Regulation of mitochondrial morphological dynamics during apoptosis by Bcl-2 family proteins - A key in Bak?

被引:97
作者
Brooks, Craig [2 ]
Dong, Zheng [1 ,2 ]
机构
[1] Med Coll Georgia, Dept Cellular Biol & Anat, Augusta, GA 30912 USA
[2] Vet Affairs Med Ctr, Augusta, GA USA
基金
美国国家卫生研究院;
关键词
Bax; Bak; mitochondria; fission; fusion; mitofusin; apoptosis;
D O I
10.4161/cc.6.24.5115
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Early during apoptosis, the mitochondrial network collapses into short punctate fragments. The seemingly morphological change, called mitochondrial fragmentation, contributes to mitochondrial injury. Mitochondrial morphology is dictated by two opposing processes, fission and fusion. It is unclear how the fission-fusion balance is tilted during apoptosis, resulting in mitochondrial fragmentation. Emerging evidence has now suggested a regulation of mitochondrial morphological dynamics by Bcl-2 family proteins. In this regulation, Bak appears to be a key. Through interaction with mitofusins, Bak may block mitochondrial fusion to induce fragmentation. By this function, Bak may collaborate with Bax to permeabilize mitochondrial outer membrane, leading to the release of apoptogenic factors.
引用
收藏
页码:3043 / 3047
页数:5
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