Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis

被引：1049

作者：

Marzo, I

Brenner, C

Zamzami, N

Jürgensmeier, JM

Susin, SA

Vieira, HLA

Prévost, MC

Xie, ZH

Matsuyama, S

Reed, JC

Kroemer, G

机构：

[1] CNRS, UPR 420, F-94801 Villejuif, France

[2] Univ Technol Compiegne, CNRS, UPRES A6022, F-60200 Compiegne, France

[3] Burnham Inst, La Jolla, CA 92037 USA

[4] Inst Pasteur, Unite Oncol Virale, F-75724 Paris 15, France

来源：

SCIENCE | 1998年 / 281卷 / 5385期

关键词：

D O I：

10.1126/science.281.5385.2027

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The proapoptotic Bax protein induces cell death by acting on mitochondria. Bax binds to the permeability transition pore complex (PTPC), a composite proteaceous channel that is involved in the regulation of mitochondrial membrane permeability. Immunodepletion of Bax from PTPC or purification of PTPC from Bax-deficient mice yielded a PTPC that could not permeabilize membranes in response to atractyloside, a proapoptotic Ligand of the adenine nucleotide translocator (ANT). Bax and ANT coimmunoprecipitated and interacted in the yeast two-hybrid system: Ectopic expression of Bax Induced cell death in wild-type but not in ANT-deficient yeast. Recombinant Bax and purified ANT, but neither of them alone, efficiently formed atractyloside-responsive channels in artificial membranes. Hence, the proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death.

引用

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页码：2027 / 2031

页数：5

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