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EPHB2 — FADD

Text-mined interactions from Literome

Varghese et al., J Biol Chem 2002 : Head involution defective ( Hid ) -triggered apoptosis requires caspase-8 but not FADD ( Fas associated death domain ) and is regulated by Erk in mammalian cells
Lüschen et al., Exp Cell Res 2005 : This conclusion is based on the following observations : ( I ) Overexpression of FADD , caspase-8, or a c-FLIP protein containing the death effector domains only leads to enhanced and prolonged ERK activation after TNF treatment
García-Fuster et al., Biol Psychiatry 2007 (Disease Models, Animal...) : Pretreatment of rats with SL 327 ( a selective MEK1/2 inhibitor that blocks ERK activation ) fully prevented the reduction of FADD content induced by SNC-80 in the cerebral cortex ( 43 % ) and corpus striatum ( 29 % ), demonstrating the direct involvement of ERK1/2 signaling in the regulation of FADD by the opiate agonist
Hasegawa et al., J Immunol 2009 : ASC mediated AP-1 activation was inhibited by chemical or protein inhibitors for caspase-8, caspase-8 targeting small interfering RNA, and p38 and JNK inhibitors, but not by a caspase-1 inhibitor, caspase-9 or Fas associated death domain protein ( FADD ) dominant negative mutants, FADD- or RICK targeting small interfering RNAs, or a MEK inhibitor, indicating that the ASC induced AP-1 activation is mediated by caspase-8, p38, and JNK, but does not require caspase-1, caspase-9, FADD, RICK, or ERK
Ramos-Miguel et al., J Psychopharmacol 2011 (Morphine Dependence...) : This inhibition of ERK1/2 , however, did not prevent the up-regulation of oligomeric p-FADD at SW 12 h and 24 h