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CRK — JUN

Text-mined interactions from Literome

Ng et al., J Biol Chem 2001 (Hypertrophy...) : In contrast, LIF promoted strong activation of ERKs, marginal activation of p38 ( MAPK ), and no c-Jun N-terminal kinase activation
Yu et al., Cancer Res 2001 (Breast Neoplasms...) : Activation of extracellular signal regulated kinase and c-Jun-NH ( 2 ) -terminal kinase but not p38 mitogen activated protein kinases is required for RRR-alpha-tocopheryl succinate induced apoptosis of human breast cancer cells
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
Hammaker et al., J Immunol 2004 (Arthritis, Rheumatoid...) : Of interest, MEKK1 immunoprecipitates from IL-1 stimulated FLS appeared to activate c-Jun through the JNK pathway and TAK1 activation of c-Jun was dependent on JNK, ERK, and p38
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
An et al., Chin Med J (Engl) 2005 (Melanoma) : The expression of phosphorylated JNK and p38 also increased after the treatment with NCTD, and inhibitors of c-Jun NH2-terminal kinase (JNK) and p38 ( SP600125 and SB203580, respectively ) had significant inhibitory effects on the upregulation of phosphorylated JNK and p38 expression
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
Kim et al., J Lipid Res 2006 : It was also found that EPA attenuated UV-induced MMP-1 and MMP-9 expression by inhibiting UV-induced c-Jun phosphorylation, which is closely related to UV-induced activator protein-1 activation, and by inhibiting JNK and p38 activation
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
Park et al., Food Chem Toxicol 2007 : Hydrophobic bile acids activate c-Jun-NH ( 2 ) -terminal kinase ( JNK ), p38 mitogen activated protein kinases ( MAPK ), and extracellular signal regulated kinase 1/2, and PF2401-SF inhibited the phosphorylation of JNK and p38
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 ... 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
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
Orlandini et al., FEBS Lett 2008 : DAB2 knockdown causes activation of the Src-FAK signal pathway, extracellular-signal regulated kinase and c-Jun NH2-terminal kinase activation, and inhibition of p38 phosphorylation
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
Röth et al., Experimental and clinical cardiology 2011 : c-Jun N-terminal kinase activation increased due to GST inhibition during I/R. EA administration led to a significant increase in p38 activation following both H ( 2 ) O ( 2 ) treatment and I/R. ERK phosphorylation increased when GST was exposed to I/R
Tanaka et al., Proc Natl Acad Sci U S A 1997 (Cell Transformation, Neoplastic) : In this study, we found that Jun kinase (JNK) is moderately activated by v-Crk in both NIH 3T3 cells and chicken embryo fibroblasts
Meucci et al., Proc Natl Acad Sci U S A 1998 (Synaptic Transmission) : Both fractalkine and macrophage derived chemokine (MDC) produced a time dependent activation of extracellular response kinases (ERK)-1/2, whereas no activation of c-JUN NH2-terminal protein kinase (JNK)/stress activated protein kinase, or p38 was evident