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NFKBIA — TNFSF11

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: TNFSF11 — NFKBIA (in vitro) Wong et al., Mol Cell 1999
• IRef Hprd Interaction: TNFSF11 — NFKBIA (in vivo) Wong et al., Mol Cell 1999
• IRef Ophid Interaction: NFKBIA — TNFSF11 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Zhang et al., J Immunol 2003 : RANKL stimulated IkappaB-alpha phosphorylation, IkappaB-alpha degradation and DNA binding ability of NF-kappaB were increased after over-expression of SHP-1 ( C453S )
Takada et al., Blood 2004 : The effect on nuclear factor-kappaB (NF-kappaB) activation correlated with RANKL induced IkappaBalpha kinase activation
Kobayashi et al., J Biol Chem 2005 : RANKL induced degradation of I kappa B alpha and phosphorylation of p38 MAPK and c-Jun N-terminal kinase in RAW264.7 cells were up-regulated by PGE2 in a cAMP dependent protein kinase A (PKA) dependent manner, suggesting that EP2 and EP4 signals cross-talk with RANK signals
Min et al., J Immunol 2005 : TRANCE induced IkappaB-alpha phosphorylation and NF-kappaB activation via a cascade of reactions involving the TNFR associated factors, phospholipase C, PI3K, and protein kinase C ( PKC-alpha and PKC-zeta )
Lee et al., Mol Cell Biochem 2006 : Osteoclast precursors expressing a dominant negative Rac1N17 are defective in TRANCE induced IKK activation and IkappaBalpha degradation resulting in inhibition of NFkappaB dependent reporter gene activity
Ichikawa et al., Mol Cancer Res 2006 (Bone Resorption...) : The suppression of NF-kappaB by ACA was mediated through suppression of RANKL induced activation of IkappaBalpha kinase, IkappaBalpha phosphorylation, and IkappaBalpha degradation
Murakami et al., Biofactors 2007 : PEITC also abrogated the RANKL induced degradation of IkappaB-alpha , a suppressive partner of nuclear factor kappaB (NFkappaB), thereby inhibiting transcription activity, as detected by a reporter assay
Tsai et al., Eur J Pharmacol 2008 : Furthermore, RANKL mediated increase of IkappaBalpha phosphorylation, p65 phosphorylation at Ser ( 536 ), kappaB-luciferase activity and NF-kappaB binding activity was inhibited by paeonol
Maruyama et al., J Bone Miner Res 2010 : RANKL still induced the degradation of I kappaB alpha and activated classical NF-kappaB, whereas processing of p100 to p52 was abolished by the aly/aly mutation