细胞色素c
Bcl-2家族
细胞生物学
线粒体
线粒体凋亡诱导通道
细胞凋亡
细胞色素
凋亡体
线粒体内膜
生物
化学
程序性细胞死亡
生物化学
半胱氨酸蛋白酶
酶
作者
Luca Scorrano,Stanley J. Korsmeyer
标识
DOI:10.1016/s0006-291x(03)00615-6
摘要
A crucial amplificatory event in several apoptotic cascades is the nearly complete release of cytochrome c from mitochondria. Proteins of the BCL-2 family which include both anti- and proapoptotic members control this step. Here, we review the proposed mechanisms by which proapoptotic BCL-2 family members induce cytochrome c release. Data support a model in which the apoptotic pathway bifurcates following activation of a "BH3 only" family member. BH3 only molecules induce the activation of the multidomain proapoptotics BAX and BAK, resulting in the permeabilization of the outer mitochondrial membrane and the efflux of cytochrome c. This is coordinated with the activation of a distinct pathway characterized by profound changes of the inner mitochondrial membrane morphology and organization. This mitochondrial remodelling insures complete release of cytochrome c and the onset of mitochondrial dysfunction that is a typical feature of many apoptotic deaths.
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