Post-translational modifications as key regulators of TNF-induced necroptosis.
Post-translational modifications as key regulators of TNF-induced necroptosis.
复制标题
翻译后修饰作为 TNF 诱导的坏死性凋亡的关键调节因子。
DOI：
10.1038/cddis.2016.197
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发表时间：
2016-07-07
影响因子：
9
通讯作者：
Cao Y
中科院分区：
文献类型：
--
作者：
Liu X;Shi F;Li Y;Yu X;Peng S;Li W;Luo X;Cao Y
坏死性下垂是一种不依赖于caspase活性的新型细胞程序性死亡。不同的刺激可以引发坏死性下垂。目前，关于坏死性下垂的信息最多的研究来自肿瘤坏死因子(TNF)触发的系统。肿瘤坏死因子诱导的坏死性下垂的发生需要受体相互作用蛋白1和3(RIP1和RIP3)的激活。目前的证据表明，RIP1和RIP3调控这一关键细胞事件的能力受到翻译后修饰的严格控制，这些修饰包括泛素化、磷酸化、caspase 8介导的切割和GlcN酰化。这些调节事件协调地决定了细胞是通过凋亡还是死于坏死下垂而存活或死亡。在这篇综述中，我们重点介绍了在肿瘤坏死因子诱导的坏死性下垂过程中翻译后修饰的最新研究进展，并讨论了这些修饰如何调控复杂而精细的程序性坏死控制。
Necroptosis is a novel form of programmed cell death that is independent of caspase activity. Different stimuli can trigger necroptosis. At present, the most informative studies about necroptosis derive from the tumor necrosis factor (TNF)-triggered system. The initiation of TNF-induced necroptosis requires the kinase activity of receptor-interacting protein 1 and 3 (RIP1 and RIP3). Evidence now reveals that the ability of RIP1 and RIP3 to modulate this key cellular event is tightly controlled by post-translational modifications, including ubiquitination, phosphorylation, caspase 8-mediated cleavage and GlcNAcylation. These regulatory events coordinately determine whether a cell will survive or die by apoptosis or necroptosis. In this review, we highlight recent advances in the study of post-translational modifications during TNF-induced necroptosis and discuss how these modifications regulate the complex and delicate control of programmed necrosis.