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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