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CHUK — NEDD9

Text-mined interactions from Literome

Lang et al., Mol Cell Biol 2003 : IKK mediated p105 phosphorylation generates a binding site for betaTrCP, the receptor subunit of an SCF-type ubiquitin E3 ligase, and depletion of betaTrCP by RNA interference blocks TNF-alpha induced p105 ubiquitination and proteolysis
Beinke et al., Mol Cell Biol 2004 (MAP Kinase Signaling System) : These data show that IKK induced p105 proteolysis is essential for LPS activation of TPL-2, thus revealing a novel function of IKK in the regulation of the ERK MAP kinase cascade
Parameswaran et al., J Biol Chem 2006 : Upon LPS stimulation, IkappaB kinase promotes phosphorylation and degradation of NFkappaB1 p105 ( p105 ) , which releases TPL2 ( a MAP3K ), which phosphorylates MEK1/2, which in turn phosphorylates ERK1/2
Loniewski et al., Mol Immunol 2007 : Furthermore, although TLR4 mediated IKK induced p105 phosphorylation is not sensitive to TRAF6 knockdown, I kappa B alpha phosphorylation ( also, IKK induced ) is significantly blocked, suggesting that TLR4 activation results in a TRAF6-sensitive and -insensitive IKK activation in macrophages
Sriskantharajah et al., Nat Immunol 2009 : To investigate the importance of proteolysis of NF-kappaB1 p105 induced by the kinase IKK in activation of the transcription factor NF-kappaB, we generated 'Nfkb1 ( SSAA/SSAA ) ' mice, in which the IKK-target serine residues of p105 were substituted with alanine
Gantke et al., Immunol Rev 2012 (Inflammation...) : Agonist stimulation releases TPL-2 from p105-inhibition by IKK mediated phosphorylation of p105 , which triggers degradation of p105 by the proteasome
Yang et al., Mol Cell Biol 2012 : Activation of TPL-2/ERK signaling by IKK induced p105 proteolysis, therefore, induced a negative feedback loop to downregulate NF-?B dependent expression of the proinflammatory cytokine interleukin-12 (IL-12) ... Unexpectedly, TPL-2 promoted soluble TNF production independently of IKK induced p105 phosphorylation and its ability to activate ERK, which has important implications for the development of anti-inflammatory drugs targeting TPL-2