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CD8A — EPHB2

Text-mined interactions from Literome

Atherly et al., J Immunol 2006 (Lymphocytic Choriomeningitis) : These studies demonstrate that the loss of Itk and Rlk impairs TCR dependent signaling, causing defects in phospholipase C-gamma1, p38, and ERK activation as well as defects in calcium flux and cytokine production in vitro and expansion and effector cytokine production by CD8 ( + ) T cells in response to viral infection
Yachi et al., Immunity 2006 : A delayed and perhaps longer lasting CD8-TCR interaction results in delayed phospho-ERK recruitment to the synapse
Reich-Zeliger et al., Transplantation 2010 : Examination of ERK phosphorylation in high and low MHC-I expressing effectors revealed marked differences, suggesting that the interaction between CD8 on the veto CTL, and MHC-I on the effector cells is likely responsible for ERK phosphorylation ... These results suggest that the interaction between CD8 on veto CTL and the MHC class I alpha3 domain on the effector cell, leads to phosphorylation of MEK/ERK in the latter cell, associated with a significant reduction of XIAP levels which, in turn, enables potent triggering of Fas-FasL mediated apoptosis on cognate binding of the veto CTLs