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细胞凋亡中癌基因对核酸内切酶激活的调控

Oncogene regulation of endonuclease activation in apoptosis.

作者信息

McConkey D J, Fernandez A, Trent J, Ananthaswamy H N

机构信息

Department of Cell Biology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.

出版信息

Cancer Lett. 1995 Jul 20;94(1):9-16. doi: 10.1016/0304-3835(95)03835-k.

Abstract

Recent work has demonstrated that oncogenes and tumor suppressor proteins regulate apoptotic cell death. Current efforts are therefore directed at determining how they exert their effects. It appears that oncogenes can control activation of the apoptosis endonuclease(s) either by regulating the signal(s) that trigger the process or via effects on expression and/or activation of key components of the effector machinery, including the endogenous endonuclease itself. This article summarizes the available information on the biochemical mechanisms underlying the effects of oncogenes on endogenous endonuclease activation and presents models to explain the observation that they also regulate alternative cell fates such as cell proliferation and differentiation.

摘要

最近的研究表明,癌基因和肿瘤抑制蛋白可调节凋亡性细胞死亡。因此,目前的研究工作旨在确定它们是如何发挥作用的。癌基因似乎可以通过调节触发该过程的信号,或者通过影响效应机制关键组分的表达和/或激活(包括内源性核酸内切酶本身)来控制凋亡核酸内切酶的激活。本文总结了关于癌基因对内源性核酸内切酶激活作用的生化机制的现有信息,并提出模型来解释它们也调节诸如细胞增殖和分化等其他细胞命运的观察结果。

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