磷脂酰肌醇 3-激酶信号通路通过抑制 XIAP 的降解来延迟仙台病毒诱导的细胞凋亡。
Phosphatidylinositol 3-kinase signaling delays sendai virus-induced apoptosis by preventing XIAP degradation.
机构信息
Department of Molecular Genetics/NE20, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
出版信息
J Virol. 2011 May;85(10):5224-7. doi: 10.1128/JVI.00053-11. Epub 2011 Mar 2.
Abstract
Sendai virus (SeV) infection causes apoptosis, which is manifested only late after infection; however, inhibition of phosphatidylinositol 3-kinase (PI3K) dramatically accelerates the process. We report here that rapid apoptosis uses the same mitochondrial apoptotic pathway as slow apoptosis. Cytoplasmic cytochrome c (cyt c) was released early in both cases, but the antiapoptotic protein XIAP prevented early activation of the caspases in cells with active PI3K. When the enzyme was inhibited, XIAP was degraded rapidly in infected cells, allowing cyt c to cause caspase activation and early apoptosis. Thus, SeV infection-mediated apoptosis is temporally regulated by the prevention of XIAP degradation by PI3K.
摘要
仙台病毒（SeV）感染会导致细胞凋亡，这种凋亡仅在感染后晚期才会出现；然而，磷脂酰肌醇 3-激酶（PI3K）的抑制作用会显著加速这一过程。我们在此报告，快速凋亡和缓慢凋亡使用相同的线粒体凋亡途径。在这两种情况下，细胞质细胞色素 c（cyt c）都较早释放，但抗凋亡蛋白 XIAP 可防止 PI3K 活性细胞中 caspase 的早期激活。当抑制该酶时，感染细胞中 XIAP 会迅速降解，从而使 cyt c 引起 caspase 激活和早期凋亡。因此，SeV 感染介导的凋亡受 PI3K 阻止 XIAP 降解的时间调控。
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