Mechanisms of apoptosis

被引:52
作者
Martin, DA [1 ]
Elkon, KB [1 ]
机构
[1] Univ Washington, Div Rheumatol, Seattle, WA 98195 USA
关键词
D O I
10.1016/j.rdc.2004.04.008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The understanding of the apoptotic program has grown exponentially over the past decade. Numerous human diseases have been directly linked to genetic defects in the apoptotic pathways, including cancer, neurodegenerative disorders, and autoimmune diseases. Caspases initiate and amplify various death signals, allowing for selective and ordered cellular demolition. The fine balance between pro- and antiapoptotic Bcl-2 family members regulates the cell fate in response to many (but not all) stress or signaling pathways. Recent discoveries highlight the complex integration of signals from various organelles that determine cell fate and the multiple functions of central players in the apoptotic process. It is likely that the knowledge obtained in a relatively time will translate into better diagnostics and therapies to enhance or retard cell death in the appropriate clinical circumstances.
引用
收藏
页码:441 / +
页数:15
相关论文
共 65 条
[1]   Three-dimensional structure of the apoptosome: Implications for assembly, procaspase-9 binding, and activation [J].
Acehan, D ;
Jiang, XJ ;
Morgan, DG ;
Heuser, JE ;
Wang, XD ;
Akey, CW .
MOLECULAR CELL, 2002, 9 (02) :423-432
[2]   Ways of dying: multiple pathways to apoptosis [J].
Adams, JM .
GENES & DEVELOPMENT, 2003, 17 (20) :2481-2495
[3]   A unified model for apical caspase activation [J].
Boatright, KM ;
Renatus, M ;
Scott, FL ;
Sperandio, S ;
Shin, H ;
Pedersen, IM ;
Ricci, JE ;
Edris, WA ;
Sutherlin, DP ;
Green, DR ;
Salvesen, GS .
MOLECULAR CELL, 2003, 11 (02) :529-541
[4]   Proapoptotic Bcl-2 relative bim required for certain apoptotic responses, leukocyte homeostasis, and to preclude autoimmunity [J].
Bouillet, P ;
Metcalf, D ;
Huang, DCS ;
Tarlinton, DM ;
Kay, TWH ;
Köntgen, F ;
Adams, JM ;
Strasser, A .
SCIENCE, 1999, 286 (5445) :1735-1738
[5]   BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes [J].
Bouillet, P ;
Purton, JF ;
Godfrey, DI ;
Zhang, LC ;
Coultas, L ;
Puthalakath, H ;
Pellegrini, M ;
Cory, S ;
Adams, JM ;
Strasser, A .
NATURE, 2002, 415 (6874) :922-926
[6]   VDAC2 inhibits BAK activation and mitochondrial apoptosis [J].
Cheng, EHY ;
Sheiko, TV ;
Fisher, JK ;
Craigen, WJ ;
Korsmeyer, SJ .
SCIENCE, 2003, 301 (5632) :513-517
[7]   BCL-2, BCL-XL sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis [J].
Cheng, EHYA ;
Wei, MC ;
Weiler, S ;
Flavell, RA ;
Mak, TW ;
Lindsten, T ;
Korsmeyer, SJ .
MOLECULAR CELL, 2001, 8 (03) :705-711
[8]   Direct activation of Bax by p53 mediates mitochondrial membrane permeabilization and apoptosis [J].
Chipuk, JE ;
Kuwana, T ;
Bouchier-Hayes, L ;
Droin, NM ;
Newmeyer, D ;
Schuler, M ;
Green, DR .
SCIENCE, 2004, 303 (5660) :1010-1014
[9]  
Chun HJ, 2001, ADV EXP MED BIOL, V490, P49
[10]   The Bcl-2 family: roles in cell survival and oncogenesis [J].
Cory, S ;
Huang, DCS ;
Adams, JM .
ONCOGENE, 2003, 22 (53) :8590-8607