INDUCTION OF APOPTOSIS BY THE BCL-2 HOMOLOG BAK

被引：686

作者：

CHITTENDEN, T ^{[1
]}

HARRINGTON, EA ^{[1
]}

OCONNOR, R ^{[1
]}

FLEMINGTON, C ^{[1
]}

LUTZ, RJ ^{[1
]}

EVAN, GI ^{[1
]}

GUILD, BC ^{[1
]}

机构：

[1] IMPERIAL CANC RES FUND, LONDON WC2A 3PX, ENGLAND

来源：

NATURE | 1995年 / 374卷 / 6524期

关键词：

D O I：

10.1038/374733a0

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：

CELLS are eliminated in a variety of physiological settings by apoptosis, a genetically encoded process of cellular suicide(1,2). Apoptosis comprises an intrinsic cellular defence against tumorigenesis, which, when suppressed, may contribute to the development of malignancies(3). The bcl-2 oncogene, which is activated in follicular lymphomas, functions as a potent suppressor of apoptosis under diverse conditions(4). Here we describe the complementary DNA cloning and functional analysis of a new Bcl-2 homologue, Bak, which promotes cell death and counteracts the protection from apoptosis provided by Bcl-2. Moreover, enforced expression of Bak induces rapid and extensive apoptosis of serum-deprived fibroblasts. This raises the possibility that Bak is directly involved in activating the cell death machinery.

引用

页码：733 / 736

页数：4