Failure of Bcl-2 to block cytochrome c redistribution during TRAIL-induced apoptosis
Failure of Bcl-2 to block cytochrome c redistribution during TRAIL-induced apoptosis
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DOI：
10.1016/s0014-5793(00)01375-2
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发表时间：
2000-04-07
期刊：
影响因子：
3.5
通讯作者：
Martin, SJ
中科院分区：
文献类型：
--
作者：
Keogh, SA;Walczak, H;Martin, SJ
肿瘤坏死因子 (TNF) 相关凋亡诱导配体 (TRAIL) 是 TNF 细胞因子家族的成员，可促进细胞凋亡和 NF-κ B 激活。在这里，我们证明重组 hu-TRAIL 启动多个半胱天冬酶的激活、线粒体跨膜电位的丧失、BID 的裂解和线粒体细胞色素 c 的重新分配。然而，虽然 Bcl-2 能有效阻断紫外线辐射诱导的细胞色素 c 释放和随后的 CEM 细胞凋亡，但在 TRAIL 治疗的情况下却无法做到这一点。因此，TRAIL 参与至少部分通过线粒体传递的死亡途径，但与参与该途径的其他刺激相比，TRAIL 诱导的细胞色素 c 释放不受 Bcl-2 调节。 (C) 2000 年欧洲生化学会联合会。
Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-kappa B activation. Here we show that recombinant hu-TRAIL initiates the activation of multiple caspases, the loss of mitochondrial transmembrane potential, the cleavage of BID and the redistribution of mitochondrial cytochrome c. However, whereas Bcl-2 efficiently blocked UV radiation-induced cytochrome c release and consequent apoptosis of CEM cells, it failed to do either in the context of TRAIL treatment. Thus, TRAIL engages a death pathway that is at least partially routed via the mitochondria, but in contrast with other stimuli that engage this pathway, TRAIL-induced cytochrome c release is not regulated by Bcl-2. (C) 2000 Federation of European Biochemical Societies.