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JUN — PI3
Text-mined interactions from Literome
Troussard et al., Mol Cell Biol 1999
:
This fibronectin dependent activation of
AP-1 activity is
inhibited in a dose dependent manner if the cells are transfected with wild-type GSK-3, and also by inhibitors of
PI 3-kinase
Guo et al., Inflammation 2000
:
IRAK-2 and
PI 3-kinase synergistically
activate NF-kappaB and
AP-1 ... As a result, antisense IRAK-2 ODN or antisense p110
PI 3-kinase ODN
inhibited IL-1 induced NF-kappaB and
AP-1 activation in HepG2 cells ... The inhibition of NF-kappaB activation by antisense IRAK-2 ODN or antisense p110
PI 3-kinase ODN and the
inhibition of
AP-1 activation by antisense IRAK-2 ODN were incomplete, whereas AP-1 activation could be inhibited by antisense p110 PI 3-kinase ODN completely ... The
effects of IRAK-2 or
PI 3-kinase on NF-kappaB and
AP-1 activation were confirmed by the results that overexpression of IRAK-2 failed to fully activate NF-kappaB and AP-1 and that overexpression of p110 PI 3-kinase is insufficient for NF-kappaB full activation but sufficient for AP-1 activation
Abounader et al., J Neurochem 2001
(Glioblastoma) :
These results support a model of c-met induction by SF/HGF in human glioma cells that uniformly involves Ras, MAPK, and
AP-1 and additionally
involves PI3-kinase and PKC in some cell lines
Funakoshi et al., Int Immunopharmacol 2001
:
Above results indicated that both
PI3-kinase and p38 MAP kinase are differentially
involved in IL-1 induced NF-kappa B and
AP-1 activation
Sarmiere et al., Mol Cell Neurosci 2001
:
In contrast to c-Rel, activated
PI 3-kinase and Akt
inhibit c-Jun phosphorylation but have only a small effect on cytochrome c release
Crossthwaite et al., J Neurochem 2004
:
Demonstrating that PI3-kinase is not ubiquitously involved in NMDA receptor signal transduction, the
PI 3-kinase inhibitors wortmannin and LY294002 did not
prevent NMDA receptor Ca2+ dependent phosphorylation of
c-Jun N-terminal kinase 1/2 ( JNK1/2 )
Rui et al., Cardiovasc Res 2005
(Myocardial Reperfusion Injury) :
An inhibitor of
phosphatidylinostol 3 (PI3)-kinase prevented the nuclear translocation of
AP-1 induced by EPO ... This beneficial effect of EPO is mediated by eNOS derived NO via a
PI3-kinase dependent activation of
AP-1
Chandrasekar et al., J Biol Chem 2005
:
Src kinase inhibitors PP1 and PP2,
phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002, Akt inhibitor, the c-Jun N-terminal kinase (JNK) inhibitor SP600125, antisense JNK and dominant negative MyD88, interleukin-1 receptor associated kinase ( IRAK)-1, IRAK4, and phosphatidylinositol 3-kinase expression all
attenuated IL-18 mediated
AP-1 binding and reporter activity, CXCL16 promoter-reporter activity, and CXCL16 expression
Wang et al., Cancer Res 2005
(MAP Kinase Signaling System) :
Because PTEN is a well-known phosphatase involved in the regulation of phosphatidylinositol 3-kinase (PI-3K)/Akt signaling pathway, taken together with the evidence that
PI-3K/Akt plays an important role in the activation of
AP-1 and NF-kappaB during tumor development, we anticipate that inhibition of AP-1 and NF-kappaB by tumor suppressor p53 seems to be mediated via PTEN, which may be a novel mechanism involved in anticancer activity of p53 protein
Butler et al., J Biol Chem 2006
:
Elafin prevents lipopolysaccharide induced
AP-1 and NF-kappaB activation via an effect on the ubiquitin-proteasome pathway ...
Elafin prevented lipopolysaccharide induced phosphorylation of
AP-1 , c-Jun, and JNK but had no effect on phosphorylation of p38
Lin et al., Rheumatol Int 2008
(Chondrosarcoma...) :
Using chondrosarcoma cells stimulated with IL-1beta, the effects of GLN on the mRNA and protein levels of MMP-3, the
activation of JNK, ERK, p38, NF-kappaB, and
AP-1 , the nuclear translocation of NF-kappaB/Rel family members, and
PI3-kinase/Akt activation were studied
Park et al., Cardiovasc Res 2011
(Disease Models, Animal...) :
Gb3 accumulation reduces K ( Ca ) 3.1 channel expression by down
regulating ERK and
AP-1 and up-regulating REST and the channel activity by decreasing intracellular levels of
PI(3)P
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
Huang et al., Toxicol Appl Pharmacol 2013
(Inflammation) :
Moreover, LTA induced increases of ?B-DNA and
AP-1-DNA binding activity were
inhibited by p38, JNK, and
PI3-kinase inhibitors
Durandy et al., J Immunol 1997
(Hypergammaglobulinemia...) :
CD40 triggered activation events, i.e.,
phosphatidylinositol 3 (PI3) kinase activation and
induction of transcription factors NF-kappaB and
AP-1 , were next analyzed in B cell lines derived from five patients
Reddy et al., J Biol Chem 1997
:
Furthermore, two
PI 3-kinase-specific inhibitors, wortmannin and a dominant negative mutant of the p85 subunit,
inhibited IL-1 induced activation of both NFkappaB and
AP-1 ... Transient transfection experiments indicated that whereas overexpression of
PI 3-kinase may be
sufficient to induce
AP-1 and increase nuclear c-Fos protein levels, PI 3-kinase may need to cooperate with other IL-1-inducible signals to fully activate NFkappaB dependent gene expression ... Our results thus indicate that
PI 3-kinase is a novel signal transducer in IL-1 signaling and that it may differentially
mediate the activation of NFkappaB and
AP-1
Skov et al., J Cell Biol 1997
:
Ligation of major histocompatability complex ( MHC ) class I molecules on human T cells induces cell death through
PI-3 kinase
induced c-Jun NH2-terminal kinase activity : a novel apoptotic pathway distinct from Fas induced apoptosis ... As the
c-Jun NH2-terminal kinase (JNK) can be
activated by
PI-3 kinase activity, and has been shown to be involved in apoptosis of lymphocytes, we examined JNK activation after MHC-I ligation