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程序性坏死(Necroptosis)的分子机制 被引量:9

The molecular mechanism of necroptosis
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摘要 程序性坏死(Necroptosis)是一种不同于凋亡及传统坏死的细胞程序性死亡方式,可由肿瘤坏死因子受体(Tumor necrosis factor receptor,TNFR)或模式识别受体(Pattern recognition receptor,PRR)调控启动。受体相互作用蛋白(Receptor-interacting protein,RIP)1和3是启动necroptosis的两个关键蛋白,necroptosis启动后需要一系列分子传递和执行死亡信号,如多核苷酸二磷酸-核糖聚合酶-1(Poly(ADP-ribose)polymerase,PARP-1)、活性氧簇(Reactive oxygen species,ROS)、Ca2+等,这些分子破坏线粒体及其他细胞器,最终使细胞在缺乏天冬氨酸半胱氨酸蛋白酶(Caspase)的情况下死亡。Necroptosis细胞可将损伤相关模式分子(Damage-associated molecular patterns,DAMPs)暴露到细胞外,被吞噬细胞识别并清除。文章对启动necroptosis的受体分子、传递执行细胞坏死的重要分子和坏死细胞的清除过程进行了概述。 Programmed necrosis called necroptosis, is different from traditional necrosis and apoptosis, it has attracted considerable attention over the last few years. Necroptosis can be initiated through many factors such as tumor necrosis factor receptor (TNFR) or pattern recognition receptor (PRR), and receptor-interacting protein (RIP) 1 and 3 are two key proteins during the process. A lot of molecules have been characterized as modulators and effectors of necroptosis, includ-ing poly(ADP-ribose) polymerase (PARP-1), reactive oxygen species (ROS), Ca2+, which can destruct mitochondria or other organelles and induce cell dead through caspase-independent pathway. Then, damage-associated molecular pattern (DAMP) molecules were released from necroptosis cells, recognized and internalized by phagocytes. Here, we briefly dis-cuss the initiation and execution of necroptosis and the clearance of death cells.
出处 《遗传》 CAS CSCD 北大核心 2014年第6期519-524,共6页 Hereditas(Beijing)
基金 国家重大基础研究发展规划(973计划)项目(编号:2013CB835304) 全国海洋公益项目(编号:201305016) 国家自然科学基金项目(编号:31170353 31202020) 大连市科技计划项目(编号:2013E11SF056)资助
关键词 程序性坏死 肿瘤坏死因子受体 受体相互作用蛋白 necroptosis tumor necrosis factor receptor(TNFR) receptor-interacting protein
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  • 1Harraz MM, Dawson TM, Dawson VL. Advances in neu-ronal cell death 2007. Stroke, 2008, 39(2): 286-288.
  • 2Yu SW, Wang H, Poitras MF, Coombs C, Bowers WJ, Federoff HJ, Poirier GG, Dawson TM, Dawson VL. Me-diation of poly(ADP-ribose)polymerase-1-dependent cell death by apoptosis-inducing factor. Science, 2002, 297(5579): 259-263.
  • 3Andrabi SA, Kim NS, Yu SW, Wang H, Koh DW, Sasaki M, Klaus JA, Otsuka T, Zhang Z, Koehler RC, Hurn PD, Poirier GG, Dawson VL, Dawson TM. Poly(ADP-ribose)(PAR)polymer is a death signal. Proc Natl Acad Sci USA, 2006, 103(48): 18308-18313.
  • 4Yu SW, Andrabi SA, Wang H, Kim NS, Poirier GG, Dawson TM, Dawson VL. Apoptosis-inducing factor medi-ates poly(ADP-ribose)(PAR)polymer-induced cell death. Proc Natl Acad Sci USA, 2006, 103(48): 18314-18319.
  • 5David KK, Andrabi SA, Dawson TM, Dawson VL. Par-thanatos, a messenger of death. Front Biosci, 2009, 14: 1116-1128.
  • 6Edinger AL, Thompson CB. Death by design: apoptosis, necrosis and autophagy. Curr Opin Cell Biol, 2004, 16(6): 663-639.
  • 7Kroemer G, El-Deiry WS, Golstein P, Peter ME, Vaux D, Vandenabeele P, Zhivotovsky B, Blagosklonny MV, Malorni W, Knight RA, Piacentini M, Nagata S, Melino G. Classification of cell death: recommendations of the No-menclature Committee on Cell Death. Cell Death Differ, 2009, 16(1): 3-11.
  • 8Galluzzi L, Kroemer G. Necroptosis: A specialized path-way of programmed necrosis. Cell, 2008, 135(7): 1161-1163.
  • 9Rosenbaum DM, Degterev A, David J, Rosenbaum PS, Roth S, Grotta JC, Cuny GD, Yuan J, Savitz SI. Necrop-tosis, a novel form of caspase-independent cell death, contributes to neuronal damage in a retinal ische-mia-reperfusion injury model. J Neurosci Res, 2010, 88(7): 1569-1576.
  • 10Miao B, Degterev A. Methods to analyze cellular necrop-tosis. Methods Mol Biol, 2009, 559: 79-93.

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