Mitochondria in Apoptosis: Bcl-2 Family Members and Mitochondrial Dynamics

被引:1207
作者
Martinou, Jean-Claude [1 ,2 ]
Youle, Richard J. [2 ]
机构
[1] Univ Geneva, Dept Cell Biol, Fac Sci, CH-1211 Geneva 4, Switzerland
[2] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA
基金
瑞士国家科学基金会;
关键词
CYTOCHROME-C RELEASE; PROGRAMMED CELL-DEATH; OUTER-MEMBRANE PERMEABILIZATION; STRESS-INDUCED APOPTOSIS; LIPIDIC PORE FORMATION; BAX-DERIVED PEPTIDE; PROAPOPTOTIC BAX; BH3-ONLY PROTEINS; SUBCELLULAR-LOCALIZATION; EMBRYONIC-DEVELOPMENT;
D O I
10.1016/j.devcel.2011.06.017
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondria participate in apoptosis through a range of mechanisms that vary between vertebrates and invertebrates. In vertebrates, they release intermembrane space proteins, such as cytochrome c, to promote caspase activation in the cytosol. This process is the result of the loss of integrity of the outer mitochondrial membrane caused by proapoptotic members of the Bcl-2 family. This event is always accompanied by a fissioning of the organelle. Fission of mitochondria has also been reported to participate in apoptosis in Drosophila and Caenorhabditis elegans. However, in these organisms, mitochondrial membrane permeabilization does not occur and the mechanism by which mitochondrial dynamics participates in cell death remains elusive.
引用
收藏
页码:92 / 101
页数:10
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