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. Author manuscript; available in PMC: 2010 Jun 15.
Published in final edited form as: Cancer Res. 2009 May 26;69(12):5023–5029. doi: 10.1158/0008-5472.CAN-08-3731

Figure 5. Caspase-8 tyrosine 380 may be involved in negative regulation of EGF signaling.

Figure 5

A) Immunoblot analysis of EGF-induced Erk and Akt pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector (E.V.), the DEDs alone (DEDs) or the “caspase domain” of caspase-8 (Casp. Dom.) (lanes 1–3, respectively). B) Immunoblot analysis of EGF-induced Erk and Akt pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector (E.V.), the catalytically inactive point mutant (C360A) or the C360A/Y380F dual mutant of caspase-8 (C360A/Y380F) (lanes 1–3, respectively). C) Immunoblot analysis of EGF-induced Erk pathway activation in NB7 cells lacking caspase-8 re-constituted with empty vector, the catalytically inactive point mutant (C360A) or the C360A/Y380F dual mutant of caspase-8 (as in Fig 5B) with or without sodium orthovanadate (200 µM) as described (lanes 1–4, respectively). D) Simplified schematic depiction of the proposed model of the critical role for caspase-8 in EGF induction of Erk pathway signaling events.