[HTML][HTML] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1-and TNF receptor–induced cell death
MP Boldin, TM Goncharov, YV Goltseve, D Wallach - Cell, 1996 - cell.com
MP Boldin, TM Goncharov, YV Goltseve, D Wallach
Cell, 1996•cell.comAbstract Fas/APO-1 and p55 tumor necrosis factor (TNF) receptor (p55-R) activate cellular
mechanisms that result in cell death. Upon activation of these receptors, Fas/APO-1 binds a
protein called MORT1 (or FADD) and p55-R binds a protein called TRADD. MORT1 and
TRADD can also bind to each other. We have cloned a novel protein, MACH, that binds to
MORT1. This protein exists in multiple isoforms, some of which contain a region that has
proteolytic activity and shows marked sequence homology to proteases of the ICE/CED-3 …
mechanisms that result in cell death. Upon activation of these receptors, Fas/APO-1 binds a
protein called MORT1 (or FADD) and p55-R binds a protein called TRADD. MORT1 and
TRADD can also bind to each other. We have cloned a novel protein, MACH, that binds to
MORT1. This protein exists in multiple isoforms, some of which contain a region that has
proteolytic activity and shows marked sequence homology to proteases of the ICE/CED-3 …
Abstract
Fas/APO-1 and p55 tumor necrosis factor (TNF) receptor (p55-R) activate cellular mechanisms that result in cell death. Upon activation of these receptors, Fas/APO-1 binds a protein called MORT1 (or FADD) and p55-R binds a protein called TRADD. MORT1 and TRADD can also bind to each other. We have cloned a novel protein, MACH, that binds to MORT1. This protein exists in multiple isoforms, some of which contain a region that has proteolytic activity and shows marked sequence homology to proteases of the ICE/CED-3 family. Cellular expression of the proteolytic MACH isoforms results in cell death. Expression of MACH isoforms that contain an incomplete ICE/CED-3 region provides effective protection against the cytotoxicity induced by Fas/APO-1 or p55-R triggering. These findings suggest that MACH is the most upstream enzymatic component in the Fas/APO-1- and p55-R-induced cell death signaling cascades.
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