Physiological and Pharmacological Control of BAK, BAX, and Beyond

被引：124

作者：

Luna-Vargas, Mark P. A. ^{[1
]}

Chipuk, Jerry Edward ^{[1
,2
,3
,4
,5
]}

机构：

[1] Icahn Sch Med Mt Sinai, Dept Oncol Sci, New York, NY 10029 USA

[2] Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA

[3] Icahn Sch Med Mt Sinai, Diabet Obes & Metab Inst, New York, NY 10029 USA

[4] Icahn Sch Med Mt Sinai, Dept Dermatol, New York, NY 10029 USA

[5] Icahn Sch Med Mt Sinai, Grad Sch Biomed Sci, New York, NY 10029 USA

来源：

TRENDS IN CELL BIOLOGY | 2016年 / 26卷 / 12期

关键词：

SELECTIVE SMALL-MOLECULE; FAMILY-MEMBER BOK; BCL-2; FAMILY; MEMBRANE PERMEABILIZATION; BH3; DOMAINS; BH3-ONLY PROTEINS; LUNG-CANCER; APOPTOSIS; POTENT; INHIBITOR;

D O I：

10.1016/j.tcb.2016.07.002

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cellular commitment to the mitochondria! pathway of apoptosis is accomplished when proapoptotic B cell chronic lymphocytic leukemia/lymphoma (BCL)-2 proteins compromise mitochondrial integrity through the process of mitochondria! outer membrane permeabilization (MOMP). For nearly three decades, intensive efforts focused on the identification and interactions of two key proapoptotic BCL-2 proteins: BCL-2 antagonist killer (BAK) and BCL-2-associated X (BAX). Indeed, we now have critical insights into which BCL-2 proteins interact with BAK/BAX to either preserve survival or initiate MOMP. In contrast, while mitochondria are targeted by BAK/BAX, a molecular understanding of how these organelles govern BAK/BAX function remains less clear. Here, we integrate recent mechanistic insights of proapoptotic BCL-2 protein function in the context of mitochondria! environment, and discuss current and potential pharmacological opportunities to control MOMP in disease.

引用

页码：906 / 917

页数：12

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