Translocation of C. elegans CED-4 to nuclear membranes during programmed cell death
Translocation of C. elegans CED-4 to nuclear membranes during programmed cell death
复制标题
DOI：
10.1126/science.287.5457.1485
复制
发表时间：
2000-02-25
期刊：
影响因子：
56.9
通讯作者：
Horvitz, HR
中科院分区：
文献类型：
--
作者：
Chen, FL;Hersh, BM;Horvitz, HR
秀丽隐杆线虫Bcl-2样蛋白CED-9通过拮抗Apaf-1样细胞死亡激活剂CED-4防止程序性细胞死亡。内源性CED-9和CED-4蛋白定位于野生型胚胎中的线粒体，其中大多数细胞存活。相比之下，在胚胎中，细胞已被诱导死亡，CED-4假定核周定位。CED-4易位诱导的细胞死亡激活剂EGL-1被ced-9中的功能获得性突变阻断，但不依赖于ced-3功能，这表明CED-4易位先于半胱天冬酶激活和程序性细胞死亡的执行阶段。因此，CED-4亚细胞定位的变化可能驱动程序性细胞死亡。
The Caenorhabditis elegans Bcl-2-like protein CED-9 prevents programmed cell death by antagonizing the Apaf-1-like cell-death activator CED-4. Endogenous CED-9 and CED-4 proteins localized to mitochondria in wild-type embryos, in which most cells survive. By contrast, in embryos in which cells had been induced to die, CED-4 assumed a perinuclear localization. CED-4 translocation induced by the cell-death activator EGL-1 was blocked by a gain-of-function mutation in ced-9 but was not dependent on ced-3 function, suggesting that CED-4 translocation precedes caspase activation and the execution phase of programmed cell death. Thus, a change in the subcellular Localization of CED-4 may drive programmed cell death.