RIP3 找到了犯罪同伙。
RIP3 finds partners in crime.
机构信息
Department of Pathology, University of Massachusetts Medical School, Worcester, MA 01505, USA.
出版信息
Cell. 2012 Jan 20;148(1-2):17-8. doi: 10.1016/j.cell.2011.12.020.
Abstract
Programmed necrosis has long been recognized as a crucial component of animal development; however, the signaling pathway beyond the protein kinases RIP1 and RIP3 remains largely unknown. Sun et al. and Wang et al. now identify critical factors downstream of RIP1 and RIP3 in programmed necrosis, extending our understanding of this form of cell death.
摘要
程序性细胞坏死长期以来被认为是动物发育的一个重要组成部分；然而，蛋白激酶 RIP1 和 RIP3 之外的信号通路在很大程度上仍然未知。孙等人和王等人现在确定了程序性细胞坏死中 RIP1 和 RIP3 下游的关键因素，扩展了我们对这种细胞死亡形式的理解。
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本文引用的文献
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The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways.线粒体磷酸酶 PGAM5 作为多个细胞坏死死亡途径的汇聚点发挥作用。
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It cuts both ways: reconciling the dual roles of caspase 8 in cell death and survival.这是一把双刃剑：caspase 8 在细胞死亡和存活中的双重角色需要调和。
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Phosphorylation-driven assembly of the RIP1-RIP3 complex regulates programmed necrosis and virus-induced inflammation.磷酸化驱动的RIP1-RIP3复合物组装调节程序性坏死和病毒诱导的炎症。
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Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha.受体相互作用蛋白激酶-3决定细胞对肿瘤坏死因子-α的坏死反应。
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RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis.RIP3，一种能量代谢调节因子，可将肿瘤坏死因子诱导的细胞死亡从凋亡转变为坏死。
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Identification of RIP1 kinase as a specific cellular target of necrostatins.鉴定RIP1激酶作为坏死素的特异性细胞靶点。
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