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EPHB2 — FASLG
Text-mined interactions from Literome
Tanimoto et al., J Biochem 2002
:
ERK activation was
essential for
FasL expression and AICD
Alcouffe et al., FASEB J 2004
:
Fas and
FasL overexpression was
dependent on reactive oxygen species ( ROS ) production as well as
ERK and JNK activation
Liu et al., J Cell Physiol 2009
(MAP Kinase Signaling System) :
Activated
ERK suppressed p38 MAPK activation and
Fas/FasL protein expression
Navenot et al., Mol Pharmacol 2009
:
Activation of GPR54 resulted in the
ERK dependent expression of tumor necrosis factor-alpha and
FasL in a lymphoid cell line, the latter being the main trigger of apoptosis
Norambuena et al., J Biol Chem 2009
:
The resulting strong
ERK1/2 activation
leads to expression of the death factor
Fas ligand and caspase mediated apoptosis
Xing et al., J Gen Virol 2010
(Influenza in Birds) :
Moreover,
ERK alone
suppressed TNF-alpha and
FasL and inhibited TNF-family mediated extrinsic apoptosis in H9N2 infected chicken macrophages
Duan et al., Dig Dis Sci 2010
(Bile Duct Neoplasms...) :
The
effects of
MAPK-ERK cascade inhibitor and c-Myc inhibition by siRNA on 67-kDa laminin receptor induced
FasL expression were determined
Shin et al., Int J Hematol 2010
:
To distinguish between the activation signalling and the death inducing pathway downstream of Fas, we generated a novel T cell line expressing a chimeric hCD8-FasC protein and found that stimulation with the anti-CD8 antibodies induced tyrosine phosphorylation of TCR-proximal proteins,
activation of
Raf-1/ERK , p38 and JNK, and increased expression of CD69, Fas, and
Fas ligand
Rapold et al., J Lipid Res 2013
:
Furthermore, Fas activation increased phosphorylation of the Ca ( 2+ ) /calmodulin dependent protein kinases II ( CaMKII ), and blocking of the CaMKII-pathway ( either by the Ca ( 2+ ) chelator BAPTA or by the CaMKII inhibitor KN62 ) blunted
FasL induced
ERK1/2 phosphorylation and glycerol release
Seidelin et al., J Mol Med (Berl) 2013
(Colitis, Ulcerative) :
Similarly,
ERK - but not NF-?B -
inhibited Fas ligand and TNF-a mediated apoptosis responses in both cell line experiments and primary IECs