Bcl-2 and Bax function independently to regulate cell death
Bcl-2 and Bax function independently to regulate cell death
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DOI：
10.1038/ng0897-358
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发表时间：
1997-08-01
期刊：
影响因子：
30.8
通讯作者：
Korsmeyer, SJ
中科院分区：
文献类型：
--
作者：
Knudson, CM;Korsmeyer, SJ
BCL-2家族有多种拮抗剂和激动剂蛋白来调节细胞凋亡，它们的功能是否相互依赖尚不确定。用遗传学的方法来解决这个问题，我们利用了Bcl2和Bax的功能获得和丧失模型，发现同样缺乏Bax的小鼠中，Bcl2缺陷小鼠的细胞凋亡和胸腺发育不良特征大部分缺失。Bax的单拷贝在缺乏Bcl2的情况下促进了细胞的凋亡。相反，在Bax缺失的情况下，Bcl2的过表达仍然抑制细胞的凋亡。虽然Bax和Bcl2之间存在体内竞争，但它们都能够独立地调节细胞凋亡。
The BCL-2 family has Various pairs of antagonist and agonist proteins that regulate apoptosis, Whether their function is interdependent is uncertain. Using a genetic approach to address this question, we utilized gain- and loss-of-function models of Bcl-2 and Bax and found that apoptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice are largely absent in mice also deficient in Bax. A single copy of Bax promoted apoptosis in the absence of Bcl-2. In contrast, overexpression of Bcl-2 still repressed apoptosis in the absence of Bax. While an in vivo competition exists between Bax and Bcl-2, each is able to regulate apoptosis independently.