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EPHB2 — TNFRSF1A

Text-mined interactions from Literome

Murakami-Mori et al., J Immunol 1999 (Acquired Immunodeficiency Syndrome...) : Using neutralizing anti-TNFR-I and TNFR-II mAbs, we have now obtained evidence that TNF-alpha induced KS cell growth and ERK1/2 activation are mediated exclusively by TNFR-I , not by TNFR-II
Tran et al., J Biol Chem 2001 : Activation of the FasR, TNF-R1 , and TRAIL-R, respectively, rapidly induced subsequent ERK1/2 activation, an event independent from caspase activity
Kunisch et al., Ann Rheum Dis 2007 (Arthritis, Rheumatoid...) : In RA- and OA-SFB, TNFalpha induced phosphorylation of p38, ERK or JNK was exclusively mediated by TNF-R1
Ogura et al., Int Immunopharmacol 2008 : In this study, we show that ERK and p38 MAP kinase are involved in the downregulation of cell surface TNF-R1 upon exposure to Ac-CHX and the subsequent inhibition of TNF-alpha induced NF-kappaB activation
Itatsu et al., Liver Int 2009 (Cholangiocarcinoma) : These data suggest that TNF-alpha/TNF-R1 interaction leads to the phosphorylation of Erk1/2 and p38MAPK and nuclear translocation of NF-kappaB, which is closely associated with the production and activation of MMP-9 in cultured CC cells of HuCTT-1 and CCKS-1
Wang et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2011 : MC3T3 cells were serum starved for 22 h, treated with MCD ( 10 g/L ) for 60 min followed by TNF-a ( 10 µg/L ) for 0, 5, 10, 15 or 30 min, or TNF-a plus CHX ( 10 mg/L ) for 4 h to induce apoptosis, then TNFR1 mediated I?Ba degradation, phosphorylation of AKT, ERK or p38, and processing of caspase-3 were analyzed by using SDS-PAGE/Western blotting method