FLAME-1, a Novel FADD-like Anti-apoptotic Molecule That Regulates Fas/TNFR1-induced Apoptosis*

S. Srinivasula,Manzoor Ahmad,S. Ottilie,F. Bullrich,Sean Banks,Yu Wang,T. Fernandes-Alnemri,C. Croce,G. Litwack,K. Tomaselli,R. Armstrong,E. Alnemri

Published 1997 in Journal of Biological Chemistry

ABSTRACT

We identified and cloned a novel human protein that contains FADD/Mort1 death effector domain homology regions, designated FLAME-1. FLAME-1, although most similar in structure to Mch4 and Mch5, does not possess caspase activity but can interact specifically with FADD, Mch4, and Mch5. Interestingly, FLAME-1 is recruited to the Fas receptor complex and can abrogate Fas/TNFR-induced apoptosis upon expression in FasL/tumor necrosis factor-sensitive MCF-7 cells, possibly by acting as a dominant-negative inhibitor. These findings identify a novel endogenous control point that regulates Fas/TNFR1-mediated apoptosis.

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