Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy

被引：2463
作者：
Czabotar, Peter E.
Lessene, Guillaume
Strasser, Andreas [1 ]
Adams, Jerry M.
机构：
[1] Univ Melbourne, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3052, Australia
来源：
NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2014年 / 15卷 / 01期
基金：
澳大利亚研究理事会;
关键词：
CHRONIC LYMPHOCYTIC-LEUKEMIA; PROGRAMMED CELL-DEATH; IN-VIVO EFFICACY; BH3-ONLY PROTEINS; CYTOCHROME-C; BH3; DOMAIN; CAENORHABDITIS-ELEGANS; CONFORMATIONAL-CHANGES; HEMATOPOIETIC-CELLS; MEMBRANE PERMEABILIZATION;
D O I：
10.1038/nrm3722
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The BCL-2 protein family determines the commitment of cells to apoptosis, an ancient cell suicide programme that is essential for development, tissue homeostasis and immunity. Too little apoptosis can promote cancer and autoimmune diseases; too much apoptosis can augment ischaemic conditions and drive neurodegeneration. We discuss the biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold. These mechanistic insights into the functions of the BCL-2 family are illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCL-2 family.
引用
收藏
页码：49 / 63
页数：15
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