BCL-2 proteins: Regulators of the mitochondrial apoptotic program

被引：70

作者：

Gross, A ^{[1
]}

机构：

[1] Weizmann Inst Sci, Dept Regulat Biol, IL-76100 Rehovot, Israel

来源：

IUBMB LIFE | 2001年 / 52卷 / 3-5期

关键词：

BCL-2; family; mitochondria; apoptosis;

D O I：

10.1080/15216540152846046

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：

BCL-2 family members are pivotal regulators of the apoptotic process. Mitochondria seem to be a major site-of-action for these proteins. Several prominent alterations occur to mitochondria during apoptosis that include the release of intermembrane space molecules, changes in the membrane potential, ionic changes, and more. All these changes seem to be part of the mitochondrial apoptotic process. The BCL-2 family members are believed to be the major regulators of this program; however, their exact mechanism of action still remains a mystery. In addition, the exact contribution of mitochondria to the apoptotic process is still unclear. This review summarizes and examines the current knowledge regarding these two issues.

引用

页码：231 / 236

页数：6

共 58 条

[21] Cytosol-to-membrane redistribution of Bax and Bcl-X-L during apoptosis [J].

Hsu, YT ;

Wolter, KG ;

Youle, RJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (08) :3668-3672

[22] Bid-induced cytochrome c release is mediated by a pathway independent of mitochondrial permeability transition pore and bax [J].

Kim, TH ;

Zhao, YG ;

Barber, MJ ;

Kuharsky, DK ;

Yin, XM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (50) :39474-39481

[23] Mitochondrial control of cell death [J].

Kroemer, G ;

Reed, JC .

NATURE MEDICINE, 2000, 6 (05) :513-519

[24] Regulation of Bcl-xl channel activity by calcium [J].

Lam, M ;

Bhat, MB ;

Nuñez, G ;

Ma, JJ ;

Distelhorst, CW .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (28) :17307-17310

[25] Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis [J].

Li, K ;

Li, YC ;

Shelton, JM ;

Richardson, JA ;

Spencer, E ;

Chen, ZJ ;

Wang, XD ;

Williams, RS .

CELL, 2000, 101 (04) :389-399

[26] Endonuclease G is an apoptotic DNase when released from mitochondria [J].

Li, LY ;

Luo, L ;

Wang, XD .

NATURE, 2001, 412 (6842) :95-99

[27] The caspase-3 precursor has a cytosolic and mitochondrial distribution: Implications for apoptotic signaling [J].

Mancini, M ;

Nicholson, DW ;

Roy, S ;

Thornberry, NA ;

Peterson, EP ;

Casciola-Rosen, LA ;

Rosen, A .

JOURNAL OF CELL BIOLOGY, 1998, 140 (06) :1485-1495

[28] Overexpression of manganese superoxide dismutase suppresses tumor necrosis factor-induced apoptosis and activation of nuclear transcription factor-KB and activated protein-1 [J].

Manna, SK ;

Zhang, HJ ;

Yan, T ;

Oberley, LW ;

Aggarwal, BB .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (21) :13245-13254

[29] Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis [J].

Marzo, I ;

Brenner, C ;

Zamzami, N ;

Jürgensmeier, JM ;

Susin, SA ;

Vieira, HLA ;

Prévost, MC ;

Xie, ZH ;

Matsuyama, S ;

Reed, JC ;

Kroemer, G .

SCIENCE, 1998, 281 (5385) :2027-2031

[30] The mitochondrial F0F1-ATPase proton pump is required for function of the proapoptotic protein Bax in yeast and mammalian cells [J].

Matsuyama, S ;

Xu, QL ;

Velours, J ;

Reed, JC .

MOLECULAR CELL, 1998, 1 (03) :327-336

← 1 2 3 4 5 6 →