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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