we demonstrate that blockade of mTOR and/or PI3K/Akt enhances prostanoid production and that
PI3K/Akt , GSK-3 and mTOR differently
regulate the expression of
mPGES-1 and COX-2 in activated primary microglia ... Taken together, we demonstrate that blockade of mTOR and/or PI3K/Akt enhances prostanoid production and that
PI3K/Akt , GSK-3 and mTOR differently
regulate the expression of mPGES-1 and
COX-2 in activated primary microglia
Lee et al., Am J Physiol Endocrinol Metab 2012
(Diabetes Mellitus, Type 2...) :
Insulin stimulated
PI3K activity in skeletal muscle and adipose tissue of DIO mice was significantly reduced ~50-65 %, but this was restored completely by INT131 therapy ... The INT131 effects on
PI3K activity are most likely
due to increased
IRS-1 tyrosine phosphorylation
Zhao et al., J Lipid Res 2012
:
Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL, decreased I?Ba and PPAR?, and also inhibited
PI3K dependent Akt and
EGFR signaling ... Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL, decreased I?Ba and PPAR?, and also inhibited
PI3K dependent
Akt and EGFR signaling
Cheng et al., Br J Pharmacol 2012
:
Renin activates
PI3K-Akt-eNOS signalling through the angiotensin AT1 and Mas receptors to modulate central blood pressure control in the nucleus tractus solitarii ... Immunoblotting and immunohistochemical studies further showed that inhibition of
PI3K significantly
blocked renin induced eNOS-Ser 117 and
Akt-Ser473 phosphorylation in situ
Tsai et al., Int Immunopharmacol 2012
:
Suppression of
PI3K expression by small interfering ( si ) RNA exhibited no
effect on LPS/IFN-? stimulated NO production or
iNOS protein expression in MES-13 cells
Li et al., J Vasc Surg 2012
(Carotid Stenosis...) :
Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing
PI3K/Akt dependent
Hsp70/eNOS signaling
Liu et al., Hepatology 2012
(Carcinoma, Hepatocellular...) :
We also found that expression of
SGK3 , which like AKT is
activated by
PI3K/PDK1 signaling, has more significance than overexpression of AKT in predicting poor outcome in HCC patients
Zhang et al., Int J Radiat Oncol Biol Phys 2012
(Lung Injury...) :
Apoptosis correlated with increased PTEN expression,
inhibition of downstream
PI3K/AKT signaling, and increased
p53 and Bax protein levels ... Apoptosis correlated with increased
PTEN expression,
inhibition of downstream
PI3K/AKT signaling, and increased p53 and Bax protein levels ... Apoptosis correlated with increased PTEN expression,
inhibition of downstream
PI3K/AKT signaling, and increased p53 and
Bax protein levels
Ghosh et al., J Biol Chem 2012
(MAP Kinase Signaling System...) :
Therefore, based on these observations, it is hypothesized that the
activation of
PI3K/AKT and p38 MAPK by VEGF results in
ETS-1 gene expression, which activates MMP-9 and MMP-13, leading to the invasion and scattering of SKOV-3 cells ... Therefore, based on these observations, it is hypothesized that the
activation of
PI3K/AKT and p38 MAPK by
VEGF results in ETS-1 gene expression, which activates MMP-9 and MMP-13, leading to the invasion and scattering of SKOV-3 cells
Chimge et al., J Cell Biochem 2012
:
Activation of
PI3K/Akt signaling is sufficient to maintain the pluripotency of mouse embryonic stem cells ( mESC ) and
results in down-regulation of
Gtf2i and Gtf2ird1 encoding TFII-I family transcription factors ... Activation of
PI3K/Akt signaling is sufficient to maintain the pluripotency of mouse embryonic stem cells ( mESC ) and
results in down-regulation of Gtf2i and
Gtf2ird1 encoding TFII-I family transcription factors
Garcia-Herreros et al., Reprod Fertil Dev 2012
:
Results showed that the expression of glycolytic proteins HK-I, PFK-1,
GAPDH and PK1/2, and the transporters GLUT-1 and GSK-3 is
regulated by
PI3-K in bovine blastocysts ... Results showed that the expression of glycolytic proteins
HK-I , PFK-1, GAPDH and PK1/2, and the transporters GLUT-1 and GSK-3 is
regulated by
PI3-K in bovine blastocysts
Min et al., J Huazhong Univ Sci Technolog Med Sci 2012
:
Our data showed that LY294002 and wortmannin, phosphatidylinositol 3-kinase (PI3K) and
PI3K-like kinase inhibitors,
increased Pim mRNA expression in ECs without altering the mRNA stability
Xu et al., Eur Rev Med Pharmacol Sci 2011
(Diabetes Mellitus, Experimental) :
Effect of insulin in combination with selenium on
Irs/PI3K mediated
GLUT4 expression in cardiac muscle of diabetic rats
Kim et al., FEBS Lett 2012
(Atherosclerosis) :
ROS mediated c-Jun NH ( 2 ) -terminal kinase ( JNK ) is also required for AP-1 activation, but Syk and
PI3K regulated
AP-1 activation independently of JNK
Ruan et al., EMBO J 2012
:
Axl is essential for
VEGF-A dependent activation of
PI3K/Akt ...
Axl is
essential for VEGF-A dependent activation of
PI3K/Akt ... These results elucidate the mechanism by which
VEGF-A activates
PI3K/Akt , and identify previously unappreciated potential therapeutic targets of VEGF-A-driven processes
Bhattacharya et al., Cancer Biol Ther 2012
(Stomach Neoplasms) :
Here, we tested the hypothesis that the dual
PI3K/mTOR inhibitor, PI103, could
synergize with the chemotherapeutic agent, 5-fluorouracil ( 5-FU ) by inhibiting
E2F1 , thymidylate synthase ( TS ) and enhancing DNA damage ... In AGS cells,
PI3K inhibition alone
enhanced 5-FU sensitivity as much as dual
PI3K/mTOR inhibition ... In AGS cells,
PI3K inhibition alone
enhanced 5-FU sensitivity as much as dual
PI3K/mTOR inhibition
Chen et al., J Biol Chem 2012
(Stomach Neoplasms) :
Moreover, CXCR4 immunoprecipitated by anti-p110ß antibody increased after CXCL12 stimulation and G ( i ) protein inhibitor pertussis toxin abrogated
CXCL12 induced activation of
PI3K
Comb et al., Mol Cell 2012
(Starvation) :
Cells expressing p85 S690A or inhibited for IKK activity exhibit increased Akt activity following cell starvation, demonstrating that
p85 phosphorylation is
required for starvation induced
PI3K feedback inhibition ... Finally, leucine deprivation is shown to be necessary and sufficient for starvation induced,
IKK mediated p85 phosphorylation and
PI3K feedback inhibition
Kim et al., Mol Cell Biochem 2012
(Burns...) :
In the
presence of inhibitors of
PI3K , Src, Smad, or reactive oxygen species, the effect of NRG1 on
CTGF expression decreased significantly
Zhang et al., Basic Res Cardiol 2012
(Calcium Signaling...) :
LPS induced reduction in
Na/K-ATPase activity was
prevented by inhibition of
PI3K , Rac1 and NADPH oxidase using LY294002, a dominant negative Rac1 adenovirus ( Ad-Rac1N17 ) and apocynin, respectively
Zito et al., PloS one 2012
(Adenocarcinoma...) :
Concurrent inhibition of PI3K and
mTOR is synergistic in vitro, and a dual
PI3K/mTOR inhibitor was highly
active
Hashikawa-Hobara et al., Diabetes 2012
(Insulin Resistance) :
These results suggest that the decrease of AT(2)R mediated neurite outgrowth in FDRs is likely to be the result of decreased
PI3K dependent
Akt activation
Tang et al., Cancer Lett 2012
(Bone Neoplasms...) :
Activations of
phosphatidylinositol 3-kinase (PI3K) , Akt, and AP-1 pathways after HMGB-1 treatment were demonstrated, and HMGB-1 induced expression of integrin and migration activity was
inhibited by the specific inhibitor and mutant of
PI3K , Akt, and AP-1 cascades
Jenkins et al., Dev Biol 2012
:
Here we report that mammary branching morphogenesis induced by transforming growth factor-alpha ( TGFa ) requires
PI3K dependent
NHE1-activation and subsequent pHi alkalization
Yuan et al., Oncogene 2013
(Adenocarcinoma...) :
Further, we used this model to test the efficacy of
GDC-0941 , a
PI3K inhibitor , in clinical development, and showed that the tumors respond to PI3K inhibition
Huang et al., J Cell Biochem 2012
:
Inhibition of calcineurin further reduced the phosphorylation of
ERK and AKT ( at thr 308 ) and inhibited the activation of Ras, but inhibitors of MAPK or
PI3K signaling did not
affect the circadian rhythm of calcineurin activity ... Inhibition of calcineurin further reduced the phosphorylation of ERK and
AKT ( at thr 308 ) and inhibited the activation of Ras, but inhibitors of MAPK or
PI3K signaling did not
affect the circadian rhythm of calcineurin activity
Hsieh et al., Br J Pharmacol 2012
:
Prodigiosin also down-regulated E2F1 ( mediates
PI3K/PKB induced
SKP2 transcription ), but E2F1 overexpression failed to restore SKP2 expression in prodigiosin treated cells
Li et al., J Ethnopharmacol 2012
(Arthritis, Experimental) :
To investigate the role of
PI3K/Akt/mTOR signaling
mediated by
BAFF/BAFF-R in antibodies production and the regulation of Pae on the signaling pathway in rats with collagen induced arthritis ( CIA ) ... To investigate the role of
PI3K/Akt/mTOR signaling
mediated by
BAFF/BAFF-R in antibodies production and the regulation of Pae on the signaling pathway in rats with collagen induced arthritis ( CIA ) ...
PI3K/Akt/mTOR signaling
mediated by
BAFF/BAFF-R participates in antibodies production by B lymphocytes of CIA rats ...
PI3K/Akt/mTOR signaling
mediated by
BAFF/BAFF-R participates in antibodies production by B lymphocytes of CIA rats
Zanou et al., J Biol Chem 2012
:
Indeed, phosphorylation of both Akt and p70S6K proteins was decreased as well as the activation of
PI3K , the main upstream
regulator of the
Akt
Blaser et al., BMC cancer 2012
(Colonic Neoplasms) :
LS174T, SW480 and DLD-1 colon cancer cell lines were treated with PP242 an ATP-competitive inhibitor of
mTOR , NVP-BEZ235, a dual
PI3K/mTOR inhibitor or rapamycin
Beauséjour et al., Apoptosis 2012
:
We report that : ( 1 ) the predominant
PI3-K complexes expressed by HIEC cells are p110a/p85ß and p110a/p55? ; ( 2 ) the inhibition and/or siRNA mediated expression silencing of p110a, but not that of p110ß, ? or d, results in Akt-1 down-activation and consequent apoptosis ; ( 3 ) the expression silencing of
p85ß or p55?, but not that of p85a, likewise
induces Akt-1 down-activation and apoptosis ; however, the impact of a loss of p55? on both Akt-1 activation and cell survival is significantly greater than that from the loss of p85ß ; and ( 4 ) both the p110a/p85ß and p110a/p55? complexes are engaged by ß1 integrin/Fak/Src signaling ; however, the engagement of p110a/p85ß is primarily Src dependent, whereas that of p110a/p55? is primarily Fak dependent ( but Src independent ) ... We report that : ( 1 ) the predominant
PI3-K complexes expressed by HIEC cells are p110a/p85ß and p110a/p55? ; ( 2 ) the inhibition and/or siRNA mediated expression silencing of p110a, but not that of p110ß, ? or d, results in Akt-1 down-activation and consequent apoptosis ; ( 3 ) the expression silencing of p85ß or
p55? , but not that of p85a, likewise
induces Akt-1 down-activation and apoptosis ; however, the impact of a loss of p55? on both Akt-1 activation and cell survival is significantly greater than that from the loss of p85ß ; and ( 4 ) both the p110a/p85ß and p110a/p55? complexes are engaged by ß1 integrin/Fak/Src signaling ; however, the engagement of p110a/p85ß is primarily Src dependent, whereas that of p110a/p55? is primarily Fak dependent ( but Src independent )
Shi et al., Br J Pharmacol 2012
:
A pharmacological profile of PI3K was created by studying the
effect of pan-PI3K, pan-Class I
PI3K and Class I PI3K isoform-selective inhibitors on ET ( A ) receptor evoked single
TRPC1/C5/C6 and TRPC3/C7 channel activities in cell attached patches from rabbit freshly isolated coronary artery VSMCs ... A pharmacological profile of PI3K was created by studying the
effect of pan-PI3K, pan-Class I
PI3K and Class I PI3K isoform-selective inhibitors on ET ( A ) receptor evoked single
TRPC1/C5/C6 and TRPC3/C7 channel activities in cell attached patches from rabbit freshly isolated coronary artery VSMCs
Bhattacharya et al., Toxicol Appl Pharmacol 2012
:
PI3K inhibition
increased AHR , NRF2 and GSTP protein level
Sinnberg et al., Exp Dermatol 2012
(MAP Kinase Signaling System...) :
MAPK and
PI3K/AKT mediated
YB-1 activation promotes melanoma cell proliferation which is counteracted by an autoregulatory loop ... We show that the
PI3K/AKT and p53 signalling, growth factors and chemotherapeutic agents
increase YB-1 promoter activity
Dai et al., J Biol Chem 2012
(Carcinoma, Hepatocellular...) :
Both
p38 MAPK promoted glucose regulated protein 78 (GRP78) expression and sustained high basal
activation of
PI3K/Akt and MEK/ERK are involved in the cytoprotective function of p190Met ( NC ) ... Both p38 MAPK promoted
glucose regulated protein 78 (GRP78) expression and sustained high basal
activation of
PI3K/Akt and MEK/ERK are involved in the cytoprotective function of p190Met ( NC )
Vinci et al., BMC biology 2012
:
Highly malignant human tumor cells were selected to exemplify therapeutic effects of three specific molecularly targeted agents : PI-103 ( phosphatidylinositol-3-kinase
(PI3K)-mammalian target of rapamycin (mTOR)
inhibitor ), 17-N-allylamino-17-demethoxygeldanamycin ( 17-AAG ) ( heat shock protein 90 (HSP90) inhibitor ) and
CCT130234 ( in-house phospholipase C ( PLC ) ? inhibitor )
Li et al., Behav Brain Res 2012
:
In cultured PC-12 cells,
BDNF activated
PI3K/Akt signaling through the TrkB receptor, whereas stimulation of ILK/Akt occurred through TrkA/p75 ( NTR ) heteroreceptor
Ishrat et al., Neuroscience 2012
(Brain Injuries...) :
The selective
PI3K inhibitor wortmannin compromised PROG induced neuroprotective effects and
reduced the elevation of pAkt levels in the ischemic
penumbra
Tajeddine et al., J Biol Chem 2012
(MAP Kinase Signaling System) :
This was associated with a decreased phosphorylation and
activation of
EGFR and with a subsequent disruption of
PI3K/Akt and MAPK downstream pathways
Hsu et al., Eur J Pharm Sci 2012
:
BBR ( 0.1-10 nM ) led to increasing insulin receptor expression,
Akt phosphorylation and enhanced oxidant-sensitive Nrf2/HO-1 induction, which were
blocked by a
PI3K inhibitor, LY294002 ... BBR ( 0.1-10 nM ) led to increasing insulin receptor expression, Akt phosphorylation and enhanced oxidant-sensitive
Nrf2/HO-1 induction, which were
blocked by a
PI3K inhibitor, LY294002
Xu et al., PloS one 2012
(Liver Neoplasms) :
Addition of recombinant human
VEGF attenuated the inhibitory effects of PP on
PI3K/AKT pathway and the cancer phenotypes
Cheng et al., PloS one 2012
(Cystadenocarcinoma, Serous...) :
The
PI3K inhibitor LY294002 had similar effects, but it could not
block the EGF induced up-regulation of N-cadherin and
ZEB1 ... The
PI3K inhibitor LY294002 had similar effects, but it could not
block the EGF induced up-regulation of
N-cadherin and ZEB1
Tang et al., Int J Biochem Cell Biol 2012
:
Therefore, we conclude that
PI3K activated by Epac
leads to the activation of
PKB/CREB signaling and the up-regulation of PPAR? expression, which in turn activate the transcription of adipogenic genes ; whereas osteogenesis is driven by Rho/FAK/MEK/ERK/Runx2 signaling, which can be inhibited by Epac via PI3K ... Therefore, we conclude that
PI3K activated by Epac
leads to the activation of
PKB/CREB signaling and the up-regulation of PPAR? expression, which in turn activate the transcription of adipogenic genes ; whereas osteogenesis is driven by Rho/FAK/MEK/ERK/Runx2 signaling, which can be inhibited by Epac via PI3K
Chakraborty et al., Proc Natl Acad Sci U S A 2012
:
EphA2 associates with c-Cbl-myosin IIA and
augmented KSHV induced Src and
PI3-K signals in LRs, leading to bleb formation and macropinocytosis of KSHV
Tabassam et al., Helicobacter 2012
(Helicobacter Infections) :
Inhibition of
PI3K or Akt kinase activity
reduced FoxO1/3a phosphorylation ... Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced
PI3K/Akt activity but did not
inhibit FoxO1/3a activation
Kim et al., Biochem Biophys Res Commun 2012
:
HMGB1 activated the JNK and PI3K/Akt signaling pathways, and inhibitors of JNK and
PI3K/Akt markedly
inhibited HMGB1 induced
MUC8 expression
Li et al., PloS one 2012
(Hypereosinophilic Syndrome) :
Interestingly,
JAK2 inhibition also
reduced PI3K , Akt and NF-?B activity in a dose dependent manner, and suppressed expression levels of c-Myc and Survivin ... Interestingly,
JAK2 inhibition also
reduced PI3K , Akt and NF-?B activity in a dose dependent manner, and suppressed expression levels of c-Myc and Survivin
Vredeveld et al., Genes Dev 2012
(Melanoma...) :
Pharmacologic
PI3K inhibition in melanoma cells
suppressed proliferation and induced the senescence associated tumor suppressor
p15(INK4B)
Mahajan et al., Thromb Haemost 2012
:
In conclusion, thrombin and FoxO factors functionally interact through
PI3K/Akt dependent
FoxO phosphorylation leading to expression of cell cycle regulating genes and ultimately SMC proliferation
Jude et al., Am J Respir Cell Mol Biol 2012
(Asthma) :
In HASM cells, regulation of
CD38 expression occurs by specific class I PI3K isoforms, independent of NF-?B or AP-1 activation, and
PI3K signaling may not be
involved in the differential elevation of CD38 in asthmatic HASM cells
Rangaswami et al., J Biol Chem 2012
(Mechanotransduction, Cellular) :
Both pathways cooperated to increase
PI3K dependent
Akt phosphorylation and were necessary for FSS to induce nuclear translocation of ß-catenin, c-fos, and cox-2 gene expression and osteoblast proliferation
Wallin et al., Clin Cancer Res 2012
(Breast Neoplasms...) :
GDC-0941 , a novel class I selective
PI3K inhibitor , enhances the efficacy of docetaxel in human breast cancer models by increasing cell death in vitro and in vivo ... The current study was intended to determine whether
GDC-0941 , an orally bioavailable class I selective
PI3K inhibitor , enhances the antitumor activity of docetaxel in human breast cancer models in vitro and in vivo
Lee et al., Mol Biol Cell 2012
:
We demonstrate that
endoglin interacts with the PI3K subunits p110a and p85 via GIPC to recruit and
activate PI3K and Akt at the cell membrane
Huang et al., Am J Pathol 2012
(Lymphoma, Large B-Cell, Diffuse) :
Taken together, our results reveal a novel target involved in miR-155 biological characteristics and provide a molecular link between the overexpression of
miR-155 and the
activation of
PI3K-AKT in DLBCL
Tenbaum et al., Nat Med 2012
(Colonic Neoplasms...) :
Simultaneous hyperactivation of the Wnt-ß-catenin pathway and inhibition of
PI3K-AKT signaling
promote nuclear accumulation of ß-catenin and
FOXO3a , respectively, promoting cell scattering and metastasis by regulating a defined set of target genes ... In the presence of high nuclear ß-catenin content,
activation of
FOXO3a by
PI3K or AKT inhibitors makes it behave as a metastasis inductor rather than a proapoptotic tumor suppressor
Gao et al., EMBO Mol Med 2012
(Disease Models, Animal...) :
This involved p38
MAPK activation by
PI3K to facilitate clathrin mediated ErbB receptor endocytosis ... This involved
p38 MAPK
activation by
PI3K to facilitate clathrin mediated ErbB receptor endocytosis
Wong et al., Blood 2012
:
Here, we show that Notch induction of
Hes1 is necessary to
repress the
PI3K/Akt pathway inhibitor, PTEN ( phosphatase and tensin homolog ), which in turn facilitates pre-TCR induced differentiation
Kittilson et al., Frontiers in endocrinology 2011
:
Although blockade of the ERK pathway had no effect on the activation of Akt, inhibition of
PI3K-Akt partially
prevented activation of
ERK , suggesting cross-talk between the ERK and PI3K-Akt pathways
Huang et al., J Mol Neurosci 2013
(MAP Kinase Signaling System) :
Besides, expression of phosphorylated-AKT and
phosphorylated-ERK1/2 in fluoxetine treated NSCs was effectively
blocked ( P < 0.05 ) by both
PI3-K inhibitor ( LY294002 ) and MEK inhibitor ( PD98059 ) ... Besides, expression of
phosphorylated-AKT and phosphorylated-ERK1/2 in fluoxetine treated NSCs was effectively
blocked ( P < 0.05 ) by both
PI3-K inhibitor ( LY294002 ) and MEK inhibitor ( PD98059 )
Choi et al., Biofactors 2012
:
Honokiol and magnolol stimulate glucose uptake by activating
PI3K dependent
Akt in L6 myotubes
Chen et al., PloS one 2012
:
Hepatocyte growth factor increases osteopontin expression in human osteoblasts through
PI3K , Akt, c-Src, and AP-1 signaling pathway ... Stimulation of osteoblasts with
HGF enhanced
PI3K , Akt, and c-Src activation
Dal-Cim et al., Neurochem Int 2012
(Neuroblastoma) :
In conclusion, our results show that guanosine can afford protection against mitochondrial oxidative stress by a signaling pathway that implicates
PI3K/Akt/GSK-3ß proteins and
induction of the antioxidant enzyme
HO-1
Tsai et al., Toxicon 2012
(MAP Kinase Signaling System...) :
These findings suggest that CTX III inhibited the EGF induced invasion and migration of MDA-MB-231 cells via
EGFR dependent
PI3K/Akt , ERK1/2, and NF-?B signaling, leading to the down-regulation of MMP-9 expression
Tasian et al., Blood 2012
(Precursor B-Cell Lymphoblastic Leukemia-Lymphoma) :
TSLP stimulation of these leukemias further
induced robust JAK/STAT and
PI3K/mTOR pathway signaling
Vitolo et al., Oncogene 2013
:
Chemical inhibition of
PI3K did not
reduce McTNs or inactivate
cofilin in PTEN ( -/- ) cells ... PTEN loss and
PI3K activation also
caused differential activation of the
cofilin regulators, LIM-kinase1 ( LIMK ) and Slingshot-1L ( SSH )
Jin et al., Oncogene 2013
:
Compared with MCF-10A cells, constitutive overexpression of
MUC1-C in breast cancer cells was unaffected by EGF stimulation, but was
blocked by inhibiting
PI3K?AKT signaling
Gulhati et al., Carcinogenesis 2012
(Colorectal Neoplasms...) :
In this study, we show that inhibition of
mTORC1 with rapamycin
leads to feedback activation of
PI3K/Akt and Ras-MAPK signaling, resulting in cell survival and possible contribution to rapamycin resistance
Bridges et al., Mol Biol Cell 2012
:
In this paper, we show that PIKFYVE and
PI3K-C2a are
necessary for activation of
mTORC1 and its translocation to the plasma membrane in 3T3-L1 adipocytes
Reddy et al., J Biol Chem 2012
:
We found that
MTA1 up-regulation
leads to a decreased expression of PTEN protein and stimulation of
PI3K as well as phosphorylation of its signaling targets ... Accordingly, selective down-regulation of MTA1 in breast cancer cells increases
PTEN expression and
inhibits stimulation of the
PI3K/AKT signaling ... Accordingly, selective down-regulation of
MTA1 in breast cancer cells increases PTEN expression and
inhibits stimulation of the
PI3K/AKT signaling
Krajewski et al., PloS one 2012
:
This study analyzes effects of ADP receptor
P(2)Y(12) and P(2)Y(1) blockade and
PI3K p110ß
inhibition on platelets and granulocytes during hypothermic ECC ... This study analyzes effects of ADP receptor P(2)Y(12) and
P(2)Y(1) blockade and
PI3K p110ß
inhibition on platelets and granulocytes during hypothermic ECC
Corbett et al., J Immunol 2012
(Neurodegenerative Diseases) :
Activation of type IA p110a PI3K and Akt by gem and abrogation of gem induced
upregulation of
IL-1Ra by inhibitors of
PI3K and Akt indicate a role of the PI3K-Akt pathway in the upregulation of IL-1Ra
Maitra et al., J Immunol 2012
:
Unlike high-dose LPS, low-dose
LPS does not
induce robust activation of NF-?B, MAPKs,
PI3K , or anti-inflammatory mediators
Chen et al., Mol Nutr Food Res 2012
:
Moreover, lycopene attenuated
VEGF receptor-2 (VEGFR2) mediated phosphorylation of extracellular signal regulated kinase ( ERK ), p38, and Akt as well as protein expression of
PI3K
Ho et al., Mol Cancer Res 2012
(Carcinoma, Renal Cell...) :
Inhibition of
PI3K/AKT by LY294002 reactivated GSK-3ß and
suppressed the TNF-a induced
EMT of RCC cells
Seljeset et al., J Recept Signal Transduct Res 2012
(MAP Kinase Signaling System) :
PI3K was relevant for GPR40- and GPR41 mediated ERK1/2 activation, and Src was
essential for
GPR40- and GPR43 induced activation
Huang et al., Free Radic Biol Med 2012
(Carcinoma...) :
Accordingly, we suggest that
PI3K/AKT signaling
mediates TGIF induced
Nox2/p67(phox) complex activation and the resultant superoxide production which reinforces the PI3K/AKT signaling to promote the cellular migration/invasion ability of UC ... Accordingly, we suggest that
PI3K/AKT signaling
mediates TGIF induced
Nox2/p67(phox) complex activation and the resultant superoxide production which reinforces the PI3K/AKT signaling to promote the cellular migration/invasion ability of UC
Park et al., Vascul Pharmacol 2012
:
These effects of GJ were attenuated not only by calcium chelators including EGTA and BAPTA-AM, but also by LY294002, a PI3K/Akt inhibitor, indicating calcium- and
PI3K/Akt dependent
activation of
eNOS by GJ
Shanmugasundaram et al., Oncogene 2013
(Carcinoma, Renal Cell...) :
Here we provide additional genetic evidence that
PI3K signaling
activates mTORC2 kinase activity
Habib et al., Genes & cancer 2011
:
These novel data provide evidence that loss of TSC-2, PTEN, and
p53 as well as
activation of
PI 3-K and mTOR is associated with kidney cancer in the Eker rat, while sustained expression of TSC-2, PTEN, and p53 may prevent progression of kidney cancer in TSC patients ... These novel data provide evidence that loss of
TSC-2 , PTEN, and p53 as well as
activation of
PI 3-K and mTOR is associated with kidney cancer in the Eker rat, while sustained expression of TSC-2, PTEN, and p53 may prevent progression of kidney cancer in TSC patients ... These novel data provide evidence that loss of TSC-2,
PTEN , and p53 as well as
activation of
PI 3-K and mTOR is associated with kidney cancer in the Eker rat, while sustained expression of TSC-2, PTEN, and p53 may prevent progression of kidney cancer in TSC patients
Yang et al., Biosci Rep 2012
(Insulin Resistance) :
In contrast, saturated fatty acid exposure caused insulin resistance, reducing
PI3K ( phosphoinositide 3-kinase ) and ERK ( extracellular-signal regulated kinase )
activation while increasing activation of stress kinases JNK ( c-Jun N-terminal kinase ) and
p38
Coso et al., PloS one 2012
:
Furthermore, activation of
PI3K/Akt by VEGF-C/VEGFR-3
resulted in phosphorylation of P70S6K, eNOS, PLC?1, and
Erk1/2 ... Furthermore, activation of
PI3K/Akt by VEGF-C/VEGFR-3
resulted in phosphorylation of P70S6K, eNOS, PLC?1, and
Erk1/2 ... Furthermore, activation of
PI3K/Akt by VEGF-C/VEGFR-3
resulted in phosphorylation of P70S6K,
eNOS , PLC?1, and Erk1/2 ... Furthermore, activation of
PI3K/Akt by VEGF-C/VEGFR-3
resulted in phosphorylation of P70S6K, eNOS,
PLC?1 , and Erk1/2 ... Furthermore,
activation of
PI3K/Akt by
VEGF-C/VEGFR-3 resulted in phosphorylation of P70S6K, eNOS, PLC?1, and Erk1/2 ... Furthermore,
activation of
PI3K/Akt by
VEGF-C/VEGFR-3 resulted in phosphorylation of P70S6K, eNOS, PLC?1, and Erk1/2
Wu et al., Antioxid Redox Signal 2013
(Hypertension) :
Redox-sensitive oxidation and phosphorylation of
PTEN contribute to enhanced activation of
PI3K/Akt signaling in rostral ventrolateral medulla and neurogenic hypertension in spontaneously hypertensive rats ... Silencing
PTEN expression in RVLM with small interfering RNA, on the other hand,
augmented PI3K/Akt signaling and promoted long-term pressor response in normotensive WKY rats
Bhatt et al., Proc Natl Acad Sci U S A 2012
(Lymphoma, B-Cell...) :
We found that aerobic glycolysis and
FAS occur in a
PI3K dependent manner and appear to be interdependent
Gentle et al., J Immunol 2012
:
Modulation required de novo protein synthesis, and PI3K, JNK, and ERK activity were necessary for enhanced IL-2 expression, whereas modulation of
IL-10 required only
PI3K activity ... Modulation required de novo protein synthesis, and
PI3K , JNK, and ERK activity were
necessary for enhanced
IL-2 expression, whereas modulation of IL-10 required only PI3K activity
Liu et al., Eur J Pharmacol 2012
(Arthritis, Experimental) :
To investigate the role of
PI3K/Akt/mTOR signaling
mediated by
B cell activating factor belonging to the TNF family ( BAFF ) involved in anti-apoptosis of B lymphocytes in rats with collagen induced arthritis ( CIA ) and the regulation of epigallo-catechin-3-gallate ( EGCG )
Han et al., PloS one 2012
(Breast Neoplasms...) :
The inhibitors of
PI3K-AKT and ERK1/2 pathways, LY294002 and U0126, both significantly
suppressed EMT and CSC phenotype, indicating that AKT and ERK1/2 pathways are required for miR-21 mediating EMT and CSC phenotype
Guo et al., Cell reports 2012
:
Here, we report that
Cbl-b does not
inhibit PI3K but rather suppresses TCR/CD28 induced inactivation of Pten
Chang et al., Gen Comp Endocrinol 2012
:
The specific inhibitors of either MEK1 ( U-0126 and PD-98059 ), JAK ( AG-490 ), JNK ( SP-600125 ), or
PI3K ( LY-294002 and wortmannin ) reduced ET-1 increased levels of SOCS-3 mRNA and respectively
inhibited ET-1 stimulated activities of
MEK1 , JAK, JNK, and PI3K ... The specific inhibitors of either MEK1 ( U-0126 and PD-98059 ),
JAK ( AG-490 ), JNK ( SP-600125 ), or PI3K ( LY-294002 and wortmannin ) reduced ET-1 increased levels of SOCS-3 mRNA and respectively
inhibited ET-1 stimulated activities of MEK1, JAK, JNK, and
PI3K
Liu et al., Brain Res Bull 2012
(Brain Ischemia...) :
Losartan, an angiotensin II type 1 receptor blocker, ameliorates cerebral ischemia-reperfusion injury via
PI3K/Akt mediated
eNOS phosphorylation
Villanueva et al., PloS one 2012
(Reperfusion Injury) :
8 ) Wortmannin, which inhibits ATM and
PI3K ,
reduces hypoxia induced
NFAT5 transcriptional activation in HEK293 cells
Wygrecka et al., Am J Respir Cell Mol Biol 2012
(Idiopathic Pulmonary Fibrosis) :
Exposure of HLFs to TGF-ß1 activated JNK in a
PI3K dependent manner and induced
Akt phosphorylation at threonine 308 and serine 473, but did not change the phosphorylation status of threonine 450
Xu et al., Immunol Cell Biol 2012
:
To understand the mechanisms of PI3K regulation during B-cell activation, we performed a series of biochemical analysis on primary B cells, and found that activity of Src family tyrosine kinases (SFK) is crucial for the
activation of
PI3K following
BCR ligation and this is regulated by the SFK Lyn ... Regulating SFK activity may thus be a central mechanism by which
Lyn regulates
PI3K activity in B cells
Zhang et al., Zhonghua Fu Chan Ke Za Zhi 2012
(Endometrial Neoplasms) :
[
Effect of
GPER on the activation of
PI3K/Akt induced by 17ß-estradiol in endometrial carcinoma cells ]
Poettler et al., Thromb Haemost 2012
:
Thus, VEGF165,
VEGF-E , FGF-2, EGF as well as HGF
induced a
PI3k dependent activation of pro-uPA when bound to uPAR, which led to an increase in cell surface fibrinolytic activity ... Thus, VEGF165,
VEGF-E , FGF-2, EGF as well as HGF
induced a
PI3k dependent activation of pro-uPA when bound to uPAR, which led to an increase in cell surface fibrinolytic activity ... Thus, VEGF165, VEGF-E, FGF-2, EGF as well as HGF induced a
PI3k dependent activation of
pro-uPA when bound to uPAR, which led to an increase in cell surface fibrinolytic activity
Meng et al., Int J Cardiol 2013
:
In summary, our research demonstrated for the first time that HIV-1
gp120 could induce autophagy of cardiomyocytes and the NMDA receptor, JNK and class III
PI3K were
involved in this process
Wangari-Talbot et al., Mol Cancer Res 2012
(MAP Kinase Signaling System...) :
We showed that suppression of
GRM1 expression in several human melanoma cell lines
resulted in a reduction in the number of viable cells and a decrease in stimulated mitogen activated protein kinase ( MAPK ) and
PI3K/AKT and suppressed tumor progression in vivo
Liu et al., J Immunol 2012
(Neoplasms) :
Overexpression of the rate limiting translation initiation factor eIF4E induced Rae1 and
ULBP1 expression in a Ras- and
PI3K dependent manner ... Overexpression of the rate limiting translation initiation factor
eIF4E induced Rae1 and ULBP1 expression in a Ras- and
PI3K dependent manner ... Overexpression of the rate limiting translation initiation factor eIF4E induced
Rae1 and ULBP1 expression in a Ras- and
PI3K dependent manner
Balzarolo et al., Eur J Immunol 2012
:
Furthermore,
PI3K signaling is
required for NAB2 mediated
TRAIL expression
Kamo et al., Hepatology 2013
(Liver Diseases...) :
A specific
PI3K blockade
inhibited Akt/ß-catenin signaling, increased Foxo1 mediated TLR4-driven local inflammation, and recreated cardinal features of liver IR injury
Steinestel et al., PloS one 2012
(Adenoma...) :
Our results support a role for Abi1 as a downstream target of inflammatory response and adenomatous change as well as oncogenic KRAS mutation via
PI3K , but not
BRAF activation
Zhou et al., Vasc Med 2012
(Cardiovascular Diseases...) :
Angiotensin ( Ang ) II inhibits insulin mediated
PI3K pathway activation, thereby impairing endothelial NO production and Glut-4 translocation in insulin-sensitive tissues, which results in vascular and systemic insulin resistance, respectively ... Angiotensin ( Ang ) II inhibits
insulin mediated
PI3K pathway activation, thereby impairing endothelial NO production and Glut-4 translocation in insulin-sensitive tissues, which results in vascular and systemic insulin resistance, respectively
Tabara et al., PloS one 2012
(Lung Neoplasms) :
However, constitutive
activation of
EGFR downstream signaling,
PI3K/Akt , was observed even after loss of the mutated EGFR gene in all resistant cell lines even in the presence of the drug
Nascimento et al., Eur J Pharmacol 2012
:
Relaxin induced AKT phosphorylation was G ( i ) - but not
PKA dependent , and it was blocked by both
PI3K and MEK inhibitors
Kurebayashi et al., Cell reports 2012
:
Inhibition of
PI3K-Akt-mTORC1-S6K1 axis
impairs the downregulation of
Gfi1 , a negative regulator of Th17 differentiation
Ahmad et al., Mol Cell Endocrinol 2012
:
Studies using chemical inhibitors and siRNAs to signaling molecules showed that
PI3K , Akt, ERK and PKC-? and the transcription factors Elk-1, c-fos and, to a lesser extent, NF-?B are
involved in
relaxin 's induction of MMP-9 ... Studies using chemical inhibitors and siRNAs to signaling molecules showed that
PI3K , Akt, ERK and PKC-? and the transcription factors Elk-1, c-fos and, to a lesser extent, NF-?B are
involved in relaxin 's induction of
MMP-9
Wang et al., Cancer Res 2012
(Disease Models, Animal...) :
Here we describe a new genetically engineered mouse model of prostate cancer in which
PI3K-Akt-mTOR signaling is
activated by inducible disruption of
PTEN , and extracellular signal regulated kinase 1/2 ( ERK1/2 ) MAPK signaling is activated by inducible expression of a BRAF ( V600E ) oncogene
Mitra et al., Cytokine 2012
(Arthritis...) :
We observed that IL-22 induced significant proliferation of NHEK and FLS which was effectively inhibited by dual kinase (
PI3K/mTOR ) inhibitor, NVP-BEZ235 and specific
mTOR inhibitor , Rapamycin
Li et al., Am J Transplant 2012
(Arteriosclerosis) :
Conditioned media from Ltv-p53 transferred SMCs activated
PI3K/Akt/mTOR and MAPK/Erk signaling in a
SDF-1a dependent manner and thereby promoted mesenchymal stem cell (MSC) migration and proliferation
Zhu et al., Glycoconj J 2012
:
Inhibition of MEK/ERK,
PI3K/AKT and NF-?B
suppressed rhOPN induced ß1,
4-GalT-I expression
Fischer et al., Lung Cancer 2012
(Mesothelioma...) :
The
PI3K/mTOR inhibitor NVP-BEZ235 and PI3K inhibitor wortmannin
reduced the phosphorylation of downstream target AKT, S6 and
4EBP1 and decreased the SP fraction ... The
PI3K/mTOR inhibitor NVP-BEZ235 and PI3K inhibitor wortmannin
reduced the phosphorylation of downstream target
AKT , S6 and 4EBP1 and decreased the SP fraction
Piccolo et al., J Mol Med (Berl) 2013
(Breast Neoplasms...) :
Production of
VEGF , that was restored by exposure of silenced cells to recombinant LGALS3BP,
required an intact
PI3k/Akt signaling
Arriola et al., J Biol Chem 2012
:
We demonstrated that FOXO1 is expressed in murine gonadotrope cells and that insulin signaling increased
FOXO1 phosphorylation and cytoplasmic localization in a
PI3K dependent manner ... We demonstrated that FOXO1 is expressed in murine gonadotrope cells and that
insulin signaling increased FOXO1 phosphorylation and cytoplasmic localization in a
PI3K dependent manner
Wu et al., Particle and fibre toxicology 2012
(MAP Kinase Signaling System) :
Pharmacological inhibition of ERK kinase and
PI3K activity
blocked DEP induced IL-8 and
IL-1ß expression ... Pharmacological inhibition of ERK kinase and
PI3K activity
blocked DEP induced
IL-8 and IL-1ß expression
Appleman et al., Mol Cancer Res 2012
:
Interestingly, we find that activation of
PI3K/AKT signaling occurs downstream of MAP-ERK kinase ( MEK ), and is
dependent on the autocrine activation of the insulin-like growth factor (IGF) receptor ( IGF1R ) by
IGF2 ... Interestingly, we find that activation of
PI3K/AKT signaling occurs downstream of MAP-ERK kinase ( MEK ), and is
dependent on the autocrine activation of the
insulin-like growth factor (IGF) receptor ( IGF1R ) by IGF2
Wang et al., Toxicological sciences : an official journal of the Society of Toxicology 2012
(Colonic Neoplasms) :
These responses are related to intracellular reactive oxygen species ( ROS ) generation,
NADPH oxidase activation , and upregulation of
PI3K/Akt and hypoxia-inducible factor 1 alpha ( HIF-1a ) signaling
Gupta et al., Mol Biol Cell 2012
(Alzheimer Disease...) :
PTEN , a widely known negative
regulator of
insulin/PI3K signaling, positively regulates neuronal insulin resistance
Yu et al., PloS one 2012
(Disease Models, Animal...) :
Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of spinal
AKT induced by ephrinB1-Fc. Inhibition of spinal
PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal c-Fos protein expression induced by intrathecal injection of ephrinB1-Fc. Inhibition of EphBs receptors by intrathecal injection of EphB1-Fc reduced formalin induced inflammation and chronic constrictive injury induced neuropathic pain behaviors accompanied by decreased expression of spinal PI3K, p-AKT and c-Fos protein ... Pre-treatment with PI3K inhibitor wortmannin or LY294002 prevented activation of spinal AKT induced by
ephrinB1-Fc. Inhibition of spinal
PI3K signaling dose-dependently prevented and reversed pain behaviors and spinal c-Fos protein expression induced by intrathecal injection of ephrinB1-Fc. Inhibition of EphBs receptors by intrathecal injection of EphB1-Fc reduced formalin induced inflammation and chronic constrictive injury induced neuropathic pain behaviors accompanied by decreased expression of spinal PI3K, p-AKT and c-Fos protein
Hatton et al., PloS one 2012
(Lymphoma, B-Cell) :
Using small molecule inhibition and siRNA strategies in human B cell lines expressing a chimeric, signaling-inducible LMP1 protein, nerve growth factor receptor (NGFR)-LMP1, we show that NGFR-LMP1 utilizes Syk to activate
PI3K/Akt signaling and
induce IL-10 production ... Using small molecule inhibition and siRNA strategies in human B cell lines expressing a chimeric, signaling-inducible LMP1 protein, nerve growth factor receptor (NGFR)-LMP1, we show that NGFR-LMP1 utilizes
Syk to
activate PI3K/Akt signaling and induce IL-10 production ... Using small molecule inhibition and siRNA strategies in human B cell lines expressing a chimeric, signaling-inducible LMP1 protein, nerve growth factor receptor (NGFR)-LMP1, we show that
NGFR-LMP1 utilizes Syk to
activate PI3K/Akt signaling and induce IL-10 production ... Using small molecule inhibition and siRNA strategies in human B cell lines expressing a chimeric, signaling-inducible LMP1 protein, nerve growth factor receptor (NGFR)-LMP1, we show that
NGFR-LMP1 utilizes Syk to
activate PI3K/Akt signaling and induce IL-10 production ... Whereas Src kinases are often required for Syk activation, we show here that
PI3K/Akt activation and autocrine IL-10 production by
NGFR-LMP1 involves the Src family kinase Fyn ... Whereas Src kinases are often required for Syk activation, we show here that
PI3K/Akt activation and autocrine IL-10 production by NGFR-LMP1
involves the Src family kinase
Fyn ... Whereas Src kinases are often required for Syk activation, we show here that
PI3K/Akt activation and autocrine IL-10 production by
NGFR-LMP1 involves the Src family kinase Fyn
Lee et al., J Clin Invest 2012
(Breast Neoplasms) :
We found that
FAM83A interacted with and
caused phosphorylation of c-RAF and
PI3K p85, upstream of MAPK and downstream of EGFR
Jie et al., Mol Cell Biochem 2012
(Ion Channel Gating) :
Taken together, these findings suggest that
NRG-1 activates
PI3K/Akt signaling and inhibits mPTP opening, and downstream apoptotic events in cardiac myocytes subjected to oxidative stress
Ren et al., J Biol Chem 2012
(Cell Transformation, Viral...) :
Tax2 efficiently immortalized CD4 ( + ) memory T lymphocytes with a CD3/TCRaß/CD4/CD25/CD45RO/CD69 immunophenotype, promoted constitutive
activation of
PI3K/Akt , I?B kinase/NF-?B,
mitogen activated protein kinase , and STAT3, and it also increased the level of Mcl-1
Troutman et al., Cell cycle (Georgetown, Tex.) 2012
(Inflammation) :
Here, we summarize the current understanding of signaling pathways activated by TLRs and provide our perspective on
TLR mediated activation of
PI3K and its impact on regulating cellular processes
Yang et al., J Mol Med (Berl) 2013
(Endotoxemia...) :
LPS caused p38
MAPK- , JNK-, and PI3K/AKT mediated Mcl-1 stabilization and prevented apoptosis, and LPS
induced GSK-3ß inactivation mainly through p38 MAPK and
PI3K/AKT ...
LPS caused p38 MAPK-, JNK-, and PI3K/AKT mediated Mcl-1 stabilization and prevented apoptosis, and LPS
induced GSK-3ß inactivation mainly through p38 MAPK and
PI3K/AKT
Tian et al., J Dig Dis 2012
(Stomach Neoplasms) :
Specific ERK1/2 inhibitor PD98059 and
PI3K inhibitor wortmannin
reduced phosphorylation of
ERK1/2 and Akt, respectively and blocked ghrelin- and des-acyl ghrelin induced AGS cell proliferation ... Specific ERK1/2 inhibitor PD98059 and
PI3K inhibitor wortmannin
reduced phosphorylation of ERK1/2 and
Akt , respectively and blocked ghrelin- and des-acyl ghrelin induced AGS cell proliferation
Ibrahim et al., Cancer Discov 2012
(Breast Neoplasms) :
PI3K inhibition
impairs BRCA1/2 expression and sensitizes BRCA-proficient triple negative breast cancer to PARP inhibition ... We show in TNBC cells that
PI3K inhibition
leads to DNA damage, downregulation of
BRCA1/2 , gain in poly-ADP-ribosylation, and subsequent sensitization to PARP inhibition
Ha et al., Neurosci Lett 2012
:
Furthermore,
PI3K activation is
responsible for
ERK1/2 phosphorylation
Harris et al., Eur J Immunol 2012
:
In this study, we reveal a novel
role for
PI3K? in the regulation of the pro-inflammatory cytokine
IL-17 ... Loss of
PI3K? or expression of a catalytically inactive mutant of PI3K? in mice
led to increased
IL-17 production both in vitro and in vivo in response to various stimuli
Busch et al., J Biol Chem 2012
:
Resveratrol suppressed
IL-1ß induced activation of NF-?B and
PI3K in a dose- and time dependent manner ... IL-1ß induced NF-?B and
PI3K activation was
inhibited by resveratrol or the inhibitors of PI3K ( wortmannin ),
c-Src ( PP1 ), and Akt ( SH-5 ) through inhibition of I?B kinase, I?Ba phosphorylation, and inhibition of nuclear translocation of NF-?B, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-?B activation ... IL-1ß induced NF-?B and
PI3K activation was
inhibited by resveratrol or the inhibitors of PI3K ( wortmannin ), c-Src ( PP1 ), and
Akt ( SH-5 ) through inhibition of I?B kinase, I?Ba phosphorylation, and inhibition of nuclear translocation of NF-?B, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-?B activation ...
IL-1ß induced NF-?B and
PI3K activation was inhibited by resveratrol or the inhibitors of PI3K ( wortmannin ), c-Src ( PP1 ), and Akt ( SH-5 ) through inhibition of I?B kinase, I?Ba phosphorylation, and inhibition of nuclear translocation of NF-?B, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-?B activation ... The modulatory effects of resveratrol on
IL-1ß induced
activation of NF-?B and
PI3K were found to be mediated at least in part by the association between Sirt-1 and scleraxis and deacetylation of NF-?B and PI3K
Banerjee et al., Breast Cancer Res Treat 2012
(Breast Neoplasms...) :
Pg extract also induced SHIP-1 expression and this was accompanied by downregulation of miRNA-155 and inhibition of
PI3K dependent phosphorylation of
AKT
Runyan et al., J Biol Chem 2012
:
As inhibiting
PI3K can
activate the endosomal fusion-regulatory small GTPase
Rab5 , we expressed GTPase-deficient Rab5 and observed endosomal enlargement and reduced SARA protein expression, similar to that seen with PI3K inhibition
Lian et al., J Biol Chem 2012
:
Furthermore, inhibition of
PI3K/Akt/mTOR signaling, but not canonical Smad signaling, downstream of TGFß,
blocked TGFß induced synthesis of
vimentin , and inhibited ATF4 dependent Ocn transcription in osteoblasts
Zong et al., PloS one 2012
(MAP Kinase Signaling System) :
Meanwhile,
PI3-K is
essential for resveratrol mediated phosphorylation of AMPK and expression of
SIRT1 ... Meanwhile,
PI3-K is
essential for resveratrol mediated phosphorylation of
AMPK and expression of SIRT1
Orita et al., Curr Eye Res 2013
:
Conclusions : The poly (
I:C ) -induced secretion of IL-6, IP-10, and RANTES from human corneal fibroblasts is
mediated by both NF-?B and
PI3K signaling pathways, whereas that of IL-8 is mediated by the NF-?B pathway
Sahu et al., J Neuroendocrinol 2013
:
In the hypothalamus, leptin stimulates
STAT3 activation, and
induces PI3K and PDE3B activities, among others ... In the hypothalamus,
leptin stimulates STAT3 activation, and
induces PI3K and PDE3B activities, among others
Staples et al., J Allergy Clin Immunol 2012
(Asthma) :
The
PI3K inhibitor LY294002
inhibited basal
CCL17 release from BAL cells and IL-4 stimulated release from MDMs
Hien et al., Biochem Pharmacol 2012
:
ER inhibition reversed
AMPK dependent
PI3K activation in response to amurensin G. Amurensin G-mediated endothelium dependent relaxation was blocked by inhibition of AMPK, ER, Src, or PI3K
Akl et al., Planta Med 2012
(Breast Neoplasms...) :
Western blot studies revealed that combined low-dose treatment of ?-tocotrienol and sesamin caused a marked reduction in
EGF induced ErbB3 and ErbB4 receptors phosphorylation ( activation ) and a relatively large decrease in intracellular levels of total and/or phosphorylated c-Raf, MEK1/2, ERK1/2,
PI3K , PDK1, Akt, p-NF?B, Jak1, Jak2, and Stat1, as compared to cells treated with only one compound or in the vehicle treated control group
Bonvin et al., Mol Cell Biol 2012
(Melanoma...) :
Collectively, our results highlight a crucial
role for
PI3K in regulating Brn-2 and
Pax3 expression, reveal a mechanism by which PI3K can regulate invasiveness, and imply that PI3K signaling is a key determinant of melanoma subpopulation diversity ... Collectively, our results highlight a crucial
role for
PI3K in regulating
Brn-2 and Pax3 expression, reveal a mechanism by which PI3K can regulate invasiveness, and imply that PI3K signaling is a key determinant of melanoma subpopulation diversity
Song et al., Journal of neuroinflammation 2012
(Neuroblastoma) :
We also found that
Src/PI3K/Akt inhibitors
prevented LLLT stimulated
Akt ( Ser473 and Thr308 ) phosphorylation and blocked Rac1 activity and actin based microglial phagocytosis, indicating the activation of Src/PI3K/Akt/Rac1 signaling pathway ... We also found that
Src/PI3K/Akt inhibitors prevented LLLT stimulated Akt ( Ser473 and Thr308 ) phosphorylation and
blocked Rac1 activity and actin based microglial phagocytosis, indicating the activation of Src/PI3K/Akt/Rac1 signaling pathway
Kenzel et al., J Immunol 2012
(Inflammation...) :
We found that GBS induced, MyD88 dependent chemokine formation of PML was specifically downmodulated by insulin via
insulin receptor mediated induction of
PI3K
Roller et al., J Immunol 2012
(Dermatitis...) :
We also show that PI3Kd and
PI3K? inhibitors
reduced IFN-? production by human TCR?d T cells and
IL-17 and IFN-? production by PBMCs from psoriatic or healthy donors
Chen et al., Genes Dev 2012
:
Surprisingly, we found that mammary differentiation was due to the
PI3K-Akt dependent synthesis and secretion of autocrine
prolactin and downstream activation of the prolactin receptor (Prlr)-Jak-Stat5 pathway ... Our findings reveal that
PI3K-Akt pathway activation is necessary and
sufficient to induce autocrine
prolactin production in the mammary gland, Stat5 activation, and terminal mammary epithelial differentiation, even in the absence of the normal developmental program that prepares the mammary gland for lactation
Patsoukis et al., Cell cycle (Georgetown, Tex.) 2012
:
The suppressive effect of
PD-1 on Skp2 expression was
mediated by inhibition of both
PI3K/Akt and Ras/MEK/Erk pathways and was only partially reversed by IL-2, which restored activation of MEK/Erk but not Akt ... The suppressive effect of PD-1 on
Skp2 expression was
mediated by inhibition of both
PI3K/Akt and Ras/MEK/Erk pathways and was only partially reversed by IL-2, which restored activation of MEK/Erk but not Akt
Shepherd et al., Leukemia 2013
(Precursor T-Cell Lymphoblastic Leukemia-Lymphoma) :
PI3K/mTOR inhibition
upregulates NOTCH-MYC signalling leading to an impaired cytotoxic response ...
PI3K/mTOR inhibition
upregulates NOTCH-MYC signalling leading to an impaired cytotoxic response
Byron et al., Molecular cancer 2012
(Melanoma) :
Resistance to E6201 was associated with disruption of
PTEN and
activation of downstream
PI3K signalling
Wang et al., Lipids in health and disease 2012
(Obesity) :
HDL and
apoA-I could
activate PI3K-Akt-mTORC1 signaling which negatively regulates autophagy
Hunzicker-Dunn et al., Proc Natl Acad Sci U S A 2012
:
PI3K activation
leads to activation of
AKT through phosphorylation of AKT on Thr ( 308 ) and Ser ( 473 )
Ma et al., Biochim Biophys Acta 2013
(Brain Ischemia...) :
We observed that overexpression of
HSPA12B activated
PI3K/Akt signaling and suppressed JNK and p38 activation following cerebral I/R. Importantly, pharmacological inhibition of PI3K/Akt signaling abrogated the protection against cerebral I/R injury in Tg mice
Song et al., Arch Biochem Biophys 2012
(Neointima) :
Specifically, overexpression of
miR-223 and miR-153 inhibited stretch stress
enhanced VSMC proliferation and the activity of
PI3K-AKT signaling
Genini et al., PloS one 2012
(Carcinoma, Non-Small-Cell Lung...) :
Induction of
VEGF was
due to both binding of PPARß/d to the VEGF promoter and
PI3K activation through a non-genomic mechanism
Stetler et al., J Neurochem 2012
(Anoxia) :
AMPK inhibition suppressed NRF1 and TFAM expression by LPS, whereas
PI3K/Akt signaling was
necessary for the nuclear translocation of NRF1 and subsequent induction of
TFAM ... AMPK inhibition suppressed NRF1 and TFAM expression by LPS, whereas
PI3K/Akt signaling was
necessary for the nuclear translocation of
NRF1 and subsequent induction of TFAM
Tsai et al., Cellular oncology (Dordrecht) 2012
(Carcinoma, Non-Small-Cell Lung...) :
In addition, we found that
HO-1 expression can be
inhibited by
PI3K and AKT inhibitors, but not by MAPK inhibitors
Yano et al., Cell communication and signaling : CCS 2012
:
PI3K/Akt dependent activation of cAMP responsive element binding protein ( CREB)-1 induced expression of matrix metalloproteinase (MMP)-9 and suppressing
MMP activity by doxycycline partially reversed FN accumulation in the InsR silenced cells ...
PI3K/Akt dependent activation of
cAMP responsive element binding protein ( CREB)-1 induced expression of matrix metalloproteinase (MMP)-9 and suppressing MMP activity by doxycycline partially reversed FN accumulation in the InsR silenced cells ...
PI3K/Akt dependent activation of cAMP responsive element binding protein (
CREB)-1 induced expression of matrix metalloproteinase (MMP)-9 and suppressing MMP activity by doxycycline partially reversed FN accumulation in the InsR silenced cells
Hsieh et al., Toxicol In Vitro 2013
(Breast Neoplasms...) :
These findings suggest that NFD inhibited the EGF induced invasion and migration of MDA-MB-231 cells via
EGFR dependent
PI3K/Akt signaling, leading to the down-regulation of MMP-9 expression
Lee et al., Apoptosis 2012
(Melanoma) :
Our data reveal that celastrol inhibits growth and induces apoptosis in melanoma cells via the activation of ROS mediated
caspase dependent and -independent pathways and the suppression of
PI3K/AKT signaling
Miyazawa et al., J Biochem 2012
:
2011 ; 149 : 265-274 ) recently indicated that
PI3K activated downstream of C5a anaphylatoxin does not
affect the induction of
IL-12 by TLR, although C5a efficiently inhibits the induction, in macrophages
Wang et al., Diabetes 2013
:
Insulin stimulated
PI3K activity and phosphoinositide ( 3,4,5 ) -triphosphate production are enhanced by Paqr3 deletion and reduced by PAQR3 overexpression in hepatocytes
Gamper et al., Frontiers in immunology 2012
:
In this review, we focus on how
PI3K activation
directs mature
CD4 T cell activation and effector function by pathways dependent on and independent of mTOR signaling
Jang et al., Br J Pharmacol 2013
(Wounds, Penetrating) :
Both an AMPK inhibitor ( compound C ) anda HO-1 activity inhibitor ( SnPPIX ) but not inhibitors of MAPKs,
PI3K and PKC
reduced the production of
VEGF by CKD712
Khaidakov et al., PloS one 2012
:
Ox-LDL also triggered phosphorylation of I?Ba coupled with nuclear translocation of NF-?B and
stimulated p44/42 MAPK,
PI3K and Akt while intracellular PTEN ( PI3K/Akt pathway inhibitor and target of miR-21 ) declined ... Further, transfection of MCF10A cells with miR-21 inhibitor prevented
ox-LDL mediated stimulation of
PI3K and Akt
Cao et al., Pharmacology 2012
:
Propofol enhances the ACE2 expression in HPAECs by increasing the transcription of
ACE2 via a
PI3K dependent mechanism, which leads to increased ACE2 activity on the cell membrane
Wang et al., Clin Exp Allergy 2012
:
The
PI3K-specific inhibitor LY294002 also completely
attenuated IL-25 induced
bFGF expression
Liu et al., Cell Signal 2013
(Stomach Neoplasms) :
PI3K/Akt dependent phosphorylation of GSK3ß and activation of
RhoA regulate Wnt5a induced gastric cancer cell migration
Zhang et al., Shock 2013
:
A specific
PI3K inhibitor, LY294002,
attenuated the inhibition of nitrite production and
iNOS expression produced by overexpressing a liver-specific Epac2 ( LEpac2 )
Takayama et al., Int Immunol 2013
(MAP Kinase Signaling System) :
We also found that the extracellular signal regulated kinase ( ERK ) signaling pathway was activated in a
PI3K dependent manner upon FceRI stimulation and that simultaneous inhibition of Akt and
ERK resulted in nearly complete blockade of FceRI induced degranulation ... We also found that the extracellular signal regulated kinase ( ERK ) signaling pathway was activated in a
PI3K dependent manner upon FceRI stimulation and that simultaneous inhibition of
Akt and ERK resulted in nearly complete blockade of FceRI induced degranulation
Marion et al., Dev Cell 2012
:
Depletion of
Bcl10 impaired Rac1 and
PI3K activation and led to an abortive phagocytic cup rich in PI ( 4,5 ) P ( 2 ), Cdc42, and F-actin, which could be rescued with low doses of F-actin depolymerizing drugs
Koutsioumpa et al., J Biol Chem 2013
(Glioma...) :
Downstream of a ( v ) ß ( 3, )
PI3K activity
mediated this phenomenon and cell surface
NCL was found to interact with both a ( v ) ß ( 3 ) and RPTPß/?. Positive correlation of cell surface NCL and a ( v ) ß ( 3 ) expression was also observed in human glioblastoma tissue arrays, and inhibition of cell migration by cell surface NCL antagonists was observed only in cells expressing a ( v ) ß ( 3 )
Boaglio et al., PloS one 2012
(Cholestasis...) :
The
PI3K inhibitor wortmannin
prevented ERK1/2 activation, whereas the cPKC inhibitor Gö6976 prevented p38 activation, suggesting that ERK1/2 and p38 are downstream of PI3K and cPKC, respectively
Del Turco et al., Curr Pharm Des 2013
(Cardiovascular Diseases...) :
These mechanisms selectively impair
PI3K dependent
insulin in vascular endothelium harming endothelial balance and strengthening the evidence of the close association between metabolic and cardiovascular disease
Finlay et al., J Exp Med 2012
:
The present study now demonstrates that
mTORC1 activity in CD8 ( + ) T cells is not
dependent on
PI3K or Akt but is critical to sustain glucose uptake and glycolysis in CD8 ( + ) T cells
Lu et al., J Clin Immunol 2013
(Arthritis, Rheumatoid...) :
We found that MAPK and Akt inhibitors, but not
PI3K inhibitor, remarkably
suppressed ACPA mediated
TNF-a production
Ding et al., Tumour Biol 2013
(Colonic Neoplasms) :
The
PI3K inhibitor LY294002
inhibited both the phosphorylation of mTOR and upregulation of
Livin ... The
PI3K inhibitor LY294002
inhibited both the phosphorylation of
mTOR and upregulation of Livin
Biswas et al., J Biol Chem 2013
:
Only p110ß was necessary for S1P iduced
Akt activation, but both
PI3K-C2a and p110ß were
required for Rac1 activation ... Only p110ß was necessary for S1P iduced Akt activation, but both
PI3K-C2a and p110ß were
required for
Rac1 activation
Lee et al., J Cell Biochem 2013
:
NaHS blocked nicotine and
LPS induced activation of p38, ERK, MKP-1,
PI3K , PKC, and PKC isoenzymes, and NF-?B
Bullone et al., J Vet Intern Med 2013
(Horse Diseases...) :
PI3K and MAPKs
regulate neutrophil migration toward the airways in heaves
Kim et al., J Neurochem 2013
(MAP Kinase Signaling System) :
Immunoblot analysis revealed that
PI3K mediated activation of
Akt preceded Erk1/2 activation in NRG1ß treated MPG neurons
Pijet et al., Cytokine 2013
(MAP Kinase Signaling System) :
Detailed acute and chronic studies with the use of metabolic inhibitors revealed that both JAK/STAT3 and MEK/MAPK but not
PI3-K/AKT/GSK-3ß signaling pathways were activated by leptin, and that
STAT3 ( Y ( 705 ) P-STAT3 ) and MEK ( T ( 202/ ) Y ( 204 ) P-ERK1/2 )
mediate these effects ... Detailed acute and chronic studies with the use of metabolic inhibitors revealed that both JAK/STAT3 and MEK/MAPK but not
PI3-K/AKT/GSK-3ß signaling pathways were
activated by
leptin , and that STAT3 ( Y ( 705 ) P-STAT3 ) and MEK ( T ( 202/ ) Y ( 204 ) P-ERK1/2 ) mediate these effects ... In contrary, insulin evoked
PI3-K dependent phosphorylation of
AKT ( S ( 473 ) ) and GSK-3ß ( S ( 9 ) ) and insulin surpassed leptin dependent inhibition of myogenic differentiation in PI3-K dependent manner
Wang et al., Toxicol Lett 2013
(Cardiovascular Diseases) :
In addition, the
PI3K inhibitor partially
blocked the effects of Sal B on the upregulation of Bcl-2 and
Bcl-xl protein expression, and downregulation of Bax protein expression ... In addition, the
PI3K inhibitor partially
blocked the effects of Sal B on the upregulation of Bcl-2 and Bcl-xl protein expression, and downregulation of
Bax protein expression ... In addition, the
PI3K inhibitor partially
blocked the effects of Sal B on the upregulation of
Bcl-2 and Bcl-xl protein expression, and downregulation of Bax protein expression
Zhu et al., Mol Endocrinol 2013
:
Although short-term activation of
PI3K and myrAkt1
increased mTOR and S6 signaling, there was no impairment in insulin mediated activation of IRS1/2
Liu et al., Biochem Biophys Res Commun 2013
:
Furthermore, in the presence of exogenous BMP-2,
PI3K and Akt inhibitors
blocked Runx2 and osteocalcin expression, although BMP-2 did not activate Akt ... Furthermore, in the presence of exogenous
BMP-2 ,
PI3K and Akt inhibitors
blocked Runx2 and osteocalcin expression, although BMP-2 did not activate Akt
Kao et al., Phytomedicine 2013
:
Glycyrrhizic acid and 18ß-glycyrrhetinic acid recover glucocorticoid resistance via
PI3K induced
AP1 , CRE and NFAT activation
Meyer et al., Frontiers in physiology 2012
:
Among others
PI3K signaling is
activated by the
hepatocyte growth factor (HGF) that regulates proliferation of hepatocytes during liver regeneration but also fosters tumor cell proliferation
Britschgi et al., Cancer Cell 2012
(Breast Neoplasms...) :
Mechanistically,
PI3K/mTOR inhibition
increased IRS1 dependent activation of
JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors ... Mechanistically,
PI3K/mTOR inhibition
increased IRS1 dependent activation of JAK2/STAT5 and secretion of
IL-8 in several cell lines and primary breast tumors ... Mechanistically,
PI3K/mTOR inhibition
increased IRS1 dependent activation of
JAK2/STAT5 and secretion of IL-8 in several cell lines and primary breast tumors
Rahmani et al., Cancer Res 2013
(Leukemia, Myeloid) :
PI3K/mTOR inhibitors markedly downregulated Mcl-1 but
increased Bim binding to
Bcl-2/Bcl-xL ; the latter effect was abrogated by ABT-737 ...
PI3K/mTOR inhibitors markedly downregulated Mcl-1 but
increased Bim binding to
Bcl-2/Bcl-xL ; the latter effect was abrogated by ABT-737
Kasukabe et al., Int J Oncol 2013
:
The
PI3K inhibitor LY294002 also
suppressed rapamycin induced phosphorylation of
Akt and combined treatment showed synergistic growth inhibition of MCF-7 cells
Shukla et al., Neurotoxicology 2013
:
Sal toxicity coincided with reduced pAkt level and its downstream effectors : pCREB, pGSK-3ß, Bcl-2 and neurotrophins
GDNF , BDNF suggesting
repressed PI3K/Akt signaling ... Sal toxicity coincided with reduced pAkt level and its downstream effectors : pCREB, pGSK-3ß,
Bcl-2 and neurotrophins GDNF, BDNF suggesting
repressed PI3K/Akt signaling
Shi et al., Biochim Biophys Acta 2013
:
Incorporation of beta-sitosterol into the membrane increases resistance to oxidative stress and lipid peroxidation via
estrogen receptor mediated
PI3K/GSK3beta signaling
Fahmi et al., Cell Signal 2013
(Hypertrophy...) :
p42/p44-MAPK and
PI3K are
sufficient for IL-6 family
cytokines/gp130 to signal to hypertrophy and survival in cardiomyocytes in the absence of JAK/STAT activation ... Both LIF and
IL-6 [ in the absence of soluble IL-6 receptor ( sIL-6Ra ) ]
activated Erk1/2, JNK1/2, p38-MAPK and
PI3K signalling peaking at 20min and induced cytoprotection against simulated ischemia-reperfusion injury which was blocked by the MEK1/2 inhibitor PD98059 but not the p38-MAPK inhibitor SB203580 ... Both
LIF and IL-6 [ in the absence of soluble IL-6 receptor ( sIL-6Ra ) ]
activated Erk1/2, JNK1/2, p38-MAPK and
PI3K signalling peaking at 20min and induced cytoprotection against simulated ischemia-reperfusion injury which was blocked by the MEK1/2 inhibitor PD98059 but not the p38-MAPK inhibitor SB203580 ... In conclusion, IL-6 can signal in cardiomyocytes independent of sIL-6R and STAT1/3 and furthermore, that Erk1/2 and
PI3K activation by
IL-6 are both necessary and sufficient for induced cardioprotection
Lai et al., J Huazhong Univ Sci Technolog Med Sci 2012
:
Western blotting was performed to examine the
effect of
EMP-1 on the
PI3K/AKT signaling
Bruning et al., Anticancer Agents Med Chem 2013
:
Inhibition of the mTOR signaling pathway by quercetin has directly been described and can further be deduced from its interference with
PI3K dependent
Akt stimulation, AMP dependent protein kinase activation and hamartin upregulation
Bhattacharya et al., Toxicol Appl Pharmacol 2013
:
PI3K inhibition
increased ( P < 0.05 )
GSTM protein by 40 % and 71 % on d4 and d6, respectively
Zhang et al., Front Biosci (Schol Ed) 2013
:
Exposure of cells to EGF activated the AKT phosphorylation, whereas EGFR and
PI3K inhibitors
blocked EGF induced
AKT phosphorylation in a dose dependent manner
Kerr et al., Cell Signal 2013
:
Interestingly, Gß? as well as
PI3K activation is
necessary for
CXCL11 induced migration of activated T-cells
Gouarné et al., Br J Pharmacol 2013
:
While
BDNF activates both the
PI3K/Akt and the ERK pathway, olesoxime induced only a late activation of the ERK pathways, which did not seem to play a major role in its neuroprotection against CPT. Rather, our results favour preserved mitochondrial membrane integrity by olesoxime
Li et al., Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 2012
:
However, the
PI3K inhibitor ( Ly294002 ) significantly down
regulated a-SMA expression ... Silica induced a-SMA expression in HBE cell line is by targeting the PI3K/Akt pathway and
PI3K inhibitor can
repress a-SMA expression
Li et al., PloS one 2012
:
Pharmacological inhibition of JAK/STAT3,
PI3K/Akt or MEK/ERK signaling by AG490, Wortmannin or U0126, respectively,
reduced leptin induced
cyclin D1 expression and NP cell proliferation
Martínez-Palacián et al., PloS one 2013
:
Interestingly, both
PI3K inhibition and/or knockdown itself
resulted in
caspase-3 activation and loss of viability in Met ( flx/flx ) oval cells, whereas no effect was observed in Met ( -/- ) oval cells ... Altogether, results presented here provide solid evidences that both paracrine and autocrine
HGF/Met signaling
requires PI3K to promote mouse hepatic oval cell survival against TGF-ß induced oxidative stress and apoptosis ... Altogether, results presented here provide solid evidences that both paracrine and autocrine
HGF/Met signaling
requires PI3K to promote mouse hepatic oval cell survival against TGF-ß induced oxidative stress and apoptosis
Zhou et al., PloS one 2013
(Cell Transformation, Neoplastic...) :
Mechanistic studies indicated
Tat activates
PI3K and AKT, and inactivates PTEN and GSK-3ß in vIL-6 expressing cells
Runne et al., Cell Adh Migr 2013
:
Previous data indicates that
RACK1 negatively
regulates Gß? mediated leukocyte migration by inhibiting Gß? stimulated PLCß and
PI3K activities
Song et al., J Biol Chem 2013
(Diabetes Mellitus, Type 2...) :
Increased insulin sensitivity was also confirmed after daily injection of emodin for 8 days using an insulin tolerance test and
insulin stimulated
PI3K phosphorylation in wild type and high fat diet induced diabetic mouse models
Kong et al., Eur J Pharmacol 2013
(Diabetes Mellitus) :
Additionally, we found that FGF21 induced PKC?/? phosphorylation in a
PI3K dependent manner ; and that a non-isoform selective PKC inhibitor blocked
FGF21 inhibition of glucose production, while an inhibitor of classical and novel PKC isoforms had no effect on FGF21 inhibitory activity
Mavila et al., PloS one 2012
(Liver Neoplasms) :
FGF Receptor ( R ) activation
resulted in the downstream activation of MAPK,
PI3K-AKT , and ß-catenin pathways, as well as cellular proliferation
Razmara et al., Cell communication and signaling : CCS 2013
:
Thus, whereas both mTORC1 and
mTORC2 are activated in a
PI3K dependent manner, different additional signaling pathways are needed ... Thus, whereas both
mTORC1 and mTORC2 are activated in a
PI3K dependent manner, different additional signaling pathways are needed
Molejon et al., Scientific reports 2013
:
Collectively, these findings reveal that
VMP1 expression recruits and
activates the Class III
PI3K complex at the site of autophagosome formation during mammalian autophagy
Park et al., Br J Pharmacol 2013
:
A
PI3K specific inhibitor ( LY294002 ), Akt inhibitor VIII ( Akti ) and NF-?B inhibitors ( Bay-11-7082 and MG-132 )
attenuated the induction of
ICAM-1 by PGE2
Ji et al., Curr Pharm Des 2013
:
Accumulating evidence has suggested
insulin induced
PI3K-Akt-eNOS survival signaling as a potent therapeutic target for cardiovascular disorders and highlighted the impaired survival signaling as a key link between insulin resistance and cardiovascular disease
Qiao et al., PloS one 2013
:
Dab2IP regulates
PI3K-AKT signaling and is associated with metastatic prostate cancer, abdominal aortic aneurysms and coronary heart disease
Tapia-Abellán et al., Liver Int 2013
(Liver Cirrhosis) :
The release of the pro-inflammatory cytokines IL-6 and TNF-a at baseline was more effectively
reduced by the
MAPK inhibitors, while the basal IL-10 anti-inflammatory cytokine secretion was only and strongly ( 90.3 % ) affected by the
PI3K inhibitor ... The release of the pro-inflammatory cytokines IL-6 and TNF-a at baseline was more effectively reduced by the MAPK inhibitors, while the basal
IL-10 anti-inflammatory cytokine secretion was only and strongly ( 90.3 % )
affected by the
PI3K inhibitor ... Finally, inhibition of
PI3K almost completely
suppressed the secretion of
IL-10 in stimulated M-DM
Ouro et al., Cell Signal 2013
(Translocation, Genetic) :
The latter action was also inhibited by
PI3K- and Akt-selective inhibitors, PTX, or by specific siRNAs to
inhibit GLUT 3 expression
Quan et al., Exp Parasitol 2013
:
The
PI3K inhibitors, LY294002 and Wortmannin, both
blocked parasite induced phosphorylation of
PKB/Akt and Bad ... The
PI3K inhibitors, LY294002 and Wortmannin, both
blocked parasite induced phosphorylation of
PKB/Akt and Bad
Huang et al., Pharm Biol 2013
(Disease Models, Animal...) :
PI3K inhibitor wortmannin not only
blocked catalpol induced
Akt activation, but also attenuated all the beneficial effects of catalpol
Takaku et al., Neurochem Int 2013
:
The GDNF induced neurite outgrowth and
GAL-1 upregulation were
attenuated by anti-GDNF family receptor (RET) antibody and phosphatidyl inositol-3'-phosphate-kinase (
PI3K ) inhibitor LY294002, suggesting that the neurite-outgrowth promoting activity of GDNF may be attributable, at least partially, to the upregulation of GAL-1 through RET-PI3K pathway
Mukherjee et al., Proc Natl Acad Sci U S A 2013
:
The innate immune receptor, Toll-like receptor 2/6 heterodimer, is exploited by Sb ( R ) LD to activate ERK and nuclear translocation of NF-?B involving p50/c-Rel leading to IL-10 induction, whereas
MDR1 up-regulation is
mediated by
PI3K/Akt and the JNK pathway
Mohan et al., Science signaling 2013
(Cardiomegaly) :
Activation of cardiac phosphoinositide 3-kinase a (PI3Ka) by growth factors, such as
insulin , or
activation of
PI3K? downstream of heterotrimeric guanine nucleotide binding protein ( G protein ) -coupled receptors stimulates the activity of the kinase Akt, which phosphorylates and inhibits glycogen synthase kinase-3 ( GSK-3 ) ...
Activation of cardiac
phosphoinositide 3-kinase a (PI3Ka) by growth factors, such as insulin, or activation of
PI3K? downstream of heterotrimeric guanine nucleotide binding protein ( G protein ) -coupled receptors stimulates the activity of the kinase Akt, which phosphorylates and inhibits glycogen synthase kinase-3 ( GSK-3 )
Ueki et al., Glia 2013
:
Interestingly,
BMP/Smad1/5/8 activation downstream of
PI3K/AKT signaling was also necessary for robust Müller glial proliferation, though activation of BMP/Smad1/5/8 signaling alone failed to stimulate their proliferation ... Interestingly,
BMP/Smad1/5/8 activation downstream of
PI3K/AKT signaling was also necessary for robust Müller glial proliferation, though activation of BMP/Smad1/5/8 signaling alone failed to stimulate their proliferation ... Interestingly,
BMP/Smad1/5/8 activation downstream of
PI3K/AKT signaling was also necessary for robust Müller glial proliferation, though activation of BMP/Smad1/5/8 signaling alone failed to stimulate their proliferation
Cai et al., Med Hypotheses 2013
(Metabolic Syndrome X) :
Since
PTEN negatively
regulates PI3K/AKT signaling and has crosstalk with 5-HT2cR, we hypothesized that the 5-HT2cR antagonism of AAPs may disrupt its crosstalk with PTEN and then trigger the PI3K/AKT signaling, and AAP induced MetS and cognitive impairments may occur via this analogous signaling pathway
Stagg et al., Am J Surg 2013
:
Rat lung microvascular endothelial cells ( RLMECs ) grown on Transwell membranes ( Corning Life Sciences, Lowell, MA ) were treated with recombinant human
TRAIL ( 10, 50, and 100 ng/mL ) for 6 hours or TRAIL ( 100 ng/mL ) + LY294002 ( a
PI3K inhibitor ; 20 µmol/L ), Z-DEVD-FMK ( a caspase-3 inhibitor ; 10 µmol/L ), or the inhibitors alone
Hyam et al., Eur J Pharmacol 2013
:
Arctigenin inhibited
LPS induced
PI3K , AKT and IKKß phosphorylation, but did not suppress LPS induced IRAK-1 phosphorylation
Xu et al., Cancer Lett 2013
(Stomach Neoplasms) :
G17 increased
COX-2 expression and cell proliferation were effectively
blocked by CCK2R antagonist and inhibitors of JAK2 and
PI3K
Kenerson et al., Gastroenterology 2013
(Carcinoma, Hepatocellular...) :
In livers of albumin (Alb)-Cre mice, we selectively deleted tuberous sclerosis (Tsc)1, a negative regulator of Ras homolog enriched in brain and mTORC1, along with
Phosphatase and tensin homolog (Pten) , a negative
regulator of
PI3K
Sauer et al., Stem Cells Dev 2013
:
In conclusion, a2M stimulates endothelial and early cardiac, but not smooth muscle differentiation of ES cells through generation of NO,
activation of ERK1/2 as well as
PI3K , and induction of
FGF-2 expression
Slouzkey et al., Biol Psychiatry 2013
:
To that end, we ( 1 ) monitored
AKT phosphorylation in the IC following CTA acquisition and extinction and ( 2 )
inhibited PI3K by local microinjection of the PI3K inhibitor LY294002 at different stages of CTA acquisition and extinction
Veillette et al., Biol Reprod 2013
:
PI3-K inhibition in vivo blocked Akt phosphorylation, reduced Smad2 phosphorylation, and
reduced both
TGF-beta2 and XIAP expression ...
PI3-K inhibition in vivo
blocked Akt phosphorylation, reduced Smad2 phosphorylation, and reduced both TGF-beta2 and XIAP expression ...
PI3-K inhibition in vivo blocked Akt phosphorylation, reduced Smad2 phosphorylation, and
reduced both TGF-beta2 and
XIAP expression ...
PI3-K inhibition in vivo blocked Akt phosphorylation,
reduced Smad2 phosphorylation, and reduced both TGF-beta2 and XIAP expression
Weidenaar et al., Mol Cancer Res 2013
(Leukemia, Myeloid, Acute...) :
Proteome profiler array analysis of downstream kinases revealed that
PTK/ZK reduced activation of
PI3K/Akt kinase signaling
Hatton et al., Am J Transplant 2013
(Epstein-Barr Virus Infections...) :
Taken together, our data indicate that
Syk activates
PI3K/Akt signaling which is required for survival of EBV+ B cell lymphomas
Huang et al., J Lipid Res 2013
(Atherosclerosis) :
However, the cell-surface protein expression of ABCA1,
ABCG1 , and SR-BI could be
regulated by
PI3K activity, and PI3K activation corrected the MCP-1 induced decreases in the cell-surface protein expression of ABCA1, ABCG1, and SR-BI ... However, the cell-surface protein expression of ABCA1, ABCG1, and
SR-BI could be
regulated by
PI3K activity, and PI3K activation corrected the MCP-1 induced decreases in the cell-surface protein expression of ABCA1, ABCG1, and SR-BI ... However, the cell-surface protein expression of
ABCA1 , ABCG1, and SR-BI could be
regulated by
PI3K activity, and PI3K activation corrected the MCP-1 induced decreases in the cell-surface protein expression of ABCA1, ABCG1, and SR-BI ... However, the cell-surface protein expression of ABCA1,
ABCG1 , and SR-BI could be
regulated by
PI3K activity, and PI3K activation corrected the MCP-1 induced decreases in the cell-surface protein expression of ABCA1, ABCG1, and SR-BI ... Our data suggest that MCP-1 impairs RCT activity in HepG2 cells by a
PI3K/Akt mediated posttranslational
regulation of ABCA1, ABCG1, and
SR-BI cell-surface expression ... Our data suggest that MCP-1 impairs RCT activity in HepG2 cells by a
PI3K/Akt mediated posttranslational
regulation of
ABCA1 , ABCG1, and SR-BI cell-surface expression ... Our data suggest that MCP-1 impairs RCT activity in HepG2 cells by a
PI3K/Akt mediated posttranslational
regulation of ABCA1,
ABCG1 , and SR-BI cell-surface expression
Shortt et al., Blood 2013
(Lymphoma, B-Cell) :
Moreover, apoptosis was initiated at drug concentrations insufficient to antagonize
PI3K/mTORC2 regulated
AKT phosphorylation
Jiang et al., Journal of thrombosis and haemostasis : JTH 2013
:
A
PI3K dependent thrombin generation and the resultant
PAR-1 activation serve as an indispensable mechanism to relay the platelet activation process induced by ADP
Liu et al., PloS one 2013
(Pleural Effusion...) :
The induction of
MCP-2/CCL8 by mycobacteria is
dependent on the activation of
TLR2/PI3K/Akt and p38 signaling pathway
Fortress et al., Learn Mem 2013
(MAP Kinase Signaling System) :
Collectively, these data demonstrate for the first time that activation of the dorsal hippocampal mTOR signaling pathway is necessary for E ( 2 ) to enhance object recognition memory consolidation and that E ( 2 ) -induced
mTOR activation is
dependent on upstream activation of ERK and
PI3K signaling
Ning et al., Arch Toxicol 2013
(Airway Remodeling...) :
PDGF induced
DNA methyltransferase 1 (DNMT1) expression was
mediated by activation of
PI3K/Akt and ERK signaling in RASM cells
Cao et al., PLoS Biol 2013
(Angelman Syndrome) :
In Ube3A deficient mice, the BDNF induced recruitment of PSD-95, as well as PLC? and Grb2 associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced activation of
PLC?-a-calcium/calmodulin dependent protein kinase II ( CaMKII ) and
PI3K-Akt , but leaving the extracellular signal regulated kinase ( Erk ) pathway intact ... In Ube3A deficient mice, the BDNF induced recruitment of PSD-95, as well as PLC? and Grb2 associated binder 1 (Gab1) with TrkB receptors was attenuated, resulting in reduced activation of
PLC?-a-calcium/calmodulin dependent protein kinase II ( CaMKII ) and
PI3K-Akt , but leaving the extracellular signal regulated kinase ( Erk ) pathway intact
Li et al., Marine drugs 2013
:
Furthermore,
PI3K inhibitor LY294002 and Erk1/2 inhibitor U0126
suppressed the induction of
HO-1 and translocation of Nrf-2 by xyloketal B, whereas P38 inhibitor SB203580 did not
Xie et al., Cancer cell international 2013
:
Klotho is a tumor suppressor in gastric cancer, which regulates
IGF-1R phosphorylation and the subsequent
activation of
IRS-1/PI3K/Akt/mTOR signaling, tumor cell proliferation, apoptosis, and autophagy
Lin et al., Int J Cancer 2013
(Brain Neoplasms...) :
Palomid 529 lacked affinity for these transporters in vitro, in contrast to
GDC-0941 , a small molecule
PI3K inhibitor , which we used as control substance for in vitro transport
Kirk-Ballard et al., PloS one 2013
(Diabetes Mellitus, Experimental...) :
The effect of
PMI5011 is
mediated by
PI3K/Akt signaling and correlates with decreased expression of Atrogin-1 and MuRF-1
Fumagalli et al., J Immunol 2013
:
These findings suggest that class IA
PI3Ks may be
activated by
PI3K? via Ras in the early phase of the response and by SFKs in the late phase
Huber et al., PloS one 2013
:
For example, DTX1 activates the
RTK/PI3K/PKB and the MAPK/ERK mitotic pathways and
induces anti-apoptotic
Mcl-1 ... For example,
DTX1 activates the
RTK/PI3K/PKB and the MAPK/ERK mitotic pathways and induces anti-apoptotic Mcl-1
Molina-Arcas et al., Cancer Discov 2013
(Carcinoma, Non-Small-Cell Lung...) :
PI3K pathway activity is
dependent on basal
IGF1R activity in KRAS-mutant, but not wild-type, lung cancer cell lines ... KRAS is needed for both MEK and PI3K pathway activity in KRAS-mutant, but not wild-type, lung cancer cells, whereas acute activation of
KRAS causes stimulation of
PI3K dependent upon IGF1R kinase activity
Liu et al., Med Hypotheses 2013
(Prostatic Neoplasms) :
More than 80 % of prostate tumors acquire mutation or deletion of tumor suppressor
phosphatase and tensin homolog (PTEN) , a negative
regulator of
PI3K/Akt signaling
Lin et al., International journal of molecular sciences 2013
:
More than 80 % of prostate tumors acquire mutation or deletion of tumor suppressor
phosphatase and tensin homolog (PTEN) , a negative
regulator of
PI3K/Akt signaling, indicating that inhibition of PI3K/Akt might be a potential therapy for advanced prostate tumors
Cao et al., PloS one 2013
(Breast Neoplasms) :
The
PI3K inhibitor LY294002 and MEK1/2 inhibitor PD98059 inhibited, but not fully
blocked , FGF-2 induced
AQP3 expression and cell migration
Bhattacharya et al., J Neurooncol 2013
(Brain Neoplasms...) :
T11TS therapy in rodent glioma model significantly downregulated expression of
VEGF along with its receptor VEGFR-2 and
inhibited the expression of pro-survival
PI3K/Akt/eNOS proteins in glioma associated brain endothelial cells
Kim et al., Int J Cancer 2013
(Colorectal Neoplasms) :
Taken together, our data suggest that targeting PI3K/MTOR sensitizes cells to apoptosis, implying that
activation of
PI3K/MTOR signaling via
KRAS or PIK3CA mutation is an important pathway in CRC cell growth
Ko et al., Arch Biochem Biophys 2013
(Diabetes Mellitus, Experimental) :
We conclude that
PI3K dependent
UCHL5 is required for high glucose induced TGF-ßR1 protein expression in mesangial cells
Wang et al., Biochem Pharmacol 2013
:
It was found that mRNA, protein, and current density of K ( Ca ) 3.1 channels were greatly enhanced in cultured cardiac fibroblasts treated with 1 µM Ang II, and the effects were countered by the
angiotensin type 1 receptor ( AT1R ) blocker losartan, the p38-MAPK inhibitor SB203580, the ERK1/2 inhibitor PD98059, and the
PI3K/Akt inhibitor LY294002
Liu et al., Autophagy 2013
(Pulmonary Fibrosis) :
In
response to
IL17A stimulation,
PI3K was activated and resulted in phosphorylation of GSK3B at Ser9, which subsequently attenuated the interaction of GSK3B with BCL2
Yan et al., Mol Cancer Res 2013
:
In addition, knocking down or inhibiting focal adhesion kinase ( FAK ),
phosphoinositide 3-kinase (PI3K) , or Src kinase significantly
reduces d-GM3 induced
p38 phosphorylation and activation
Dilly et al., Int J Cancer 2013
(Neoplasm Invasiveness...) :
Specific inhibitors of 12-LOX,
PI3K or NF-?B
inhibited MMP9 expression in 12-LOX expressing PC-3 cells and resulted in the blockade of the migratory ability of endothelial cells
Mondal et al., The Ochsner journal 2013
:
Insulin induced
PI3K/Akt signaling and endothelial nitric oxide ( NO ) -synthase ( eNOS ) phosphorylation regulates NO production by ECs that maintain vascular homeostasis
Liu et al., Exp Mol Med 2013
:
Similar to the changes in neurite outgrowth, the
PI3K/Akt activation by
NGF was potentiated by PIP5Ka KD, but was attenuated by the reintroduction of PIP5Ka
Purpura et al., Oncotarget 2013
:
In addition, KGFR induced a ligand dependent decrease of
p63 through a miR-203 independent mechanism and this effect was
blocked by inhibition of the
PI3K/Akt signaling, which is the main pathway involved in KGFR dependent keratinocyte differentiation, suggesting that alterations of the KGFR/p63 crosstalk are responsible for the impairment of keratinocyte differentiation induced by 16E5 and that the opposite tumor-suppressive action of KGFR and oncogenic role of E5 might both involve p63
Haeussler et al., J Biol Chem 2013
:
Knockdown of H-Ras blocked VEGF induced
PI3K dependent
Akt ( Ser-473 ) and eNOS ( Ser-1177 ) phosphorylation and nitric oxide dependent cell migration, demonstrating the essential role of H-Ras ... Knockdown of H-Ras blocked VEGF induced
PI3K dependent Akt ( Ser-473 ) and
eNOS ( Ser-1177 ) phosphorylation and nitric oxide dependent cell migration, demonstrating the essential role of H-Ras
Cao et al., J Mol Endocrinol 2013
:
6Cl-TGQ induced
Akt phosphorylation was completely
blocked by IR and
PI3K inhibitors, while the induced glucose uptake was blocked by the same compounds and a Glut4 inhibitor
Yang et al., Journal of biomedical research 2011
:
Activation of
Rac1-PI3K/Akt is
required for epidermal growth factor induced
PAK1 activation and cell migration in MDA-MB-231 breast cancer cells ... Furthermore, expression of dominant negative
Rac1 ( T17N ) could largely
block EGF induced
PI3K/Akt-PAK1 activation and cell migration ... Furthermore, expression of dominant negative Rac1 ( T17N ) could largely block
EGF induced
PI3K/Akt-PAK1 activation and cell migration ... Interestingly,
EGF could
induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF induced ROS generation, cell migration, as well as activation of
PI3K/Akt and PAK, but not Rac1
Lau et al., PloS one 2013
(Neoplasm Invasiveness...) :
The pharmacological inhibition of phosphatidylinositol-3-kinase (PI3K), mammalian target of rapamycin (mTOR), and MEK suggests that both
PI3K/Akt/mTOR and MAPK/ERK signaling are
required for FGF2 induced
E-cadherin down-regulation
Owada et al., PloS one 2013
:
We have reported glucose deprivation rapidly
induces AKT phosphorylation through
PI3K activation
Brennan-Minnella et al., Cell death & disease 2013
:
The
PI3K inhibitor wortmannin
prevented NMDA induced
NOX2 activation and cell death, without preventing cell swelling, calcium elevation, or mitochondrial depolarization
Blank et al., Exp Cell Res 2013
:
In conclusion, we herein demonstrated that
STAT1 serine phosphorylation is
mediated by the sequential activation of
PI3K , PKCd and p38 MAPK
Cho et al., Life Sci 2013
:
Glucose deprivation induced activation of
PI3K-Akt-GSK3ß , p38 and AMPK, and inhibition of these pathways using LY294002, SB203580 and compound C significantly
inhibited glucose deprivation induced
tPA down-regulation, demonstrating the essential role of these pathways in tPA regulation in glucose deprived astrocytes
Trott et al., Eur J Appl Physiol 2013
:
Collectively, these results indicate that impaired NO-mediated, endothelium dependent dilation in old SFA is due, in part, to an impaired potential for
PI3K/Akt dependent phosphorylation of
eNOS on ser ( 1177 )
Schmid et al., PloS one 2013
(Inflammation...) :
We show here that
PI3K? activates
PLC? , leading to RasGrp/CalDAG-GEF-I & II mediated, Rap1a dependent activation of integrin a4ß1, extravasation of monocytes and granulocytes, and inflammation associated tumor progression ... Genetic depletion of PLC?, CalDAG-GEFI or II,
Rap1a , or the Rap1 effector RIAM was
sufficient to prevent integrin a4 activation by chemoattractants or activated
PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1 ... Genetic depletion of PLC?, CalDAG-GEFI or II, Rap1a, or the Rap1 effector
RIAM was
sufficient to prevent integrin a4 activation by chemoattractants or activated
PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1 ... Genetic depletion of
PLC? , CalDAG-GEFI or II, Rap1a, or the Rap1 effector RIAM was
sufficient to prevent integrin a4 activation by chemoattractants or activated
PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1 ... Genetic depletion of PLC?,
CalDAG-GEFI or II, Rap1a, or the Rap1 effector RIAM was
sufficient to prevent integrin a4 activation by chemoattractants or activated
PI3K? ( p110?CAAX ), while activated Rap ( RapV12 ) promoted constitutive integrin activation and cell adhesion that could only be blocked by inhibition of RIAM or integrin a4ß1
Bhowmick et al., J Virol 2013
(Rotavirus Infections) :
This function of NSP1 was independent of its interferon or phosphatidylinositol 3-kinase (PI3K)/AKT modulation activity since
p53 degradation was observed in Vero cells as well as in the
presence of
PI3K inhibitor
Heskamp et al., Neurobiol Dis 2013
(Disease Models, Animal...) :
Furthermore, the neurite growth promoting and disinhibitory effects of CXCL12 were abrogated by a specific
CXCR4 antagonist and by
inhibition of the
PI3K/AKT/mTOR- , but not the JAK/STAT3-pathway
Muscolini et al., J Immunol 2013
:
Hence, PIP2 is a crucial substrate in driving the PI3K downstream signaling pathways, and PIP2 turnover may be an essential regulatory step to ensure the
activation of
PI3K following
CD28 engagement
Furuya et al., J Biol Chem 2013
:
The inhibition of
p85a expression by siRNA or the
inhibition of
PI3K by LY294002 prevents the expression of Pdx1, Ngn3, and MafA and the reprogramming to insulin producing cells
Fransson et al., Journal of molecular signaling 2013
:
PI3K activity subsequently
activates Akt/PKB , and as mutations of PI3K are rare in neuroblastoma and high levels of PI3K subunit p110delta is associated with favorable disease with low p-Akt/PKB, the levels of other PI3K subunits could be important for Akt activation ...
PI3K activity subsequently
activates Akt/PKB , and as mutations of PI3K are rare in neuroblastoma and high levels of PI3K subunit p110delta is associated with favorable disease with low p-Akt/PKB, the levels of other PI3K subunits could be important for Akt activation
Qi et al., J Biol Chem 2013
(Colonic Neoplasms) :
Stimulation of LD density in human colon cancer cells led to a
PI3K dependent loss of
FOXO3 and a decrease in the negative regulator of lipid metabolism in Sirtuin6 (SIRT6)
Chowdhury et al., Diabetologia 2013
:
PI3K inhibition only slightly
attenuated glucose stimulated
insulin secretion from monolayers, but substantially reduced that from pseudoislets and human and mouse islets without suppressing the glucose induced [ Ca ( 2+ ) ] c response ... We propose that islet architecture is critical for proper beta cell mitochondrial metabolism and IRS-1 signalling, and that
PI3K regulates
insulin secretion at a step distal to the elevation of [ Ca ( 2+ ) ] c
Chung et al., J Endocrinol 2013
(MAP Kinase Signaling System) :
Our data also suggest that
PI3K/Akt mediated inactivation of GSK-3ß and
activation of
mTOR/p70 ( S6K ) contribute to the proliferative effect of ghrelin ... Our data also suggest that
PI3K/Akt mediated inactivation of GSK-3ß and
activation of
mTOR/p70 ( S6K ) contribute to the proliferative effect of ghrelin
Kumari et al., Indian J Dermatol Venereol Leprol 2013
(Acne Vulgaris...) :
Milk consumption and hyperglycemic diets can induce insulin and
IGF-1 mediated
PI3K / Akt-activation inducing sebaceous lipogenesis, sebocyte, and keratinocyte proliferation, which can aggravate acne
Carpentier et al., Traffic 2013
:
A substractive approach, comparing in Opossum Kidney ( OK ) cells a pan-class I/II/III PI3K inhibitor ( LY294002 ) with a class I/II PI3K inhibitor ( ZSTK474 ), suggested that class III
PI3K/VPS34 inhibition
induced selective apical endosome swelling and sequestration of the endocytic receptor,
megalin/LRP-2 , causing surface down-regulation
Henao-Mejia et al., Immunity 2013
:
Mechanistically, miR-181 modulated expression of the phosphatase
PTEN to
control PI3K signaling, which was a primary stimulus for anabolic metabolism in immune cells
Suzuki et al., Mol Cell 2013
:
Surprisingly,
PI3K-Akt signaling, which is a major anabolic signaling and normally inhibits GSK3 activity,
promotes GSK3 phosphorylation and inhibition of
AMPK , thus revealing how AMPK senses anabolic environments in addition to cellular energy levels
Das et al., Mol Cell Endocrinol 2013
:
PI3K inhibitors, wortmannin and LY294002
blocked insulin , but not 17a, 20ß-DHP induced GVBD
Martinelli et al., Int J Cancer 2013
(Colorectal Neoplasms...) :
The in vitro and in vivo anti-tumor activity of pimasertib, a selective MEK 1/2 inhibitor, alone or in combination with a
PI3K inhibitor (PI3Ki) , a
mTOR inhibitor ( everolimus ), or with multi targeted kinase inhibitors ( sorafenib and regorafenib ), that block also BRAF and CRAF, were tested in a panel of eight human lung and colon cancer cell lines
Willimott et al., Clin Cancer Res 2013
:
PI3K inhibitors and 4EGI-1 also reduced cap-complex formation but only 4EGI-1 consistently
reduced BCL2L1 and
BCL2A1 protein levels ...
PI3K inhibitors and 4EGI-1 also reduced cap-complex formation but only 4EGI-1 consistently
reduced BCL2L1 and BCL2A1 protein levels
Du et al., PloS one 2013
(Neoplasms) :
In this study, we show that IGF-1 up-regulates
MDM2 protein levels in a
PI3K/AKT dependent manner
Pang et al., International journal of molecular sciences 2013
:
Furthermore, resistin enhanced DNA binding activity of
Sp1 with VEGF promoter in a
PI3K/Akt dependent manner ...
PI3K/Akt activated by resistin
led to increasing interaction with
Sp1 , triggering a progressive phosphorylation of Sp1 on Thr453 and Thr739, resulting in the upregulation of VEGF expression
Kan-o et al., Biochem Biophys Res Commun 2013
:
Poly IC-induced upregulation of
B7-H1 was profoundly
suppressed by a
pan-PI3K inhibitor and partially by an inhibitor or a small interfering ( si ) RNA for PI3Kd in BEAS-2B cells
Xu et al., Mol Med Report 2013
:
However, LY294002, a
PI3K inhibitor, attenuated the anti-apoptotic effect of salidroside and
blocked the increase of
Akt and mTOR ; however, did not affect the antioxidative effect of salidroside ... However, LY294002, a
PI3K inhibitor, attenuated the anti-apoptotic effect of salidroside and
blocked the increase of Akt and
mTOR ; however, did not affect the antioxidative effect of salidroside
Lo et al., International journal of molecular sciences 2013
:
In parallel,
VEGF induced JNK,
PI3K and Akt activation
Chou et al., Toxicol In Vitro 2013
:
A specific
PI3K inhibitor
attenuated the UVB induced ERK1/2 and
p53 phosphorylation ... A specific
PI3K inhibitor
attenuated the UVB induced
ERK1/2 and p53 phosphorylation
Chiron et al., Cell cycle (Georgetown, Tex.) 2013
(Lymphoma) :
PIK3IP1 , a negative
PI3K regulator , appears to mediate pG1 sensitization to PI3K inhibition ; it is markedly reduced in MCL tumor cells compared with normal peripheral B cells, profoundly induced in pG1 and required for pG1 sensitization to GS-1101 ...
PIK3IP1 , a negative
PI3K regulator , appears to mediate pG1 sensitization to PI3K inhibition ; it is markedly reduced in MCL tumor cells compared with normal peripheral B cells, profoundly induced in pG1 and required for pG1 sensitization to GS-1101
Cipriano et al., Oncotarget 2013
(Cell Transformation, Neoplastic...) :
FAM83B mediated
activation of
PI3K/AKT and MAPK signaling cooperates to promote epithelial cell transformation and resistance to targeted therapies
Yu et al., Cell death & disease 2013
(Cell Transformation, Neoplastic...) :
Our studies are the first to demonstrate that reduced CTGF as an unfavorable prognosis factor mediates the
activation of
miR-18b , an oncomir directly suppresses CTGF expression, by
PI3K/AKT/C-Jun and C-Myc and promotes cell growth of NPC
Uranga et al., J Biol Chem 2013
:
Levels of
phospho-FoxO3a ( inactive form ) increased in the cytosolic fraction of cells treated with iron in a
PI3K dependent manner
Berdichevsky et al., J Neurosci 2013
:
Inhibition of
PI3K and Akt
prevented activation of
mTOR , and was as effective as inhibition of mTOR in reducing ictal activity and cell death
Hsieh et al., Chem Biol Interact 2013
(Breast Neoplasms) :
Additionally, treatment of SB203580 ( p38
MAPK inhibitor ) or wortmannin (
PI3K inhibitor ) resulted in a reduced activity and expression of MMP-2 as well as inhibition on cell migration and invasion in MDA-MB-231 cells ... Additionally, treatment of SB203580 (
p38 MAPK inhibitor ) or wortmannin (
PI3K inhibitor ) resulted in a reduced activity and expression of MMP-2 as well as inhibition on cell migration and invasion in MDA-MB-231 cells
Yu-Shengyou et al., BioMed research international 2013
:
The
PI3K inhibitor LY294002
blocked p-Akt and p-GSK3 ß expressions in podocytes
Yang et al., Biochim Biophys Acta 2013
(Cardiomegaly) :
And
PI3K inhibitor, LY294002, effectively
prevented LPA induced
miR-23a expression in cardiomyocytes, suggesting that LPA might induce miR-23a elevation by activating LPA3 and PI3K/AKT pathway
Zheng et al., Exp Cell Res 2013
:
TMP significantly inhibited
TNF-a induced phosphorylation of Syk and
PI3K ... Our data indicate that TMP might repress iNOS expression, at least in part, through its inhibitory effect of
Syk mediated
PI3K phosphorylation in TNF-a stimulated HUVECs
Hanihara et al., Int Immunol 2013
:
The PI3K inhibitor LY294002 inhibited BCR mediated, but not TLR mediated, induction of I?B-?, consistent with the
role of
PI3K in
BCR signaling and its suppression by Fc?R. Analysis of I?B-?-deficient B cells demonstrated that I?B-? was essential upon stimulation of BCR or TLR for the expression of several genes including IL-10 and CTLA4
Shoeb et al., Free Radic Biol Med 2013
(Colonic Neoplasms) :
We found that AR inhibition regulates
AKT/PI3K dependent
activation of forkhead transcription factor
FOXO3a
Beckham et al., Oncogenesis 2013
:
This signaling pathway proceeds through
S1P receptor 2 (S1PR2) dependent stimulation of
PI3K
Díaz-Muñoz et al., J Immunol 2013
:
Cyclooxygenase-2 deficiency in macrophages
leads to defective p110?
PI3K signaling and impairs cell adhesion and migration
Huang et al., Hypertension 2013
(Hypertension...) :
In conclusion, global null deletion of Ceacam1 caused an increase in blood pressure with increased renin-angiotensin system activation together with upregulation of PRR via
PI3K-Akt activation of cAMP response element binding protein 1,
ATF-1 , ATF-2, and NF-?B p65 transcription factors ... In conclusion, global null deletion of Ceacam1 caused an increase in blood pressure with increased renin-angiotensin system activation together with upregulation of PRR via
PI3K-Akt activation of cAMP response element binding protein 1, ATF-1,
ATF-2 , and NF-?B p65 transcription factors
Chang et al., Microvasc Res 2013
:
PI3K activity
regulated the expression of
Slug , which was required for survival in Notch activated endothelial cells ... Homocysteine, but not
LPS ,
blocked both
PI3K activity and Slug expression in Notch activated cells, leading to increased endothelial apoptosis
Chakraborty et al., J Mol Cell Cardiol 2013
:
Inhibition of
PI3K/AKT/GSK3ß/ß-catenin signaling reduces, but does not eliminate,
Tbx20 mediated
increases in cell proliferation, providing evidence for parallel regulatory pathways downstream of BMP/Smad1/5/8 signaling in promoting cardiomyocyte proliferation after birth
Zhen et al., PloS one 2013
:
Mechanistic analysis revealed that
CTGF suppression
activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs
Zenzmaier et al., Prostate 2013
(Prostatic Hyperplasia...) :
DKK3 knockdown did not affect subcellular localization or levels of ß-catenin but
attenuated AKT phosphorylation in PrSCs. Consistently the
PI3K/AKT inhibitor LY294002 mimicked the effects of DKK3 knockdown
Jin et al., PloS one 2013
:
Moreover, sCD40L strongly stimulates neutrophil oxidative burst via
CD40 dependent activation of
PI3K/NF-KB , but independent of Mac-1 and PKC?
Chow et al., Biology open 2013
:
The inhibition of
PI3K or Akt activities, by the specific kinase inhibitors ( wortmannin, LY294002 or SH6 ),
stimulates Ostf1 expression, while a reduction of GSK3ß activity by LiCl reduces Ostf1 expression
Chen et al., Am J Physiol Lung Cell Mol Physiol 2013
(Anoxia) :
Thus, our findings indicate that
Trx1 contributes to hypoxia induced PASMC proliferation by modulating HIF activation and subsequent
PI3K-Akt activation
Sampath et al., Neoplasia (New York, N.Y.) 2013
:
GDC-0980 , a dual
PI3K/mTOR inhibitor , was found to reduce micro-CT angiography vascular density, while VSI MRI demonstrated a significant reduction in vessel density and an increase in mean vessel size, consistent with a loss of small functional vessels and a substantial antivascular response ... Interestingly, comparable antivascular effects were observed for both GDC-980 and
GNE-490 ( a selective class I
PI3K inhibitor )
Randhawa et al., BMC cancer 2013
(Breast Neoplasms...) :
Inhibition of the MEK/ERK, but not
PI3K or mTOR, pathway
reduced the expression of PDF and
MAP1D in both colon and lung cancer cell lines
Iqbal et al., Molecular cancer 2013
(Neoplasms) :
We observed that insulin up-regulated PKM2 expression, through
PI3K/mTOR mediated
HIF1a induction, but significantly reduced PKM2 activity independent of this pathway
Pfeifer et al., Proc Natl Acad Sci U S A 2013
(Lymphoma, Large B-Cell, Diffuse) :
Reexpression of PTEN induced cytotoxicity in PTEN-deficient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of
GCB DLBCLs.
PI3K/AKT inhibition induced down-regulation of the transcription factor MYC
Nowak et al., eLife 2013
:
We exploited mitotic recombination in developing Drosophila imaginal tissues to analyze the behavior of cells devoid of the tumor suppressor
PTEN , a negative
regulator of
PI3K signaling, under varying nutritional conditions
Dufour et al., Biochem Biophys Res Commun 2013
(Neoplasms, Experimental) :
In particular,
PI3K blockade
leads to the inhibition of
AKT , a major downstream effector responsible for the oncogenic activity of PI3K ... However, we report here that small molecule inhibitors of
PI3K only transiently
block AKT signaling ... This study shows that
PI3K inhibitors only transiently
inhibit AKT which limits their antitumor activities
Managlia et al., Inflamm Bowel Dis 2013
(Chronic Disease...) :
Therefore,
5-ASA reduces CUC induced reactive oxygen species in colonic progenitor cells and enhances PTEN activity, thus
attenuating PI3K/Akt signaling
Iliev et al., Fish Shellfish Immunol 2013
:
The basal
phospho-ERK level increased gradually throughout a 5-day culture period and was
PI3K dependent as demonstrated by its sensitivity to Wortmannin suggesting it is influenced by growth factors
Wang et al., Acta Pharmacol Sin 2013
:
The growth of prostate cancer PC-3 cells and B cell type leukemia Raji cells was determined using SRB assay and CCK-8 assay, respectively.Results : The phosphorylation of
Akt in Rh30-Myr-p110a, ß, ?, d cells was preferentially
inhibited by
PI3K isoform-selective inhibitors A66 ( PI3Ka ), TGX221 ( PI3Kß ), AS604850 ( PI3K? ) and CAL-101 ( PI3Kd ), respectively
Sun et al., PloS one 2013
:
Our results show that baicalein induced Epo and
VEGF expression in a HIF1a- and
PI3K/Akt dependent manner in neurons ... Our results show that baicalein induced
Epo and VEGF expression in a HIF1a- and
PI3K/Akt dependent manner in neurons
Ji et al., PloS one 2013
:
Moreover, the
PI3K inhibitor wortmannin significantly
inhibited activation of Akt and AMPK, reduced
GLUT4 translocation, glucose uptake and ultimately, depressed IPC induced cardioprotection ... Moreover, the
PI3K inhibitor wortmannin significantly
inhibited activation of
Akt and AMPK, reduced GLUT4 translocation, glucose uptake and ultimately, depressed IPC induced cardioprotection ... Moreover, the
PI3K inhibitor wortmannin significantly
inhibited activation of Akt and
AMPK , reduced GLUT4 translocation, glucose uptake and ultimately, depressed IPC induced cardioprotection
O'Farrell et al., PLoS Biol 2013
:
Both Stit and
insulin receptor (InR) signaling
activate PI3K-I and drive cellular proliferation and tissue growth
Seo et al., PloS one 2013
:
MS-enhanced
MMP-2 expression and activity were
inhibited by molecular inhibition of Akt using Akt siRNA as well as by
PI3K/Akt inhibitors, LY293002 and AI, but not by MAPK inhibitors such as PD98059, SP600125 and SB203580
Hu et al., PloS one 2013
:
Although stretch activated the kinases AMPKa, PKA, Akt, and ERK1/2, stretch induced
eNOS activation was only
inhibited by kinase-specific inhibitors of PKA and
PI3K/Akt , but not of AMPKa and Erk1/2
Yang et al., Oxidative medicine and cellular longevity 2013
:
In conclusion, these results suggest that SPD induces
PI3K/Akt-Nrf2 mediated
HO-1 expression in human endothelial cells, which may have a role in cytoprotection of the cells against oxidative stress induced death ... In conclusion, these results suggest that
SPD induces
PI3K/Akt-Nrf2 mediated HO-1 expression in human endothelial cells, which may have a role in cytoprotection of the cells against oxidative stress induced death
Basquin et al., Communicative & integrative biology 2013
:
Our recent work reveals that
PI3K regulates
Rac1 during IL-2R uptake in two ways : via its catalytic activity ( p110 ) and via its regulatory factor ( p85 ) ... Thus,
PI3K regulates both the activation of
Rac1 and its recruitment during IL-2R endocytosis
Glauer et al., Blood cancer journal 2013
:
Phosphatidylinositol-3-kinase (PI3K) activation may be associated with tumor progression and drug resistance, and inhibiting
PI3K can
induce apoptosis in MM cells
Marra et al., FEBS Lett 1995
:
The results of this study show that in hepatic stellate cells
PI 3-K is
involved in
ERK activation, although it is not necessary
Truitt et al., J Exp Med 1994
(Mast-Cell Sarcoma) :
These observations suggest that phosphorylation of
Tyr 173 may
mediate the interaction between CD28 and
PI3-K
Monfar et al., Mol Cell Biol 1995
:
We demonstrate that these kinases lie on the same signalling pathway and that
PI3K mediates the activation of pp70 by the cytokine
interleukin-2 (IL-2) ... Like rapamycin, PKA appears to act downstream of cPKC mediated pp70S6k activation, and like wortmannin, PKA antagonizes
IL-2 dependent activation of
PI3K
Johnson et al., Biochem Mol Biol Int 1995
(Second Messenger Systems) :
In both M23 and MM55 cells,
HGF induces association with MET/HGFR and
increased tyrosine phosphorylation of the SH2-domain containing proteins
PI3K , GAP and NCK
Truitt et al., J Immunol 1995
(Second Messenger Systems) :
Stimulation of CD28 induces its association with phosphatidylinositol 3'-kinase (PI3-K), raising the possibility that
PI3-K plays a critical role in
CD28 signaling
Skorski et al., Blood 1995
(Blast Crisis...) :
Phosphatidylinositol-3 kinase activity is
regulated by
BCR/ABL and is required for the growth of Philadelphia chromosome positive cells ...
Phosphatidylinositol-3 kinase activity is
regulated by
BCR/ABL and is required for the growth of Philadelphia chromosome positive cells
Burgering et al., Nature 1995
:
Activation of
PKB was
inhibited by the phosphatidylinositol-3-OH kinase (
PI(3)K ) inhibitor wortmannin and by coexpression of a dominant negative mutant of PI(3)K
Kovacsovics et al., J Biol Chem 1995
:
However,
PI 3-K stimulation is
necessary for prolonged
GPIIb-IIIa activation and irreversible platelet aggregation
Lu et al., Eur J Immunol 1995
:
Wortmannin added to cell cultures partially inhibits CD28 induced tyrosine phosphorylation of the putative p110 catalytic subunit of PI3-K, but does not block
CD28 induced association of the p85
PI3-K regulatory subunit with the CD28 receptor
Rordorf-Nikolic et al., J Biol Chem 1995
:
Phosphatidylinositol 3'-kinase ( PI 3'-kinase ) is
activated in insulin stimulated cells by the binding of the SH2 domains in its 85-kDa regulatory subunit to
insulin receptor substrate-1 (IRS-1)
Zhang et al., J Biol Chem 1995
:
Activation of
PI 3-K is
dependent upon
GTP binding protein ( s ), since PI 3-K in permeabilized platelets is stimulated by GTP gamma S ( guanosine 5'-3-O- ( thio ) triphosphate ), and stimulation of platelet cytosolic PI 3-K by GTP gamma S requires a functional small G-protein, Rho
Berger et al., Biochem Biophys Res Commun 1994
:
Phosphatidylinositol 3-kinase ( PI 3-kinase ) is acutely
stimulated by
insulin but its role in regulating glucose metabolism is still not fully understood
Cheatham et al., Mol Cell Biol 1994
:
Phosphatidylinositol 3-kinase ( PI 3-kinase ) is
stimulated by
insulin and a variety of growth factors, but its exact role in signal transduction remains unclear
von Willebrand et al., Eur J Immunol 1994
:
Here we show that
TcR/CD3 induced tyrosine phosphorylation and activation of
PI3K in Jurkat T leukemia cells depend on the presence of the p56lck tyrosine kinase : in a variant of the Jurkat T cell line lacking p56lck, JCaM1, these responses were absent ... We also show that
p56lck directly
activates PI3K purified from transfected COS-1 cells, indicating that other T cell-specific proteins are not required for the process ... Our results suggest that
p56lck is
required for activation of
PI3K in Jurkat T cells and can itself directly activate it by phosphorylating one or several stimulatory sites
Roche et al., Proc Natl Acad Sci U S A 1994
:
A second
tyrosine kinase receptor , the epidermal growth factor receptor, also
required the
PI 3-K for efficient signaling
Okamoto et al., Biochem J 1993
:
These results indicate that the specific activity of
PI3K is
increased by
insulin stimulation without detectable tyrosine phosphorylation of PI3K itself in Fao cells ... The majority of the insulin activated portion of PI3K is associated with pTyr containing proteins including IRS-1, which suggests that this is important for
activation of
PI3K by
insulin
Heydrick et al., J Clin Invest 1993
(Diabetes Mellitus, Type 2...) :
Insulin did not
affect total
PI3K activity
Stephens et al., J Biol Chem 1993
:
A number of characteristics of these responses, including their relative sensitivities to inhibition by pertussis toxin and guanosine 5'-beta- ( thio ) diphosphate, suggested that fMLP and
PAF increased this
PI3K activity via the actions of heterotrimeric G-proteins
Shimizu et al., J Cell Biol 1995
(Leukemia, Promyelocytic, Acute) :
A role for PI 3-K in CD2 mediated increases in beta 1 integrin function is suggested by : ( a ) the ability of the PI 3-K inhibitor wortmannin to completely inhibit CD2 induced increases in beta 1 integrin activity ; ( b ) the association of PI 3-K with
CD2; and (c) induced
PI 3-K activity upon CD2 stimulation
Ghiotto-Ragueneau et al., Eur J Immunol 1996
:
We demonstrate in this report that both
CD28-B7.1 and CD28-B7.2 interactions
induce the association of
PI3-K to CD28 in the CD4 subpopulation, whereas it was barely detectable in CD8 cells ... Worthmannin, a specific inhibitor of
PI3-K enzymatic activity within the nanomolar range also
inhibits the
interleukin-2 production induced by costimulation mediated by either the B7.1- and B7.2 transfected cells or CD28 monoclonal antibodies
Chacko et al., J Biol Chem 1996
:
activation of platelets with anti-Fc gamma RIIA antibodies resulted in the noncovalent association of PI 3-K with
Fc gamma RIIA as well as an
increase in Fc gamma RIIA associated
PI 3-K activity
Fuhrer et al., Exp Hematol 1996
:
Immunoprecipitation studies with anti-PI3K revealed for the first time that p62yes associated with
PI3K in
response to
IL-11 ... To summarize,
IL-11 activates p60src, p62yes and
PI3K but not p59fyn, and this activation of p62yes leads to its association with PI3K and PI3K activation
Lu et al., Eur J Immunol 1996
(Leukemia) :
Engagement of
CD28 caused the rapid receptor association and activation of
PI3-K but did not activate phospholipase C gamma ...
CD28 induced tyrosine phosphorylation and
PI3-K activation was independent of p56lck protein tyrosine kinase ( PTK ) activity ( previously reported to be associated with CD28 ) and was insensitive to inhibition by the PTK inhibitor herbimycin A ... CD28 induced tyrosine phosphorylation and
PI3-K activation was
independent of p56lck
protein tyrosine kinase ( PTK ) activity ( previously reported to be associated with CD28 ) and was insensitive to inhibition by the PTK inhibitor herbimycin A ... Two structurally and mechanistically dissimilar inhibitors of PI3-K, wortmannin and 2- ( 4-morpholinyl ) -8-phenyl-4H-1-benzopyran-4-one ( LY294002 ) also failed to block
CD28 dependent tyrosine phosphorylation events or the association of
PI3-K with the CD28 receptor ... Although herbimycin A did not significantly block the observed
CD28 dependent tyrosine phosphorylation or
PI3-K activation, herbimycin did block CD28 dependent cytotoxicity in a dose dependent manner ... These data support a role for PI3-K activation in the CD28 dependent initiation of cytotoxic effector function and suggest that a herbimycin sensitive step ( s ) is either CD28 independent, resides within a PI3-K independent CD28 signaling pathway, or is downstream of
CD28 dependent
PI3-K activation
Mèndez et al., Mol Cell Biol 1996
:
The behavior of cell lines containing IRS-1 variants and inhibition by wortmannin and rapamycin indicate that the phosphorylation of both proteins requires
IRS-1 mediated stimulation of
PI3K and pp70S6K but not mitogen activated protein kinase or SH-PTP2
Lavie et al., J Neurochem 1996
(Neuroblastoma) :
Preincubation with 1 mM carbachol inhibited the
insulin stimulated
PI3K activity in a time dependent manner, with half-maximal and maximal inhibition times of 4 and 15 min, respectively ... Addition of the cell-permeable homologue didecanoyl-CDP-DAG to intact cells inhibited
insulin stimulated
PI3K activity up to 75 %, with an IC50 of 0.5 microM, a result that further supports a proposed lipid mediated inhibition of PI3K
Abrams et al., J Biol Chem 1996
:
Depending upon its phosphorylation/charged state,
pleckstrin inhibits PI3Kgamma, but not
p85/PI3K
Klinghoffer et al., Mol Cell Biol 1996
:
Thus, activation of
PI3K requires not only binding of PI3K to the tyrosine phosphorylated
PDGFR but accumulation of GTP bound Ras as well
Quon et al., Biochem Biophys Res Commun 1996
:
In adipose cells, stimulation of endogenous
PDGF receptors (PDGF-R) results in increased
PI3K activity without causing recruitment of GLUT4 ... Our data suggest that overexpression of PDGF-R mediates positive effects on
GLUT4 translocation by a wortmannin sensitive pathway not
dependent on direct interaction of the PDGF-R with
PI3K
Knall et al., Proc Natl Acad Sci U S A 1997
:
Recently we reported that
IL-8 caused the activation of the Ras/Raf/extracellular signal regulated kinase ( ERK ) pathway in human neutrophils and that this activation was
dependent on
PI3K activity
Hamburger et al., Anticancer Res 1997
:
The purpose of these experiments was to determine the
effects of
heregulin beta 1 (HRG) on growth and
PI3K activation of a nonneoplastic human mammary epithelial cell line, 184B5 ... Similarly,
HRG at all concentrations
stimulated the association of
PI3K with erbB3 ... We conclude that both the growth inhibitory and stimulatory effects of
HRG in nonneoplastic human mammary epithelial cells are
mediated by activation of
PI3K
Chan et al., J Immunol 1997
:
CD7 stimulation of both Jurkat T cells and resting human peripheral blood CD4+ T cells
results in rapid association and activation of
PI 3-K with CD7
Freychet et al., Bull Mem Acad R Med Belg 1996
(Disease Models, Animal...) :
Insulin activation of
PI3-K is markedly diminished in obese mice ; starving the obese animals restores normal responses of PI3-K, glucose transport, and glycogen synthesis, to insulin
King et al., Mol Cell Biol 1997
:
Phosphatidylinositol 3-kinase is
required for integrin stimulated AKT and
Raf-1/mitogen activated protein kinase pathway activation ...
Phosphatidylinositol 3-kinase is
required for integrin stimulated
AKT and Raf-1/mitogen activated protein kinase pathway activation ...
Phosphatidylinositol 3-kinase is
required for integrin stimulated AKT and
Raf-1/mitogen activated protein kinase pathway activation
Mendez et al., Mol Cell Biol 1997
:
The fact that PKC zeta stimulates general protein synthesis but not activation of p70S6K indicates that PKC zeta activation does not involve the proto-oncogene
Akt , which is also
activated by
PI3K
Mañes et al., J Biol Chem 1997
:
IGFBP-1 complex with hST-3 restores
IGF-I induced proliferation and
PI 3-K kinase activity in these cells
Flamigni et al., Biochem Biophys Res Commun 1997
(Leukemia L1210) :
These results indicate that
PI3K activity is
required for the induction of
ODC , possibly affecting both ODC mRNA level and translation ... However, LY294002 and wortmannin at concentrations which inhibited almost completely PI3K activity did not decrease p70S6K activity, suggesting that p70S6K does not mediate the
PI3K effects on
ODC , but may lie on a separate pathway in this experimental model
Sharma et al., Mol Cell Biol 1997
:
Thus, interference with the IRS-1-IR interaction inhibits
insulin stimulated IRS-1 and Shc phosphorylation,
PI 3-K enzymatic activity, p70s6k activation, MAPK phosphorylation and cell cycle progression ... Thus, interference with the
IRS-1-IR interaction
inhibits insulin stimulated IRS-1 and Shc phosphorylation,
PI 3-K enzymatic activity, p70s6k activation, MAPK phosphorylation and cell cycle progression
Yamada et al., J Biol Chem 1997
:
We examined how
BDNF activates
PI3-K in cultured cerebral cortical neurons ... IRS-1 and -2 were tyrosine phosphorylated and bound to
PI3-K in
response to
BDNF ... On the other hand, we observed no association of
PI3-K with TrkB in
response to
BDNF ... These results indicate that the activation of TrkB by
BDNF induces the activation of
PI3-K via IRS-1 and -2 rather than by a direct interaction of TrkB with PI3-K in cultured cortical neurons ... These results indicate that the activation of
TrkB by BDNF
induces the activation of
PI3-K via IRS-1 and -2 rather than by a direct interaction of TrkB with PI3-K in cultured cortical neurons
Phung et al., J Biol Chem 1997
:
Current studies demonstrate that the PI 3-K inhibitor wortmannin inhibits both basal and
insulin stimulated
PI 3-K activities ... To link PI 3-K activation to insulin action on apoB, we investigated whether
insulin induced localization of activated
PI 3-K to the endoplasmic reticulum ( ER ), where apoB biogenesis is initiated ...
Insulin stimulates a significant increase in
PI 3-K activity associated with insulin receptor substrate-1 as well as an increase in insulin receptor substrate-1/PI 3-K mass in LDM ...
Insulin stimulates
PI 3-K activity in smooth and rough microsomes isolated from rat hepatocytes, the latter of which contain rough ER as demonstrated by electron microscopy ... Studies indicate that 1 ) PI 3-K activity is necessary for insulin dependent inhibition of apoB secretion by rat hepatocytes ; 2 )
insulin action
leads to the activation and localization of
PI 3-K in an ER fraction containing apoB ; and 3 ) insulin stimulates PI 3-K activity in the rough ER
Brennan et al., Immunity 1997
:
Inhibition of
PI3K inhibits phosphorylation of Rb, induction of
cyclin D3 , and degradation of p27kip1 ... Inhibition of
PI3K inhibits phosphorylation of Rb, induction of cyclin D3, and degradation of
p27kip1 ... Inhibition of
PI3K inhibits phosphorylation of Rb, induction of cyclin D3, and degradation of
p27kip1
Andjelković et al., J Biol Chem 1997
:
Our results indicate that
PI3-K activity is
required for translocation of
PKB to the plasma membrane, where its activation occurs through phosphorylation of the same sites that are induced by insulin or IGF-1
Keely et al., Nature 1997
(Cell Transformation, Neoplastic...) :
PI(3)K inhibition also disrupts actin structures, suggesting that
activation of
PI(3)K by
Cdc42 and Rac1 alters actin organization, leading to increased motility and invasiveness ... PI(3)K inhibition also disrupts actin structures, suggesting that
activation of
PI(3)K by Cdc42 and
Rac1 alters actin organization, leading to increased motility and invasiveness
Banfić et al., J Biol Chem 1998
:
Both this novel pathway and the activation of PKB/Akt are inhibited by the
PI3K inhibitor, wortmannin, and the calpain inhibitor, calpeptin, constituting the first evidence that PtdIns ( 3,4 ) P2 can
stimulate PKB/Akt in vivo in the absence of PtdIns ( 3,4,5 ) P3 ... Both this novel pathway and the activation of PKB/Akt are inhibited by the
PI3K inhibitor, wortmannin, and the calpain inhibitor, calpeptin, constituting the first evidence that PtdIns ( 3,4 ) P2 can
stimulate PKB/Akt in vivo in the absence of PtdIns ( 3,4,5 ) P3
Kosaki et al., J Biol Chem 1998
:
The specific activity of the PI3K in the former was approximately half of that in the latter, suggesting that 14-3-3beta protein bound to IRS-1 inhibits
insulin stimulated lipid kinase activity of
PI3K in 3T3L1 adipocytes
Geltz et al., Blood 1998
:
The
protein tyrosine kinase inhibitor, erbstatin analog, partially inhibited p85 and p110 phosphorylation but did not appear to
affect PI3K lipid kinase activity
Conus et al., J Biol Chem 1998
:
Furthermore, although PI3K in anti-phosphotyrosine immunoprecipitates is only very weakly activated by ionomycin, the calcium induced stimulation of
p70 ( S6k ) is completely
inhibited by the specific
PI3K inhibitor wortmannin
Capodici et al., J Immunol 1998
:
Aggregation of human neutrophils is associated with activation of the mitogen activated protein kinases Erk1 and -2, and
Erk is activated in
response to
PI 3-K in some cell types
Yin et al., Nature 1998
:
We report here that the protein
p85 , a regulator of the signalling protein phosphatidyl-3-OH kinase ( PI(3)K ), participates in the cell death process that is induced in response to oxidative stress and that this role of p85 in apoptosis does not
involve PI(3)K
Cichy et al., J Biol Chem 1998
:
Constitutively active
PI3K and PKB/Akt are each
sufficient to mediate effects of insulin on the
IGFBP-1 promoter in a nonadditive fashion
Van Lint et al., J Biol Chem 1998
:
Although the presence of a pleckstrin homology domain makes PKD a potential PI3K target,
PKD was not
stimulated by selective
PI3K activation, and wortmannin, an inhibitor of PI3K, did not inhibit PDGF signaling to PKD
Lipson et al., J Pharmacol Exp Ther 1998
:
A synthetic EGF receptor kinase inhibitor showed selective inhibitor properties when tested for
EGF induced receptor autophosphorylation, MAPK activation,
PI3K activation, entry into S phase and cyclin E-associated kinase activity
Misra et al., J Biol Chem 1998
:
We conclude that
PI3K is
involved in alpha2M* induced mitogenesis in macrophages and intracellular
Ca2+ plays a role in PI3K activation
Lin et al., Biochem Biophys Res Commun 1998
(Carcinoma, Hepatocellular...) :
Phosphatidylinositol 3-kinase is
required for the regulation of hepatitis B
surface antigen production and mitogen activated protein kinase activation by insulin but not by TPA ...
Phosphatidylinositol 3-kinase is
required for the regulation of hepatitis B surface antigen production and
mitogen activated protein kinase activation by insulin but not by TPA ...
Phosphatidylinositol 3-kinase is
required for the regulation of hepatitis B surface antigen production and mitogen activated protein kinase activation by
insulin but not by TPA
Zhang et al., J Biol Chem 1998
:
HsC2-PI3K , identifiable by Western blotting and immunoprecipitatable activity, is sensitive to wortmannin ( IC50 6-10 nM ),
requires Mg2+ , and shows strong preference for PtdIns over PtdIns4P or phosphatidylinositol 4,5-bisphosphate as substrate
Di Guglielmo et al., Mol Cell Biochem 1998
:
Furthermore, studies with isolated rat adipocytes reveal the EN to be the principle site of
insulin stimulated IRS-1 tyrosine phosphorylation and associated
PI3K activation
Liu et al., Am J Physiol 1998
:
In contrast,
PDGF-BB stimulation
triggered PDGFR associated
PI3K activity ... Both
PDGF-BB induced
PI3K activation and GAG synthesis were abolished by the PI3K inhibitors wortmannin and LY-294002
Scheid et al., Proc Natl Acad Sci U S A 1998
:
Interleukin 3 (IL-3) , on the other hand,
requires PI3K for survival, and blocking PI3K partially inhibited Bad phosphorylation
Zundel et al., Genes Dev 1998
:
Ceramide inhibition of
PI(3)K is
dependent on
acid-sphingomyelinase
Gliozzo et al., J Cell Biochem 1998
(Breast Neoplasms) :
In MDA-MB157 and MCF-10A cells,
insulin stimulated
PI3-K activity three- to fourfold ... In ZR-75-1 cells, however,
insulin did not
stimulate PI3-K activity ... Next, we studied
insulin receptor substrate-1 (IRS-1) , a major endogenous substrate for the insulin receptor which, when tyrosine is phosphorylated by the insulin receptor, interacts with and
activates PI3-K
Wang et al., Cell Growth Differ 1998
:
Serum and
EGF induction of the core SRE was partially
inhibited by rho and
PI3K inhibitors
Simonsen et al., Nature 1998
:
The association of
EEA1 with the endosomal membrane
requires Rab5-GTP and
PI(3)K activity, and excess Rab5-GTP stabilizes the membrane association of EEA1 even when PI(3)K is inhibited ... The association of EEA1 with the endosomal membrane requires Rab5-GTP and
PI(3)K activity, and excess
Rab5-GTP stabilizes the membrane association of EEA1 even when PI(3)K is inhibited
Milani et al., AIDS 1998
:
Extracellular
Tat induced a rapid increase of p125FAK tyrosine phosphorylation and p125FAK associated
PI 3-K activity
Kivens et al., Mol Cell Biol 1998
:
Mutation of the proline residues in the K-G-P-P-L-P motif to alanines prevented
CD2 mediated activation of integrin function and
PI 3-K activity but not mitogen activated protein ( MAP ) kinase activity
Kunapuli et al., J Biol Chem 1998
(Cardiomegaly) :
However, both wortmannin, a
PI3K inhibitor, and rapamycin, an
inhibitor of
p70 ( S6K ) activity, inhibit 8,12-iso-iPF2alpha-III -induced myocyte hypertrophy, with IC50 values of 60 +/- 12 and 3 +/- 1.7 nM, respectively, whereas neither compound abrogates the PGF2alpha mediated response
Paradis et al., Genes Dev 1998
:
This demonstrates that
Akt/PKB activity is not necessarily
dependent on AGE-1
PI3K activity ... This demonstrates that
Akt/PKB activity is not necessarily
dependent on AGE-1
PI3K activity
Bragado et al., Gastroenterology 1998
(Diabetes Mellitus, Experimental) :
Rapamycin and
PI 3K inhibitors, wortmannin and LY294002,
blocked CCK stimulated
p70 S6K activity
Polakiewicz et al., J Biol Chem 1998
:
Phosphorylation of p70 S6 kinase and
4E-BP1 is also
repressed by
PI3K inhibitors as well as by rapamycin, the selective inhibitor of FRAP/mTOR
Delcommenne et al., Proc Natl Acad Sci U S A 1998
:
We also demonstrate here that ILK is an upstream effector of the
Pi(3)K dependent regulation of both
protein kinase B ( PKB/AKT ) and glycogen synthase kinase 3 ( GSK-3 ) ... We also demonstrate here that ILK is an upstream effector of the
Pi(3)K dependent regulation of both protein kinase B ( PKB/AKT ) and
glycogen synthase kinase 3 ( GSK-3 ) ... ILK is thus a receptor-proximal effector for the
Pi(3)K dependent , extracellular matrix and growth factor mediated, activation of
PKB/AKT , and inhibition of GSK-3 ... ILK is thus a receptor-proximal effector for the
Pi(3)K dependent , extracellular matrix and growth factor mediated, activation of
PKB/AKT , and inhibition of GSK-3
Staubs et al., J Biol Chem 1998
:
The
PI3K inhibitors wortmannin and LY294002
inhibit the PDGF induced phosphorylation of
IRS-1 , whereas the MEK inhibitor PD98059 was without a major effect ... 2 ) This PDGF induced phosphorylation of
IRS-1 leads to a significant decrease in insulin stimulated
PI3K activity ... 2 ) This PDGF induced phosphorylation of IRS-1 leads to a significant decrease in
insulin stimulated
PI3K activity
Bhargavi et al., Biochem Mol Biol Int 1998
:
Recently Singh et al., ( Biochemistry, 35, 16544-16549, 1996 ) have shown that
profilin activates
PI3-K activity in a concentration dependent manner
Lu et al., J Immunol 1998
:
Phosphatidylinositol 3-kinase is
required for
CD28 but not CD3 regulation of the TEC family tyrosine kinase EMT/ITK/TSK : functional and physical interaction of EMT with phosphatidylinositol 3-kinase ... CD28 induced association of EMT with
PI3K also
requires functional expression of
LCK ...
CD28 induced association of EMT with
PI3K also requires functional expression of LCK
Kim et al., Endocrinology 1998
(Neuroblastoma) :
We also observed a concomitant increase in the mobility of IRS-2, suggesting that
PI 3-K mediates or is required for IRS-2 serine/threonine phosphorylation, and that this phosphorylation
inhibits IRS-2 tyrosine phosphorylation ... However, even though the
PI 3-K inhibitors
enhanced the association of
Grb2 with IRS-2, these compounds suppressed IGF-I induced mitogen activated protein kinase activation and neurite outgrowth
Mohr et al., Gastroenterology 1998
:
Tyrosyl phosphorylation of IRS-1, association of
IRS-1 with PI3K, and
activation of downstream
PI3K and MAPK pathways were greatly reduced as a result of long-term ethanol consumption
Saci et al., J Biol Chem 1999
:
Our results suggest that
Cbl is
involved in platelet signal transduction by the recruitment of PI 3-K to the FcgammaRIIa pathway, possibly by increasing
PI 3-K activity
Bavelloni et al., J Cell Sci 1999
(Osteosarcoma) :
Phosphatidylinositol 3-kinase translocation to the nucleus is
induced by
interleukin 1 and prevented by mutation of interleukin 1 receptor in human osteosarcoma Saos-2 cells
Terauchi et al., Nat Genet 1999
(Hypoglycemia) :
Insulin stimulated
PI3K activity associated with insulin receptor substrates (IRSs) was mediated via full-length p85 alpha in wild-type mice, but via the p50 alpha alternative splicing isoform of the same gene in Pik3r1-/- mice