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

被引：2545
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
相关论文
共 217 条
[41]   Context-dependent Bcl-2/Bak Interactions Regulate Lymphoid Cell Apoptosis [J].
Dai, Haiming ;
Meng, X. Wei ;
Lee, Sun-Hee ;
Schneider, Paula A. ;
Kaufmann, Scott H. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (27) :18311-18322
[42]   Bax dimerizes via a symmetric BH3:groove interface during apoptosis [J].
Dewson, G. ;
Ma, S. ;
Frederick, P. ;
Hockings, C. ;
Tan, I. ;
Kratina, T. ;
Kluck, R. M. .
CELL DEATH AND DIFFERENTIATION, 2012, 19 (04) :661-670
[43]   To trigger apoptosis, Bak exposes its BH3 domain and homodimerizes via BH3: Groove interactions [J].
Dewson, Grant ;
Kratina, Tobias ;
Sim, Huiyan W. ;
Puthalakath, Hamsa ;
Adams, Jerry M. ;
Colman, Peter M. ;
Kluck, Ruth M. .
MOLECULAR CELL, 2008, 30 (03) :369-380
[44]   Bak Activation for Apoptosis Involves Oligomerization of Dimers via Their α6 Helices [J].
Dewson, Grant ;
Kratina, Tobias ;
Czabotar, Peter ;
Day, Catherine L. ;
Adams, Jerry M. ;
Kluck, Ruth M. .
MOLECULAR CELL, 2009, 36 (04) :696-703
[45]   Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition [J].
Du, CY ;
Fang, M ;
Li, YC ;
Li, L ;
Wang, XD .
CELL, 2000, 102 (01) :33-42
[46]   Bcl-xL Retrotranslocates Bax from the Mitochondria into the Cytosol [J].
Edlich, Frank ;
Banerjee, Soojay ;
Suzuki, Motoshi ;
Cleland, Megan M. ;
Arnoult, Damien ;
Wang, Chunxin ;
Neutzner, Albert ;
Tjandra, Nico ;
Youle, Richard J. .
CELL, 2011, 145 (01) :104-116
[47]   Bim is a suppressor of Myc-induced mouse B cell leukemia [J].
Egle, A ;
Harris, AW ;
Bouillet, P ;
Cory, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (16) :6164-6169
[48]   Bax loss impairs Myc-induced apoptosis and circumvents the selection of p53 mutations during Myc-mediated lymphomagenesis [J].
Eischen, CM ;
Roussel, MF ;
Korsmeyer, SJ ;
Cleveland, JL .
MOLECULAR AND CELLULAR BIOLOGY, 2001, 21 (22) :7653-7662
[49]  
Elkholi Rana, 2011, Genes Cancer, V2, P523, DOI 10.1177/1947601911417177
[50]   Loss of the pro-apoptotic BH3-only Bcl-2 family member Bim inhibits BCR stimulation-induced apoptosis and deletion of autoreactive B cells [J].
Enders, A ;
Bouillet, P ;
Puthalakath, H ;
Xu, YK ;
Tarlinton, DM ;
Strasser, A .
JOURNAL OF EXPERIMENTAL MEDICINE, 2003, 198 (07) :1119-1126
12345678910