Lethal weapons: DAP-kinase, autophagy and cell death DAP-kinase regulates autophagy
Lethal weapons: DAP-kinase, autophagy and cell death DAP-kinase regulates autophagy
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DOI：
10.1016/j.ceb.2009.11.004
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发表时间：
2010-04-01
影响因子：
7.5
通讯作者：
Kimchi, Adi
中科院分区：
文献类型：
--
作者：
Bialik, Shani;Kimchi, Adi
近年来，DAP-K被认为是自噬的重要调节因子之一，受细胞因子和内质网应激等信号的激活。DAP-K是一种肿瘤抑制因子，可介导多种细胞死亡途径，如细胞凋亡和程序性坏死。同样，功能研究表明，DAP-激酶可能会引导自噬特异性地导致自噬细胞死亡。最近的几项研究已经将DAP-激酶的功能定位到自噬信号的不同阶段。其中包括Beclin-1/磷脂酰肌醇3-激酶(PI(3)K)复合体，这是自噬小体形成所必需的，以及与LC3结合蛋白MAP1B的相互作用，MAP1B可能调节囊泡运输。本文综述了将DAP-K与自噬，特别是自噬细胞死亡的调控联系在一起的功能和机制研究。
Recently, DAP-kinase was identified as one of the essential regulators of autophagy, activated by signals such as cytokines and ER stress. DAP-kinase is a tumor suppressor that mediates several cell death pathways, such as apoptosis and programmed necrosis. Likewise, functional studies suggest that DAP-kinase may direct autophagy specifically towards autophagic cell death. Several recent studies have mapped DAP-kinase function to distinct stages in autophagy signaling. These include the Beclin-1/phosphatidylinositol 3-kinase (PI(3)K) complex, which is necessary for autophagosome formation, and an interaction with the LC3 binding protein, MAP1B, which may regulate vesicle trafficking. This review will summarize the functional and mechanistic studies that have linked DAP-kinase to the regulation of autophagy in general, and autophagic cell death, in particular.