Apoptosis: Overview and signal transduction pathways

被引:73
作者
Bredesen, DE
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif San Francisco, San Francisco, CA 94143 USA
关键词
programmed cell death; caspase; physiological cell death; neurodegeneration; neurotrauma;
D O I
10.1089/neu.2000.17.801
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Apoptosis is a form of cell death that is driven by an intrinsic cellular suicide program, The roles of apoptosis and other forms of programmed cell death in neural development, maintenance, and disease states are increasingly being recognized and defined, Therapies directed at the apoptotic program have seen at least some degree of success in animal models of neurodegenerative disease, vascular disease, and traumatic CNS injury, This article describes the signal transduction pathways that mediate apoptosis, Broadly speaking, intrinsic and extrinsic pathways for apoptosis activation may be distinguished, as can be cross-talk between these two, These pathways converge on a system of proteases referred to as "capases" (cysteinyl aspartic proteinases), and modulators exist that multimerize, activate, amplify, or inhibit caspases, Activated caspases are the executioners of the apoptotic program, and carry out this function by cleaving specific cellular substrates, Modulation of this process holds promise as a therapeutic approach in neurotrauma.
引用
收藏
页码:801 / 810
页数:10
相关论文
共 74 条
[1]   The RET proto-oncogene induces apoptosis: a novel mechanism for Hirschsprung disease [J].
Bordeaux, MC ;
Forcet, C ;
Granger, L ;
Corset, V ;
Bidaud, C ;
Billaud, M ;
Bredesen, DE ;
Edery, P ;
Mehlen, P .
EMBO JOURNAL, 2000, 19 (15) :4056-4063
[2]   Keeping neurons alive: The molecular control of apoptosis .2. [J].
Bredesen, DE .
NEUROSCIENTIST, 1996, 2 (04) :211-216
[3]   p75NTR and the concept of cellular dependence:: seeing how the other half die [J].
Bredesen, DE ;
Ye, X ;
Tasinato, A ;
Sperandio, S ;
Wang, JJL ;
Assa-Munt, N ;
Rabizadeh, S .
CELL DEATH AND DIFFERENTIATION, 1998, 5 (05) :365-371
[4]   Keeping neurons alive: The molecular control of apoptosis .1. [J].
Bredesen, DE .
NEUROSCIENTIST, 1996, 2 (03) :181-190
[5]  
BREDESEN DE, 1999, NEURAL NOTES, V70, P31
[6]   INHIBITION OF ICE FAMILY PROTEASES BY BACULOVIRUS ANTIAPOPTOTIC PROTEIN P35 [J].
BUMP, NJ ;
HACKETT, M ;
HUGUNIN, M ;
SESHAGIRI, S ;
BRADY, K ;
CHEN, P ;
FERENZ, C ;
FRANKLIN, S ;
GHAYUR, T ;
LI, P ;
LICARI, P ;
MANKOVICH, J ;
SHI, LF ;
GREENBERG, AH ;
MILLER, LK ;
WONG, WW .
SCIENCE, 1995, 269 (5232) :1885-1888
[7]   Conversion of Bcl-2 to a Bax-like death effector by caspases [J].
Cheng, EHY ;
Kirsch, DG ;
Clem, RJ ;
Ravi, R ;
Kastan, MB ;
Bedi, A ;
Ueno, K ;
Hardwick, JM .
SCIENCE, 1997, 278 (5345) :1966-1968
[8]   FADD, A NOVEL DEATH DOMAIN-CONTAINING PROTEIN, INTERACTS WITH THE DEATH DOMAIN OF FAS AND INITIATES APOPTOSIS [J].
CHINNAIYAN, AM ;
OROURKE, K ;
TEWARI, M ;
DIXIT, VM .
CELL, 1995, 81 (04) :505-512
[9]   DEVELOPMENTAL CELL-DEATH - MORPHOLOGICAL DIVERSITY AND MULTIPLE MECHANISMS [J].
CLARKE, PGH .
ANATOMY AND EMBRYOLOGY, 1990, 181 (03) :195-213
[10]   PREVENTION OF APOPTOSIS BY A BACULOVIRUS GENE DURING INFECTION OF INSECT CELLS [J].
CLEM, RJ ;
FECHHEIMER, M ;
MILLER, LK .
SCIENCE, 1991, 254 (5036) :1388-1390