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JUN — MAP3K7

Text-mined interactions from Literome

Lee et al., J Biochem Mol Biol 2002 : TAK1 dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB ... The AP1 activation by TRAF2, TRAF5, and TRAF6 was also greatly suppressed by the dominant negative TAK1
Li et al., J Biol Chem 2003 : Ectopic expression of a phosphatase negative mutant of PP2Cepsilon, PP2Cepsilon ( D/A ), which acted as a dominant negative form, enhanced both the association between TAK1 and MKK4 or MKK6 and the TAK1 induced activation of an AP-1 reporter gene
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
Kaminska et al., Acta biochimica Polonica 2005 (Neoplasms) : Furthermore, TGF-beta activated kinase-1 (TAK1) is a component of TGF-beta signalling and activates stress activated kinases : p38 through MKK6 or MKK3 and c-Jun N-terminal kinases (JNKs) via MKK4
Sakurai et al., FEBS Lett 2005 : CD28-responsive element/activator protein-1 binding site ( RE/AP ) within the IL-2 promoter was a functional target for TAK1
Ishizawa et al., Biol Cell 2006 : xFADD and xRIP1 synergistically induced the activation of AP-1 and NF-kappaB, both of which were partially mediated by TRAF2 ( tumour-necrosis-factor-receptor associated factor 2 ) and TAK1 ( transforming-growth-factor-beta activated kinase 1 )
Tang et al., J Exp Med 2008 (Bone Marrow Diseases...) : Activation of TAK1 by proinflammatory cytokines and T and B cell receptors induces the nuclear localization of nuclear factor kappaB (NF-kappaB) and the activation of c-Jun N-terminal kinase (JNK)/AP1 and P38, which play important roles in mediating inflammation, immune responses, T and B cell activation, and epithelial cell survival
Yu et al., J Biol Chem 2008 : Consistently, TAK1 mutant with alanine substitution of these two residues severely inhibits IL-1 induced NFkappaB and AP-1 activities, whereas TAK1 mutant with replacement of these two sites with acidic residues slightly enhances IL-1 induced NFkappaB and AP-1 activities compared with the TAK1 wild-type ... Consistently, TAK1 mutant with alanine substitution of these two residues severely inhibits IL-1 induced NFkappaB and AP-1 activities, whereas TAK1 mutant with replacement of these two sites with acidic residues slightly enhances IL-1 induced NFkappaB and AP-1 activities compared with the TAK1 wild-type
Kumar et al., J Immunol 2009 (Inflammation) : TAK1 was also required for the activation of AP-1 in response to TWEAK
Nijboer et al., Stroke 2009 (Cerebral Infarction...) : We now show that TAT-NBD treatment increased HI-induced AP-1 activation concomitantly with reduced Gadd45beta, XIAP, and increased ( P ) -TAK1 expression
Dey et al., Virology 2011 : TAK1 regulates NF-?B and AP-1 activation in airway epithelial cells following RSV infection ... Inhibition of TAK1 activation, by overexpression of kinase inactive TAK1 or using cells lacking TAK1 expression, significantly reduced RSV induced NF-?B and AP-1 nuclear translocation and DNA binding activity, as well as NF-?B dependent gene expression, identifying TAK1 as an important upstream signaling molecule regulating RSV induced NF-?B and AP-1 activation
Jin et al., Dev Biol 2013 : Second, MAP3K1 potentiated AP-2a expression and SRF and AP-1 activity, but its target genes were enriched for binding motifs of AP-2a and SRF, and not AP-1, suggesting the existence of novel MAP3K1-AP-2a/SRF modules in gene regulation
Wang et al., J Biol Chem 1997 : This report shows that TAK1 is also a strong activator of c-Jun N-terminal kinase (JNK)