线粒体在细胞凋亡中的作用：Bcl-2 家族蛋白与线粒体动力学。
Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics.
机构信息
Department of Cell Biology, University of Geneva, Faculty of Sciences, 30 quai Ernest-Ansermet, Geneva 4, Switzerland.
出版信息
Dev Cell. 2011 Jul 19;21(1):92-101. doi: 10.1016/j.devcel.2011.06.017.
Abstract
Mitochondria participate in apoptosis through a range of mechanisms that vary between vertebrates and invertebrates. In vertebrates, they release intermembrane space proteins, such as cytochrome c, to promote caspase activation in the cytosol. This process is the result of the loss of integrity of the outer mitochondrial membrane caused by proapoptotic members of the Bcl-2 family. This event is always accompanied by a fissioning of the organelle. Fission of mitochondria has also been reported to participate in apoptosis in Drosophila and Caenorhabditis elegans. However, in these organisms, mitochondrial membrane permeabilization does not occur and the mechanism by which mitochondrial dynamics participates in cell death remains elusive.
摘要
线粒体通过多种机制参与细胞凋亡，这些机制在脊椎动物和无脊椎动物之间有所不同。在脊椎动物中，它们释放跨膜间隙蛋白，如细胞色素 c，以促进细胞质中半胱天冬酶的激活。这个过程是由促凋亡 Bcl-2 家族成员引起的外膜完整性丧失的结果。这一事件总是伴随着细胞器的分裂。线粒体的分裂也被报道参与了果蝇和秀丽隐杆线虫的细胞凋亡。然而，在这些生物中，线粒体膜通透性不会发生，线粒体动力学参与细胞死亡的机制仍然难以捉摸。
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