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JUN — PIK3CA

Text-mined interactions from Literome

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
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
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
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
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
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
Song et al., Gut 2007 (Adenocarcinoma...) : 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
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
Choi et al., Stem Cells Dev 2008 (MAP Kinase Signaling System) : 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
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
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
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
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
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
Kao et al., Phytomedicine 2013 : Glycyrrhizic acid and 18ß-glycyrrhetinic acid recover glucocorticoid resistance via PI3K induced AP1 , CRE and NFAT activation