Executionary pathway for apoptosis: lessons from mutant mice

被引：42

作者：

Woo, M

Hakem, R

Mak, TW

机构：

[1] Univ Toronto, Amgen Inst, Toronto, ON M5G 2C1, Canada

[2] Univ Toronto, Ontario Canc Inst, Dept Immunol, Toronto, ON, Canada

[3] Univ Toronto, Ontario Canc Inst, Dept Med Biophys, Toronto, ON, Canada

来源：

CELL RESEARCH | 2000年 / 10卷 / 04期

关键词：

apoptosis; progammed cell death; caspases; death receptors; mitochondria;

D O I：

10.1038/sj.cr.7290054

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Apoptosis or programmed cell death (PCD) is an evolutionarily conserved cellular process that is essential for normal development and homeostasis of multicellular organisms. Defects in the apoptosis signaling result in many diseases including autoimmune diseases and cancer. The apoptosis signaling pathway was first described genetically in the nematode Caenorhabditis elegans which serves as a framework for the more complex apoptotic pathways that exist in mammals. In this review, we will discuss the apoptotic pathways that are emerging in mammals as elucidated by studies of gene-targeted mutant mice.

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收藏

页码：267 / 278

页数：12

相关论文

共 68 条

[1] The Bcl-2 protein family: Arbiters of cell survival [J].

Adams, JM ;

Cory, S .

SCIENCE, 1998, 281 (5381) :1322-1326

[2] Cellular environments and apoptosis: Tissue microenvironments control activated T-cell death [J].

Akbar, AN ;

Salmon, M .

IMMUNOLOGY TODAY, 1997, 18 (02) :72-76

[3] Early activation of caspases during T lymphocyte stimulation results in selective substrate cleavage in nonapoptotic cells [J].

Alam, A ;

Cohen, LY ;

Aouad, S ;

Sékaly, RP .

JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 190 (12) :1879-1890

[4] Apoptosis control by death and decoy receptors [J].

Ashkenazi, A ;

Dixit, VM .

CURRENT OPINION IN CELL BIOLOGY, 1999, 11 (02) :255-260

[5] Defects in regulation of apoptosis in caspase-2-deficient mice [J].

Bergeron, L ;

Perez, GI ;

Macdonald, G ;

Shi, LF ;

Sun, Y ;

Jurisicova, A ;

Varmuza, S ;

Latham, KE ;

Flaws, JA ;

Salter, JCM ;

Hara, H ;

Moskowitz, MA ;

Li, E ;

Greenberg, A ;

Tilly, JL ;

Yuan, JY .

GENES & DEVELOPMENT, 1998, 12 (09) :1304-1314

[6] Human CARD4 protein is a novel CED-4/Apaf-1 cell death family member that activates NF-κB [J].

Bertin, J ;

Nir, WJ ;

Fischer, CM ;

Tayber, OV ;

Errada, PR ;

Grant, JR ;

Keilty, JJ ;

Gosselin, ML ;

Robison, KE ;

Wong, GHW ;

Glucksmann, MA ;

DiStefano, PS .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (19) :12955-12958

[7] A NOVEL PROTEIN THAT INTERACTS WITH THE DEATH DOMAIN OF FAS/APO1 CONTAINS A SEQUENCE MOTIF RELATED TO THE DEATH DOMAIN [J].

BOLDIN, MP ;

VARFOLOMEEV, EE ;

PANCER, Z ;

METT, IL ;

CAMONIS, JH ;

WALLACH, D .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (14) :7795-7798

[8] Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death [J].

Boldin, MP ;

Goncharov, TM ;

Goltsev, YV ;

Wallach, D .

CELL, 1996, 85 (06) :803-815

[9] Biochemical pathways of caspase activation during apoptosis [J].

Budihardjo, I ;

Oliver, H ;

Lutter, M ;

Luo, X ;

Wang, XD .

ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, 1999, 15 :269-290

[10] Apaf-1 oligomerizes into biologically active ∼700-kDa and inactive ∼1.4-MDa apoptosome complexes [J].

Cain, K ;

Bratton, SB ;

Langlais, C ;

Walker, G ;

Brown, DG ;

Sun, XM ;

Cohen, GM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (09) :6067-6070

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