The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis

被引:4189
作者
Kluck, RM [1 ]
BossyWetzel, E [1 ]
Green, DR [1 ]
Newmeyer, DD [1 ]
机构
[1] LA JOLLA INST ALLERGY & IMMUNOL,DIV CELLULAR IMMUNOL,SAN DIEGO,CA 92121
关键词
D O I
10.1126/science.275.5303.1132
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
In a cell-free apoptosis system, mitochondria spontaneously released cytochrome c, which activated DEVD-specific caspases, leading to fodrin cleavage and apoptotic nuclear morphology. Bcl-2 acted in situ on mitochondria to prevent the release of cytochrome c and thus caspase activation. During apoptosis in intact cells, cytochrome c translocation was similarly blocked by Bcl-2 but not by a caspase inhibitor, zVAb-fmk. In vitro, exogenous cytochrome c bypassed the inhibitory effect of Bcl-2. Cytochrome c release was unaccompanied by changes in mitochondrial membrane potential. Thus, Bcl-2 acts to inhibit cytochrome c translocation, thereby blocking caspase activation and the apoptotic process.
引用
收藏
页码:1132 / 1136
页数:5
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