RIPK-dependent necrosis and its regulation by caspases: a mystery in five acts.
RIPK-dependent necrosis and its regulation by caspases: a mystery in five acts.
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DOI：
10.1016/j.molcel.2011.09.003
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发表时间：
2011-10-07
期刊：
影响因子：
16
通讯作者：
Salvesen, Guy S.
中科院分区：
文献类型：
--
作者：
Green, Douglas R.;Oberst, Andrew;Dillon, Christopher P.;Weinlich, Ricardo;Salvesen, Guy S.
Caspase-8、FADD和FLIP响应于死亡受体连接而协调细胞凋亡。然而，不幸的是，这些蛋白质也是正常胚胎发育和免疫细胞增殖所必需的，这一观察结果导致了它们在几个非凋亡过程中的作用。虽然已经提出了许多方案，但最近的遗传和生物化学证据表明，受体相互作用蛋白激酶-1（RIPK 1）和RIPK 3的不受调节的信号传导是半胱天冬酶-8，FADD和FLIP缺陷动物和组织中的致命缺陷。RIPK是已知的杀手，负责具有类似于坏死的特征的非凋亡形式的细胞死亡。然而，caspase-8、FADD和FLIP阻止失控的RIPK激活的机制尚不清楚，在发育和免疫细胞激活过程中触发这些事件的信号仍然不清楚。在这篇评论中，我们将展示目前的证据，根据新的线索重新解释早期的观察结果，并考虑调查可能导致的结果。
Caspase-8, FADD, and FLIP orchestrate apoptosis in response to death receptor ligation. Mysteriously however, these proteins are also required for normal embryonic development and immune cell proliferation, an observation that has led to their implication in several non-apoptotic processes. While many scenarios have been proposed, recent genetic and biochemical evidence points to unregulated signaling by the receptor interacting protein kinases-1 (RIPK1) and RIPK3 as the lethal defect in caspase-8, FADD and FLIP deficient animals and tissues. The RIPKs are known killers, being responsible for a non-apoptotic form of cell death with features similar to necrosis. However, the mechanism by which caspase-8, FADD, and FLIP prevent runaway RIPK activation is unknown, and the signals that trigger these events during development and immune cell activation remain at large. In this review, we will lay out the evidence as it now stands, reinterpreting earlier observations in light of new clues and considering where the investigation might lead.
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