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EGFR — FADD
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
FADD
→
Complex of EGFR-FAS
(increases, EGFR/FAS Activity, FADD Translocation)
Reinehr et al., J Biol Chem 2005*
Evidence: Activated Yes rapidly associated with the epidermal growth factor receptor (EGFR), which became phosphorylated at Tyr845 and Tyr1173 but not at Tyr1045. Activated EGFR then triggered an AG1478-sensitive CD95-tyrosine phosphorylation, which was a signal for membrane targeting of the EGFR/CD95 complex, subsequent recruitment of Fas-associated death domain and caspase 8, and apoptosis induction. All of these events were significantly blunted by inhibitors of sphingomyelinase, PKCzeta, NADPH oxidase...
Text-mined interactions from Literome
Iwase et al., Oral Oncol 2008
(Carcinoma, Squamous Cell...) :
Although
EGFR inhibitors did not
affect the expression of Fas, the
Fas associated death domain protein , or procaspase-8 in OSCC cells, the inhibition downregulated cellular FLICE-inhibitory protein ( c-FLIP )
Lokeshwar et al., Cancer Res 2010
(Neoplasm Invasiveness...) :
4-MU
induced caspase-8, caspase-9, and caspase-3 activation, PARP cleavage, upregulation of Fas-L, Fas,
FADD and DR4, and downregulation of bcl-2, phosphorylated bad, bcl-XL, phosphorylated Akt, phosphorylated IKB, phosphorylated ErbB2, and phosphorylated
epidermal growth factor receptor