Bcl-2 family: Life-or-death switch

被引:620
作者
Tsujimoto, Y [1 ]
Shimizu, S [1 ]
机构
[1] Osaka Univ, Grad Sch Med, Biomed Res Ctr, Dept Med Genet,CREST,Japan Sci & Technol Corp, Osaka 5650871, Japan
关键词
apoptosis; Bcl-2; mitochondrion; cytochrome c; VDAC;
D O I
10.1016/S0014-5793(99)01761-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The Bcl-2 family of proteins that consists of anti-apoptotic and pro-apoptotic members determines life-or-death of a cell by controlling the release of mitochondrial apoptogenic factors, cytochrome c and apoptosis-inducing factor (AIF), that activate downstream executional phases, including the activation of death proteases called caspases, Cytochrome c release is, thus, central to apoptotic signal transduction in mammals, making study of the mechanism for cytochrome c release a major issue. Several models for cytochrome c release have been proposed, including rupture of mitochondrial outer membrane and involvement of a specific channel. Here, we pro,ide an overview of recent findings on the role of Bcl-2 family members in the life-or-death decision of a cell. (C) 2000 Federation of European Biochemical Societies.
引用
收藏
页码:6 / 10
页数:5
相关论文
共 56 条
[31]   BCL-2 HETERODIMERIZES IN-VIVO WITH A CONSERVED HOMOLOG, BAX, THAT ACCELERATES PROGRAMMED CELL-DEATH [J].
OLTVAI, ZN ;
MILLIMAN, CL ;
KORSMEYER, SJ .
CELL, 1993, 74 (04) :609-619
[32]   Caspase-9, Bcl-XL, and Apaf-1 form a ternary complex [J].
Pan, GH ;
O'Rourke, K ;
Dixit, VM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (10) :5841-5845
[33]   The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex [J].
Puthalakath, H ;
Huang, DCS ;
O'Reilly, LA ;
King, SM ;
Strasser, A .
MOLECULAR CELL, 1999, 3 (03) :287-296
[34]   Structure of Bcl-x(L)-Bak peptide complex: Recognition between regulators of apoptosis [J].
Sattler, M ;
Liang, H ;
Nettesheim, D ;
Meadows, RP ;
Harlan, JE ;
Eberstadt, M ;
Yoon, HS ;
Shuker, SB ;
Chang, BS ;
Minn, AJ ;
Thompson, CB ;
Fesik, SW .
SCIENCE, 1997, 275 (5302) :983-986
[35]   Channel formation by antiapoptotic protein Bcl-2 [J].
Schendel, SL ;
Xie, ZH ;
Montal, MO ;
Matsuyama, S ;
Montal, M ;
Reed, JC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (10) :5113-5118
[36]   Ion channel activity of the BH3 only Bcl-2 family member, BID [J].
Schendel, SL ;
Azimov, R ;
Pawlowski, K ;
Godzik, A ;
Kagan, BL ;
Reed, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (31) :21932-21936
[37]   Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2 [J].
Schlesinger, PH ;
Gross, A ;
Yin, XM ;
Yamamoto, K ;
Saito, M ;
Waksman, G ;
Korsmeyer, SJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (21) :11357-11362
[38]   Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC [J].
Shimizu, S ;
Narita, M ;
Tsujimoto, Y .
NATURE, 1999, 399 (6735) :483-487
[39]   Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux [J].
Shimizu, S ;
Eguchi, Y ;
Kamiike, W ;
Funahashi, Y ;
Mignon, A ;
Lacronique, V ;
Matsuda, H ;
Tsujimoto, Y .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (04) :1455-1459
[40]  
SHIMIZU S, 1999, IN PRESS P NATL ACAD