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PI3 — VEGFA

Text-mined interactions from Literome

Thakker et al., J Biol Chem 1999 : Inhibition studies with both a dominant negative p85 mutant and the PI 3-kinase inhibitor, wortmannin, were employed to show for the first time that VEGF stimulated PI 3-kinase modulates MAP kinase activation and nuclear events such as transcription from c-fos promoter and entry into the synthesis ( S ) -phase
Jiang et al., Proc Natl Acad Sci U S A 2000 : These results suggest that PI 3-kinase plays an important role in angiogenesis and regulates VEGF expression
Qi et al., Exp Cell Res 2001 : Thus, VEGF-A stimulation leads to complex formation between FAK and PI3-kinase and overexpression of dominant negative FAK decreases VEGF-A induced PI3-kinase activation ... These data show that VEGF-A induced FAK and PI3-kinase activation are required for migration of cells expressing VEGFR-2, via a pathway independent of direct interaction with the receptor
Suzuma et al., J Biol Chem 2002 : In contrast, DN PI 3-kinase as well as pharmacologic inhibitors of PI 3-kinase blocked stretch induced VEGF expression ... We present novel findings demonstrating that stretch induced VEGF expression in retinal capillary pericytes is mediated by phosphatidylinositol (PI) 3-kinase and protein kinase C (PKC)-zeta but is not mediated by ERK1/2, classical/novel isoforms of PKC, Akt, or Ras despite their activation by stretch
Kim et al., FASEB J 2002 : However, unexpectedly, phosphatidylinositol (PI) 3'-kinase inhibitor enhanced the VEGF- and TNF-a induced expression and activity of TF
Podar et al., J Biol Chem 2002 (Multiple Myeloma) : VEGF stimulates activation of PI 3-kinase, and both MM cell adhesion and migration are PI 3-kinase dependent ... Moreover, both VEGF induced PI 3-kinase activation and beta ( 1 ) integrin mediated binding to fibronectin are required for the recruitment and activation of PKC alpha
Poulaki et al., J Clin Invest 2002 (Diabetes Mellitus...) : Insulin induced VEGF expression requires p38 MAPK and PI 3-kinase , whereas hyperglycemia induced VEGF expression is HIF-1alpha independent and requires PKC and p42/p44 MAPK
Senthil et al., Biochem J 2002 : VEGF also increased association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3-kinase ( PI 3-kinase ), and PI 3-kinase activity in IRS-1 immunoprecipitates was increased in VEGF treated cells ... Incubation of epithelial cells with antisense IRS-1 oligonucleotide, but not sense oligonucleotide, reduced expression of the protein and VEGF induced PI 3-kinase activity in IRS-1 immunoprecipitates ... This association may account for some of the increase in VEGF induced PI 3-kinase activity, and the increase in de novo protein synthesis seen in renal epithelial cells
Woods et al., Neuro Oncol 2002 (Astrocytoma...) : In this study, pharmacologic inhibitors were used to specifically inhibit PI3-kinase and MEK1/2 activity in human malignant astrocytoma cell lines, and their effects on VEGF expression were determined
Reisinger et al., J Cell Sci 2003 (Neovascularization, Pathologic) : Herein, we provide evidence that PI 3-kinase , MEK1/2 and PKC-zeta play a significant role in HGF/SF induced VEGF/VPF promoter activation
Yin et al., FASEB J 2003 (Cell Transformation, Neoplastic...) : Specific inhibitors of protein kinase C ( PKC ), Src, and phosphatidylinositol 3-kinase (PI3K) inhibit Par1 induced VEGF expression, suggesting the participation of these kinases in the process
Eriksson et al., Circulation 2003 : We further found that phosphatidylinositol-3-OH kinase (PI3K) acted upstream of Rac and Akt-eNOS in VEGF/VEGFR-2 signaling
Kanda et al., Biochem Biophys Res Commun 2003 : However, VEGFR-2, insulin receptor substrate-1, and c-Src were also involved in VEGF-A induced activation of PI3-kinase , resulting in the compensation in cells expressing kinase-inactive c-Fes ... Considered collectively, VEGF-A activated PI3-kinase partly through c-Fes and increase in c-Fes kinase activity enhanced capillary morphogenesis by yet unknown signaling pathways
Roy et al., Surgery 2003 (Anoxia...) : ( 1 ) Morphine inhibits hypoxia induced VEGF transcription, in part, through an HIF-1alpha mediated mechanism and ( 2 ) morphine inhibition of hypoxia induced HIF-1alpha may be mediated by inhibition of ERK 1,2 MAP kinase activity and PI3 kinase activity
Gao et al., Toxicol Appl Pharmacol 2004 (Ovarian Neoplasms) : To explore the mechanism of 4-OHE2 induced HIF-1alpha and VEGF-A expression, we studied whether phosphatidylinositol 3-kinase (PI3K) or mitogen activated protein kinase ( MAPK ) signaling pathways are involved in 4-OHE2 induced HIF-1alpha and VEGF-A expression
Spagnuolo et al., Blood 2004 : Overall these data indicate that Gas1 induction by VE-cadherin and VEGF in endothelial cells requires activation of PI3-kinase
Wu et al., Mol Endocrinol 2005 (Breast Neoplasms...) : Inhibitors of PI3-kinase or SP-1 blocked both progesterone- and MPA induced increases in VEGF mRNA levels in T47-DCO cells
Hellwig-Bürgel et al., Cell Physiol Biochem 2005 : Thus, PI3K signaling is required for HIF-1alpha accumulation and VEGF synthesis, whereas MAPKK-1 signaling is required for VEGF synthesis only
Kim et al., Br J Dermatol 2005 : The PI3-kinase inhibitor also inhibited the expression of VEGF by IGF-II
Beierle et al., J Surg Res 2005 (Neuroblastoma) : We have found that exposure of human neuroblastoma cells to exogenous VEGF results in an increased expression of survivin protein and phosphorylated Akt, and inhibition of PI3-kinase abrogates those effects
Trisciuoglio et al., Mol Biol Cell 2005 (MAP Kinase Signaling System...) : Pharmacological inhibition of mitogen activated protein kinase ( MAPK ) and phosphatidylinositol 3-kinase (PI3K) signaling pathways reduced the induction of VEGF and HIF-1 in response to bcl-2 overexpression in hypoxia
Kawano et al., Growth Factors 2005 (MAP Kinase Signaling System) : WISH cells were cultured, and the effect of epidermal growth factor (EGF), mitogen activated protein ( MAP ) kinase kinase or extracellular signal regulated kinase ( ERK ) kinase ( MEK ) inhibitors ( U0126 ) or phosphatidylinositol (PI) 3-kinase on the production of VEGF was examined
Karihaloo et al., Mol Cell Biol 2005 : We demonstrate that VEGF-165 but not VEGF-121 induces single-cell branching morphogenesis and multicellular tubulogenesis in mouse renal tubular epithelial cells and that these morphogenic effects require activation of the phosphatidylinositol 3-kinase (PI 3-K) and, to a lesser degree, the extracellular signal regulated kinase and protein kinase C signaling pathways
Li et al., Mol Cell Biochem 2005 (Calcium Signaling) : PI-3K is partially involved in VEGF induction by vanadium, while p38K and mTOR are not involved
Ouyang et al., Mol Cell Biochem 2005 (Calcium Signaling) : Essential role of PI-3K , ERKs and calcium signal pathways in nickel induced VEGF expression ... In the present study, we investigated the potential roles of PI-3K , ERKs, p38 kinase and calcium signalling in VEGF induction by nickel in Cl 41 cells ... Collectively these data demonstrate that PI-3K , ERKs and cytosolic calcium, but not p38 kinase, play essential roles in VEGF induction by nickel compounds
Nie et al., J Biol Chem 2006 (Neovascularization, Pathologic...) : An increase in PI 3-kinase activity was found in 12-LOX transfected PC-3 cells and inhibition of PI 3-kinase by LY294002 significantly reduced VEGF expression
Fu et al., Acta Pharmacol Sin 2006 : Moreover, the inhibitor of the PI3-kinase , but not the inhibitor of the PKC, significantly inhibited the shh mediated proliferation, migration and VEGF production
Tang et al., Mol Cancer Res 2006 (Breast Neoplasms...) : To explore the underlying signaling pathways used by EMMPRIN, we studied the involvement of phosphoinositide 3-kinase (PI3K)-Akt , mitogen activated protein kinase ( MAPK ), JUN, and p38 kinases in EMMPRIN mediated VEGF regulation
Kobayashi et al., Pathobiology 2006 (Adenocarcinoma...) : We investigated the role of phosphatidyl inositol-3 OH kinase (PI3K)-Akt signaling in the regulation of HIF-1alpha and VEGF expression in human gastric adenocarcinoma
Solà-Villà et al., Kidney Int 2006 : SB 203580, a p38 mitogen activated protein kinase inhibitor, weakly inhibited the induction of VEGF by IL-1beta in a concentration dependent manner, whereas LY 294002, a phosphoinoside 3-kinase (PI3-K) inhibitor, and rapamycin, a mammalian target of rapamycin (mTOR) inhibitor, strongly inhibited both IL-1beta- and tumor necrosis factor-alpha induced VEGF formation in a concentration dependent manner
Takai et al., Mol Cell Endocrinol 2007 : Taken together, our findings strongly suggest that PI3-kinase/Akt plays an inhibitory role in FGF-2 induced VEGF release in osteoblasts
Bian et al., Exp Eye Res 2007 : Moreover, TGF-beta2 induced RPE VEGF secretion was significantly reduced by inhibitors of mitogen activated protein ( MAP ) kinase ( MEK ) ( U0126 ), p38 ( SB202190 ), c-Jun NH2-terminal kinase (JNK), Sp600125, protein tyrosine kinase ( PTK ) ( Genistein ), and phosphatidylinositol 3-kinase (PI3K) ( Ly294002 )
Hasaneen et al., Am J Physiol Lung Cell Mol Physiol 2007 : Our results show : 1 ) a significant increase in human lung microvascular endothelial cell ( HMVEC-L ) proliferation, migration, and tube formation following incubation in conditioned media ( CM ) from HASM cells exposed to mechanical strain ; 2 ) mechanical strain of HASM cells induced VEGF expression and release ; 3 ) VEGF neutralizing antibodies inhibited the proliferation, migration, and tube formations of HMVEC-L induced by the strained airway smooth muscle CM ; 4 ) mechanical strain of HASM induced a significant increase in hypoxia-inducible factor-1alpha ( HIF-1alpha ) mRNA and protein, a transcription factor required for VEGF gene transcription ; and 5 ) mechanical strain of HASM induced HIF-1alpha/VEGF through dual phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and ERK pathways
Wang et al., Biochem Biophys Res Commun 2008 : Moreover, Ly 294002, a specific inhibitor of phosphatidylinositol-3-kinase (PI3K)/Akt significantly attenuated the VEGF synthesis stimulated by TGF-beta1
Cezar-de-Mello et al., Br J Pharmacol 2008 (Neovascularization, Pathologic) : Pretreatment of EC with ATL-1 strongly decreased VEGF dependent phosphorylation of phosphainositide 3-kinase (PI3-K) and extracellular signal regulated kinase-2 ( ERK-2 ), two signalling kinases involved in EC proliferation
Kim et al., Cancer Lett 2008 (Breast Neoplasms...) : In addition, the basal activities of Akt and GSK-3beta were deregulated in MCF-7/ADR cells, and either the activation of PI3-kinase or the inhibition of GSK-3 restored the diminished transcription of VEGF
Kawahara et al., Int J Mol Med 2008 (Atherosclerosis...) : The PI3-kinase inhibitor LY294002 significantly inhibited VEGF production in HMGB1 stimulated macrophages, while other kinase inhibitors did not
Xiao et al., Diabetes Metab Res Rev 2009 : Visfatin induced protein kinase B ( Akt ) phosphorylation and phosphoinositide 3 kinase (PI3K) inhibitors could suppress visfatin induced upregulation of DDAH2 and VEGF expressions
Fontijn et al., Cell Oncol 2009 (Melanoma) : Basic fibroblast growth factor mediated overexpression of vascular endothelial growth factor in 1F6 human melanoma cells is regulated by activation of PI-3K and p38 MAPK ... PI-3K, p38 MAPK and ERK1/2 MAPK pathways were activated, while inhibition of PI-3K or p38 resulted in, respectively, 55 % and up to 70 % reduction of VEGF mRNA overexpression
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
He et al., Rheumatol Int 2011 (Arthritis, Rheumatoid) : TNFa- or hypoxia induced secretion of VEGF and IL-8 and expression of HIF-1a were hampered by treatment with the PI3 kinase inhibitor LY294002, suggesting that inhibition of PI3 kinase/Akt activation might inhibit VEGF and IL-8 secretion and HIF-1a expression induced by TNFa or hypoxia
Demyanets et al., Basic Res Cardiol 2011 (Atherosclerosis...) : STAT3 inhibitor WP1066, p38 MAPK inhibitors SB-202190 and BIRB 0796, extracellular signal regulated kinase1/2 ( Erk1/2 ) inhibitor U0126, and phosphatidylinositol 3-kinase (PI3K) inhibitors LY-294002 and PI-103 reduced OSM induced VEGF synthesis
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
Lo et al., International journal of molecular sciences 2013 : In parallel, VEGF induced JNK, PI3K and Akt activation
Mazure et al., Blood 1997 (Cell Transformation, Neoplastic...) : In contrast to the c-Raf-1/MAP kinase pathway, hypoxia increases phosphatidylinositol 3-kinase ( PI 3-kinase ) activity in a Ras dependent manner, and inhibition of PI 3-kinase activity genetically and pharmacologically results in inhibition of VEGF induction