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JUN — TAB1

Text-mined interactions from Literome

Lee et al., J Biochem Mol Biol 2002 : The AP1 activation by TRAF2, TRAF5, and TRAF6 was also greatly suppressed by the dominant negative TAK1
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
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
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