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RELA — TPX2

Text-mined interactions from Literome

Vatsyayan et al., EMBO Rep 2008 : SUMO1 modification of NF-kappaB2/p100 is essential for stimuli induced p100 phosphorylation and processing
Yao et al., J Clin Invest 2009 (Bone Resorption) : These findings suggest that upregulation of TRAF3 or NF-kappaB p100 expression or inhibition of NF-kappaB p100 degradation in OCPs could limit bone destruction and inflammation induced bone loss in common bone diseases
Sun et al., Proc Natl Acad Sci U S A 1994 : Subsequent studies have revealed that ( i ) cytoplasmic RelA is stably associated not only with I kappa B alpha but also with other ankyrin motif-rich proteins including the products of the NF-kappa B2 ( p100 ) and NF-kappa B1 ( p105 ) genes ; ( ii ) in contrast to RelA-I kappa B alpha, RelA-p100 cytoplasmic complexes are not dissociated following tumor necrosis factor alpha activation ; ( iii ) p100 functions as a potent inhibitor of RelA mediated transcription in vivo ; ( iv ) the interaction of RelA and p100 involves the conserved Rel homology domain of both proteins but not the nuclear localization signal of RelA, which is required for I kappa B alpha binding ; ( v ) p100 inhibition of RelA function requires the C-terminal ankyrin motif domain, which mediates cytoplasmic retention of RelA ; and ( vi ) as observed with I kappa B alpha, nuclear RelA stimulates p100 mRNA and protein expression