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CSK — EPHB2

Text-mined interactions from Literome

Gu et al., Mol Cell Biochem 2001 : Overexpression of Csk that inactivates Src family tyrosine kinases also inhibited ERK activation evoked by GH
Shah et al., J Biol Chem 2003 (MAP Kinase Signaling System) : The Src inhibitor, PP2, the C-terminal Src kinase (Csk) , and dominant negative Pyk2 attenuated ERK1/2 activation by GnRH and PMA but not by EGF
Zhang et al., Mol Cell 2004 : Shp2 regulates SRC family kinase activity and Ras/Erk activation by controlling Csk recruitment
Dey et al., Exp Cell Res 2005 : CSK overexpression caused a profound inhibition of NGF induced activation of FYN, YES, RAS, and ERK and inhibited neurite outgrowth, NGF stimulated integrin directed migration and blocked the NGF induced conversion of GDP-RAC to its GTP bound active state ... In contrast, kinase-dead CSK augmented the activation of FYN, RAS, and ERK and increased neurite outgrowth ... These data suggest a distinct requirement for CSK in the regulation of NGF/TrkA activation of RAS, RAC, ERK , and AKT via the differential control of SFKs in the orchestration of neuronal differentiation
Beaulieu et al., Blood 2011 : Using Meg-01 cells and mouse megakaryocytes, we found that NF?B, ERK-MAPK , and PI3K/Akt pathways, known downstream pathways of TLRs, are activated by Pam3CSK4 , a TLR2-specific ligand
Zou et al., Circ Res 1998 : Overexpression of C-terminal Src kinase (Csk) , which inactivates Src family tyrosine kinases, suppressed the activation of transfected ERK in cardiac fibroblasts ... Overexpression of Csk or the dominant negative mutant of Ras had no effects on Ang II-induced ERK activation in cardiac myocytes