Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8
Regulation of an ATG7-beclin 1 program of autophagic cell death by caspase-8
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DOI：
10.1126/science.1096645
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发表时间：
2004-06-04
期刊：
影响因子：
56.9
通讯作者：
Lenardo, MJ
中科院分区：
文献类型：
--
作者：
Yu, L;Alva, A;Lenardo, MJ
半胱天冬酶在细胞凋亡中起核心作用，细胞凋亡是一种研究充分的程序性细胞死亡途径。可能存在其他可能涉及坏死和自噬的死亡程序，但它们与凋亡的关系和调控机制仍不清楚。我们去。一种新的分子途径，其中受体相互作用蛋白（丝氨酸-苏氨酸激酶）和Jun氨基末端激酶的激活诱导细胞死亡，具有自噬的形态。自噬性死亡需要基因ATG 7和beclin 1，并由caspase-8抑制诱导。涉及半胱天冬酶抑制剂的临床治疗可能会阻止细胞凋亡，但也有促进自噬细胞死亡的意外作用。
Caspases play a central role in apoptosis, a well-studied pathway of programmed cell death. Other programs of death potentially involving necrosis and autophagy may exist, but their relation to apoptosis and mechanisms of regulation remains unclear. We de. ne a new molecular pathway in which activation of the receptor-interacting protein (a serine-threonine kinase) and Jun amino-terminal kinase induced cell death with the morphology of autophagy. Autophagic death required the genes ATG7 and beclin 1 and was induced by caspase-8 inhibition. Clinical therapies involving caspase inhibitors may arrest apoptosis but also have the unanticipated effect of promoting autophagic cell death.