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EPHB2 — ZAP70

Text-mined interactions from Literome

Shan et al., Mol Cell Biol 2001 : The tyrosine kinase ZAP-70 has been implicated as a critical intermediary between T-cell antigen receptor ( TCR ) stimulation and Erk activation on the basis of the ability of dominant negative ZAP-70 to inhibit TCR stimulated Erk activation, and the reported inability of anti-CD3 antibodies to activate Erk in ZAP-70 negative Jurkat cells
Sánchez et al., Eur J Immunol 2004 : CD46 enhanced TCR/CD3 induced tyrosine phosphorylation of CD3zeta and ZAP-70 , as well as the activation of the ERK , JNK, and p38, but did not modify intracellular calcium
Wang et al., J Immunol 2008 : The transient activation of ERK1/2 under pro-apoptotic conditions of stimulation is at least partially due to the rapid polyubiquitination and subsequent degradation of ZAP70 , whereas the sustained activation of ERK1/2 under survival promoting conditions is paralleled by the induction/phosphorylation of anti-apoptotic molecules such as protein kinase B and Bcl-x ( L )
Griffith et al., J Biol Chem 1998 : Consistent with the hypothesis that ZAP-70 is required for activation of Erk in response to an oxidative stimulus, Erk1 and Erk2 could be rapidly activated in Jurkat cells but not in P116 cells upon addition of H2O2 ... Surprisingly, although ZAP-70 was required for H2O2 mediated Erk activation, Erk activation in response to T cell antigen receptor engagement did not require ZAP-70 ... In addition to demonstrating a requirement for ZAP-70 in H2O2 stimulated Erk activation, these results provide the first evidence for the existence of a ZAP-70 independent pathway for Erk activation in T cells