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Wilmer et al., Kidney Int 2001
:
This current study investigated the mechanisms of HG-mediated activation of p38 MAPK in cultured human mesangial cells ( HMCs ) and the
effects of
p38 MAPK activation on the transcription factor
activator protein-1 (AP-1)
Jijon et al., Am J Physiol Cell Physiol 2002
:
Furthermore,
AP-1 and NF-kappaB DNA binding was not
affected by ERK and
p38 inhibition
Shimada et al., Carcinogenesis 2003
(Prostatic Neoplasms) :
The results suggest that not only p53 induction through
p38/JNK dependent
NFkappaB/AP-1 activation but also JNK dependent Bcl-2 phosphorylation are required for 2-ME induced apoptosis ; moreover, inhibition of these pathways may be involved in androgen mediated resistance to apoptosis
Dolganiuc et al., Gastroenterology 2004
(Hepatitis C...) :
HCV core and NS3 induced interleukin (IL)-1 receptor associated kinase ( IRAK ) activity, phosphorylation of
p38 , extracellular regulated ( ERK ), and c-jun N-terminal ( JNK ) kinases and induced
AP-1 activation
Sawai et al., Oncogene 2006
(Disease Progression...) :
Overexpressed ILK enhances the IL-1alpha induced
p38 MAPK phosphorylation more strongly through glycogen synthase kinase 3 ( GSK-3 ) activation, and subsequently
induces AP-1 activation, which promotes aggressive capabilities of pancreatic cancer cells
Ueno et al., Cardiovasc Toxicol 2006
(Atherosclerosis) :
Our results indicate that nicotine enhances the expression of ICAM-1 and VCAM-1 on the endothelial cell surface via a second messenger pathway which involves PKC and
p38 MAPK mediated
activation of NF-kappaB and
AP-1 , resulting in increased expression of these cellular adhesion molecules
Qi et al., J Biol Chem 2007
(Breast Neoplasms) :
Analyses of MAPK kinase 6 ( MKK6 ) -p38 fusion proteins showed that constitutively active
p38alpha ( MKK6-p38alpha ) and p38gamma ( MKK6-p38gamma ) stimulates and inhibits c-Jun phosphorylation respectively,
leading to a distinct
AP-1 regulation
Coss et al., Mol Endocrinol 2007
:
Inhibition of
p38 by either of two different inhibitors or a dominant negative p38 kinase abrogates synergy on FSHbeta expression,
reduces c-Fos induction by GnRH, and prevents the further increase in c-Fos levels that occurs with cotreatment
Chiu et al., J Cell Physiol 2008
:
p38 inhibitor, SB203580 or JNK inhibitor, SP600125 but not ERK inhibitor, PD98059
attenuated the US-induced MMP-13,
c-Fos , and c-Jun expression ; these results were further substantiated by transfecting with the dominant negative mutants of p38 or JNK
Hasegawa et al., J Immunol 2009
:
ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced
AP-1 activation is
mediated by caspase-8,
p38 , and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK
Khan et al., Mol Cell Biochem 2010
(Escherichia coli Infections...) :
In this article, we have shown that EAEC induced activation of mitogen activated protein kinases ( MAPK ) ( ERK-1/2, JNK and
p38MAPK ) in cultured human intestinal epithelial cells ( INT-407 )
leads to the induction of DNA binding activity of NF-kappaB and
AP-1 , resulting in IL-8 production
Boucher et al., Viral Immunol 2010
(HIV Infections...) :
In primary monocytes, ERK and
p38 inhibition
increased binding of
AP-1 and Sp1, respectively, to the IL-12p40 promoter, while JNK inhibition increased NF-kappaB, AP-1, and Sp1 binding
Sullivan et al., J Pharmacol Exp Ther 2011
:
Expression of JunB mRNA, but not other
AP-1 proteins, increased in TGF-ß1 treated MMNK-1 cells, and induction of JunB expression was
p38 dependent