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JUN — PIK3R1
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