Control of mitochondrial permeability by Bcl-2 family members

被引：329

作者：

Sharpe, JC ^{[1
]}

Arnoult, D ^{[1
]}

Youle, RJ ^{[1
]}

机构：

[1] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2004年 / 1644卷 / 2-3期

关键词：

Bax; Bid; mitochondrion; channel;

D O I：

10.1016/j.bbamcr.2003.10.016

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：

Programmed cell death (apoptosis) is regulated by the Bcl-2 family of proteins. Although it remains unclear how these family members control apoptosis, they clearly have the capacity to regulate the permeability of intracellular membranes to ions and proteins. Proapoptotic members of the Bcl-2 family, especially Bax and Bid, have been extensively analyzed for the ability to form channels in membranes and to regulate preexisting channels. Anti-apoptotic members of the family tend to have the opposing effects on membrane channel formation. The molecular mechanisms of the different models for the permeabilization of membranes by the Bcl-2 family members and the regulation of Bcl-2 family member subcellular localizations are discussed. (C) 2003 Elsevier B.V. All rights reserved.

引用

页码：107 / 113

页数：7

共 73 条

[1] Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria [J].

Antonsson, B ;

Montessuit, S ;

Lauper, S ;

Eskes, R ;

Martinou, JC .

BIOCHEMICAL JOURNAL, 2000, 345 :271-278

[2] Inhibition of Bax channel-forming activity by Bcl-2 [J].

Antonsson, B ;

Conti, F ;

Ciavatta, A ;

Montessuit, S ;

Lewis, S ;

Martinou, I ;

Bernasconi, L ;

Bernard, A ;

Mermod, JJ ;

Mazzei, G ;

Maundrell, K ;

Gambale, F ;

Sadoul, R ;

Martinou, JC .

SCIENCE, 1997, 277 (5324) :370-372

[3] Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells [J].

Antonsson, B ;

Montessuit, S ;

Sanchez, B ;

Martinou, JC .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (15) :11615-11623

[4] Mitochondrial release of AIF and EndoG requires caspase activation downstream of Bax/Bak-mediated permeabilization [J].

Arnoult, D ;

Gaume, B ;

Karbowski, M ;

Sharpe, JC ;

Cecconi, F ;

Youle, RJ .

EMBO JOURNAL, 2003, 22 (17) :4385-4399

[5] Caspase inhibition prevents the mitochondrial release of apoptosis-inducing factor [J].

Arnoult, D ;

Karbowski, M ;

Youle, RJ .

CELL DEATH AND DIFFERENTIATION, 2003, 10 (07) :845-849

[6] Mitochondrial release of apoptosis-inducing factor occurs downstream of cytochrome c release in response to several proapoptotic stimuli [J].

Arnoult, D ;

Parone, P ;

Martinou, JC ;

Antonsson, B ;

Estaquier, J ;

Ameisen, JC .

JOURNAL OF CELL BIOLOGY, 2002, 159 (06) :923-929

[7] Bax-type apoptotic proteins porate pure lipid bilayers through a mechanism sensitive to intrinsic monolayer curvature [J].

Basañez, G ;

Sharpe, JC ;

Galanis, J ;

Brandt, TB ;

Hardwick, JM ;

Zimmerberg, J .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (51) :49360-49365

[8] Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations [J].

Basañez, G ;

Nechushtan, A ;

Drozhinin, O ;

Chanturiya, A ;

Choe, E ;

Tutt, S ;

Wood, KA ;

Hsu, YT ;

Zimmerberg, J ;

Youle, RJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (10) :5492-5497

[9] Biphasic translocation of Bax to mitochondria [J].

Capano, M ;

Crompton, M .

BIOCHEMICAL JOURNAL, 2002, 367 :169-178

[10] Involvement of the N-terminus of Bax in its intracellular localization and function [J].

Cartron, PF ;

Moreau, C ;

Oliver, L ;

Mayat, E ;

Meflah, K ;

Vallette, FM .

FEBS LETTERS, 2002, 512 (1-3) :95-100

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