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预的BAX和BAK:是线粒体功能障碍和死亡的必要门户
1Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Science (New York, N.Y.)
|April 28, 2001
概括
激活BAX或BAK蛋白对于启动线粒体功能障碍和细胞死亡至关重要. 缺乏BAX和BAK的细胞抵抗多个亡刺激,突出显示它们在亡中的关键作用.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 线粒体功能障碍是亡的一个关键事件,但启动触发器仍然不清楚.
- 只有BH3的蛋白tBID激活了亲细胞突变的BAX或BAK,导致细胞染色体c的释放.
- 在体内引发线粒体亡的BAX和BAK的确切作用尚未完全理解.
研究的目的:
- 为了确定在亡过程中线粒体功能障碍的关键启动事件.
- 调查BAX和BAK在tBID诱导的亡和其他死亡刺激中的重要作用.
- 阐明线粒体外膜透的网关机制.
主要方法:
- 使用了缺乏Bax和/或Bak.的淘汰细胞模型.
- 使用各种刺激诱导亡,包括tBID,稳定体,紫外线辐射和ER压力剂.
- 评估细胞染色体c释放和细胞活力以测量细胞亡.
主要成果:
- 缺乏Bax和Bak的细胞完全抵抗tBID诱导的细胞染色体c释放和亡.
- 双重缺陷的细胞对多种亡性刺激产生了抵抗力,包括稳素,紫外线,生长因子剥夺,以托波西德,thapsigargin和tunicamycin.
- 单次缺乏BAX或BAK并不能使人具有完全的抗药性.
结论:
- 激活BAX或BAK是线粒体功能障碍在亡中的关键通道.
- BAX 和 BAK 作为各种细胞亡刺激的关键融合点,导致细胞死亡.
- 这些发现澄清了BAX/BAK在启动 mitochondrial apoptosis in vivo中的核心作用.
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