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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