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EPHB2 — VAV1

Text-mined interactions from Literome

Villalba et al., Eur J Immunol 2000 : Here, we analyzed the effects of Vav on three known downstream targets of Ras, i. e. activation of ERK and NFAT, and up-regulation of the activation antigen CD69 ... The MEK inhibitor PD90859 inhibited Vav induced activation of ERK , and Vav- or anti-CD3 induced activation of NFAT, suggesting that MEK and ERK are involved in Vav mediated NFAT activation ... Conversely, however, dominant negative Vav did not inhibit NFAT and ERK activation or CD69 expression induced by an active Ras mutant
Hebeis et al., Blood 2005 : In addition, activation of ERK ( extracellular signal regulated kinase ) required Vav1 and Vav2 in response to CD180 but was Vav1 and vav2 independent in response to LPS
Wilsbacher et al., Cell communication and signaling : CCS 2006 : In contrast, mutations in the SH2 and C-SH3 domains did not affect Rac activation by Vav1Y3F, but reduced the ability of Vav1Y3F to induce EGF independent migration and constitutive ERK phosphorylation ... Lastly, treatment of cells with the EGF receptor inhibitory antibody blocked the Vav1Y3F induced , EGF independent stimulation of ERK phosphorylation, but had no effect on Rac1 activation or PAK phosphorylation
Dorn et al., Blood 2007 : Although RhoH is not required for TCR induced activation of ZAP70 and ZAP70 mediated activation of p38, it is crucial for the tyrosine phosphorylation of LAT, PLCgamma1, and Vav1 and for the activation of Erk and calcium influx