JNK1的选择性激活对于hILP的抗凋亡活性是必要的。
Selective activation of JNK1 is necessary for the anti-apoptotic activity of hILP.
作者信息
Sanna M G, Duckett C S, Richter B W, Thompson C B, Ulevitch R J
机构信息
The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 May 26;95(11):6015-20. doi: 10.1073/pnas.95.11.6015.
Abstract
The balance between the inductive signals and endogenous anti-apoptotic mechanisms determines whether or not programmed cell death occurs. The widely expressed inhibitor of apoptosis gene family includes three closely related mammalian proteins: c-IAP1, c-IAP2, and hILP. The anti-apoptotic properties of these proteins have been linked to caspase inhibition. Here we show that one member of this group, hILP, inhibits interleukin-1beta-converting enzyme-induced apoptosis via a mechanism dependent on the selective activation of c-Jun N-terminal kinase 1. These data demonstrate that apoptosis can be inhibited by an endogenous cellular protein by a mechanism that requires the activation of a single member of the mitogen-activating protein kinase family.
摘要
诱导信号与内源性抗凋亡机制之间的平衡决定了程序性细胞死亡是否会发生。广泛表达的凋亡抑制基因家族包括三种密切相关的哺乳动物蛋白：c-IAP1、c-IAP2和hILP。这些蛋白的抗凋亡特性与半胱天冬酶抑制有关。在此我们表明，该家族的一个成员hILP通过一种依赖于c-Jun氨基末端激酶1选择性激活的机制来抑制白细胞介素-1β转化酶诱导的凋亡。这些数据表明，细胞内一种内源性蛋白可通过一种需要激活丝裂原活化蛋白激酶家族单个成员的机制来抑制凋亡。
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