Is MAC the knife that cuts cytochrome c from mitochondria during apoptosis?

被引：121

作者：

Dejean, L. M. ^{[1
]}

Martinez-Caballero, S. ^{[1
]}

Kinnally, K. W. ^{[1
]}

机构：

[1] NYU, Coll Dent, Dept Basic Sci, New York, NY 10010 USA

来源：

CELL DEATH AND DIFFERENTIATION | 2006年 / 13卷 / 08期

关键词：

MAC; mitochondrial apoptosis-induced channel; apoptosis; cytochrome c; patch-clamp; Bcl-2; Bax; t-Bid;

D O I：

10.1038/sj.cdd.4401949

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Apoptosis is a phenomenon fundamental to higher eukaryotes and essential to mechanisms controlling tissue homeostasis. Bcl-2 family proteins tightly control this cell death program by regulating the permeabilization of the mitochondrial outer membrane and, hence, the release of cytochrome c and other proapoptotic factors. Mitochondrial apoptosis-induced channel (MAC) is the mitochondrial apoptosisinduced channel and is responsible for cytochrome c release early in apoptosis. MAC activity is detected by patch clamping mitochondria at the time of cytochrome c release. The Bcl-2 family proteins regulate apoptosis by controlling the formation of MAC. Depending on cell type and apoptotic inducer, Bax and/or Bak are structural component(s) of MAC. Overexpression of the antiapoptotic protein Bcl-2 eliminates MAC activity. The focus of this review is a biophysical characterization of MAC activity and its regulation by Bcl-2 family proteins, and ends with some discussion of therapeutic targets.

引用

页码：1387 / 1395

页数：9

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