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ASIP — EPHB2

Text-mined interactions from Literome

Shinohara et al., Cancer Res 2000 (Glioma...) : We report here that : ( a ) in gliomas, [ 3H ] TdR incorporation was enhanced by anti-Fas IgM monoclonal antibody CH-11 and conversely inhibited by anti-FasL monoclonal antibody NOK-2 ; ( b ) cross linking of Fas with CH-11 drove both cell cycle progression and apoptosis as demonstrated by the induction of the S-G2 phase of DNA and RNA and fragmented nuclei ; ( c ) phosphorylation of extracellular signal regulated kinase ( ERK ), but not of c-Jun NH2-terminal kinase or p38, was induced by cross linking of Fas ; ( d ) a mitogen activated protein kinase/ERK kinase 1 ( MEK1 ) inhibitor PD98059 completely blocked CH-11 induced ERK phosphorylation as well as cell cycle progression without affecting induction of apoptosis ; and ( e ) a broad-spectrum caspase inhibitor Z-Asp-CH2-DCB inhibited CH-11 induced ERK phosphorylation, cell cycle progression, and apoptosis
Zamah et al., J Biol Chem 2002 : Activation of ERK by wild type and Ser -- > Asp receptors is inhibited by pertussis toxin
Rakatzi et al., Diabetes 2003 (MAP Kinase Signaling System) : This finding correlated with a prominent Shc/IGF-I receptor interaction, tyrosine phosphorylation of Shc, activation of extracellular signal regulated protein kinase ( ERK ) -1 and -2, and stimulation of DNA synthesis by HMR 1153 and Asp ( B10 ) insulin
Karanian et al., Eur J Pharmacol 2005 : Interestingly, the integrin antagonist Gly-Arg-Gly-Asp-Ser-Pro also caused the disruption of R-methanandamide mediated ERK and FAK responses and upset the integrity of excitatory synapses