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EPHB2 — F2R

Text-mined interactions from Literome

Seo et al., J Biol Chem 2000 : Like alpha-thrombin receptor mediated Erk activation, the effect of rPMT was insensitive to the protein kinase C inhibitor GF109203X, but was blocked by the epidermal growth factor receptor-specific tyrphostin, AG1478 and by dominant negative mutants of mSos1 and Ha-Ras
Robey et al., Kidney Int 2000 : Thrombin increases mesangial cell HK activity via a PTX-insensitive mechanism involving thrombin receptor activation, PKC dependent activation of ERK1/2 , and both ongoing gene transcription and de novo protein synthesis
Wang et al., Am J Physiol Cell Physiol 2002 (Calcium Signaling...) : Thrombin stimulated ERK1/2 activation is mainly mediated by PAR-1 via two branches : 1 ) the PTX-sensitive G protein/ ( betagamma-subunits ) -phosphatidylinositol 3-kinase branch, and 2 ) the G ( q ) -PLC- ( InsP ( 3 ) receptor ) /Ca2+ -PKC pathway ... Thrombin- or PAR-1-AP induced ERK activation is partially blocked by a selective EGF receptor inhibitor, AG1478
Darmoul et al., Mol Cancer Res 2004 (Colonic Neoplasms) : Finally, PAR1 activation induces Src phosphorylation, which is reversed by using the Src tyrosine kinase inhibitor PP2, suggesting that Src activation plays a permissive role for PAR1 mediated ERK1/2 activation and cell proliferation probably acting downstream of the EGFR
Nicole et al., J Neurosci 2005 (Brain Injuries...) : The mechanisms by which PAR-1 stimulates glial proliferation appear to be related to the ability of PAR-1 receptor signaling to induce sustained extracellular receptor kinase (ERK) activation ... In contrast to the transient activation of ERK by cytokines and growth factors, PAR-1 stimulation induces a sustained ERK activation through its coupling to multiple G-protein linked signaling pathways, including Rho kinase
Syeda et al., J Biol Chem 2006 : PAR-1 and PAR-2 stimulation rapidly activated both ERK1/2 and p38MAPK, and pharmacological blockade of MEK with either PD98059 or U0126 or of p38MAPK by SB203580 or SB202190 strongly inhibited thrombin- and SLIGKV induced COX-2 expression and 6-keto-PGF1alpha formation
Kuo et al., Cell Signal 2006 : Our results show that PAR1 mediated activation of Src and ERK1/2 in HEK 293 cells was increased with overexpression of beta-arrestin1 or depletion of beta-arrestin2 ... PAR1 mediated activation of Src and ERK1/2 in HEK 293 cells was decreased or eliminated with depletion of beta-arrestin1 or overexpression of beta-arrestin2
Sekiguchi et al., Biochem Pharmacol 2007 : PAR1-AP caused persistent ( 6h or more ) and transient ( 5min ) phosphorylation of ERK and p38 MAPK, respectively, followed by delayed reinforcement at 18h ... The PAR1 mediated persistent ERK phosphorylation was reduced by inhibitors of Src and EGFR-TK. PAR1-AP actually phosphorylated EGF receptors and up-regulated mRNA for heparin-binding-EGF (HB-EGF), the latter effect being blocked by inhibitors of Src, EGFR-TK and MEK
Zhang et al., J Am Soc Nephrol 2007 (Disease Models, Animal...) : These findings support important profibrotic roles for plasmin that include PAR-1 dependent ERK signaling and EMT induction
Cisowski et al., Am J Pathol 2011 (Adenocarcinoma...) : Unlike i1 pepducins, the i3 loop pepducins were effective inhibitors of PAR1 mediated ERK activation and tumor growth
Lin et al., J Biol Chem 2013 : Moreover, thrombin activated PAR1-PAR2 heterodimers enhance ß-arrestin mediated ERK1/2 activation in the cytoplasm, whereas activated ERK1/2 induced by the thrombin activated PAR1 protomer redistributes to the nucleus