Bcl-2 family regulation of neuronal development and neurodegeneration

被引：168
作者：
Akhtar, RS
Ness, JM
Roth, KA
机构：
[1] Univ Alabama Birmingham, Dept Pathol, Div Neuropathol, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Dept Neurobiol, Birmingham, AL 35294 USA
[3] Univ Alabama Birmingham, Dept Pediat, Div Pediat Neurol, Birmingham, AL 35294 USA
来源：
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2004年 / 1644卷 / 2-3期
关键词：
apoptosis; programmed cell death; caspase; Bcl-X; Bax; neuropathology;
D O I：
10.1016/j.bbamcr.2003.10.013
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：
Neuronal cell death is a key feature of both normal nervous system development and neuropathological conditions. The Bcl-2 family, via its regulation of both caspase-dependent and caspase-independent cell death pathways, is uniquely positioned to critically control neuronal cell survival. Targeted gene disruptions of specific bcl-2 family members and the generation of transgenic mice overexpressing anti- or proapoptotic Bel-2 family members have confirmed the importance of the Bcl-2 family in the nervous system. Data from studies of human brain tissue and experimental animal models of neuropathological conditions support the hypothesis that the Bcl-2 family regulates cell death in the mature nervous system and suggest that pharmacological manipulation of Bcl-2 family action could prove beneficial in the treatment of human neurological conditions such as stroke and neurodegenerative diseases. (C) 2003 Elsevier B.V. All rights reserved.
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收藏
页码：189 / 203
页数：15
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