受体相互作用蛋白3——细胞凋亡与坏死的调节阀
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国家自然科学基金(30721001, 30973373, 30772507, 81071811), 国家高技术发展计划(863)(2006AA02A403, 2006AA02A308)和国际科技合作与交流专项(2008DFA31130)资助项目


RIP3: a Possible Trigger of Apoptosis or Necrosis
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This work was supported by grants from The National Natural Science Foundation of China (30721001, 30973373, 30772507, 81071811), Hi-Tech Research and Development Program of China(2006AA02A403, 2006AA02A308) and International Science & Technology Cooperation and Exchanges Program of China(2008DFA31130)

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    摘要:

    综述了受体相互作用蛋白(RIPs)蛋白结构和RIP3调控细胞凋亡与坏死机制的研究进展.受体相互作用蛋白3(receptor-interacting protein 3, RIP3)是丝/苏氨酸蛋白激酶家族成员之一,该蛋白质家族包含一类高度保守的丝/苏氨酸激酶结构域.RIP家族激酶作为细胞应激传感分子,在调控细胞凋亡、细胞坏死和存活通路中发挥重要作用.近年发现,RIP3参与肿瘤坏死因子TNFα诱导的细胞程序化坏死的生物学过程.认识RIP3调控TNFα诱导的细胞凋亡与坏死不同死亡途径转换的分子机制,有助于发现肿瘤治疗的新策略.

    Abstract:

    The receptor-interacting protein 3 (RIP3) is a member of RIP kinase family, which has highly conserved serine/threonine kinase activity. Increasing number of evidences has revealed RIPs to be essential sensors of cellular stress and a key regulator of cell apoptosis, necrosis and survival. Recent studies demonstrating RIP3 as a possible trigger for cellular necrosis in response to TNF-α family of death inducing cytokines may lead to new strategies for developing cancer therapy. This review focuses on the biological characteristics and structure of RIP3 protein, and its cell death control function between apoptotic and necrotic.

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许杨,赵晓航.受体相互作用蛋白3——细胞凋亡与坏死的调节阀[J].生物化学与生物物理进展,2010,37(10):1067-1073

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  • 收稿日期:2010-04-06
  • 最后修改日期:2010-06-09
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  • 在线发布日期: 2010-06-17
  • 出版日期: 2010-10-20