Mitochondrial involvement in the point of no return in neuronal apoptosis
Mitochondrial involvement in the point of no return in neuronal apoptosis
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DOI：
10.1016/s0300-9084(02)01372-x
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发表时间：
2002-02-01
期刊：
影响因子：
3.9
通讯作者：
Johnson, EM
中科院分区：
文献类型：
--
作者：
Chang, LK;Putcha, GV;Johnson, EM
程序性细胞死亡（PCD）有助于各种组织（包括神经系统）的发育、维持和病理学。许多分子、生物化学和遗传事件发生在经历PCD的细胞内。其中一些事件与细胞的长期存活不相容，因为它们具有不可逆转的灾难性后果。这种变化的开始标志着不可逆转的点，一个决定性的监管事件被称为“死亡承诺”。在这篇综述中，我们讨论了在神经生长因子剥夺诱导的交感神经元死亡中死亡承诺的基础事件。在这个模型系统中的研究结果牵连作为一个重要的网站的监管承诺，以死在存在或不存在的半胱天冬酶抑制剂的peption。(C)2002法国生物化学与生物分子学会/科学与医学版Elsevier SAS。All rights reserved.
Programmed cell death (PCD) contributes to development, maintenance, and pathology in various tissues, including the nervous system. Many molecular, biochemical, and genetic events occur within cells undergoing PCD. Some of these events are incompatible with long-term cell survival because they have irreversible, catastrophic consequences. The onset of such changes marks the point of no return, a decisive regulatory event termed 'the commitment-to-die.' In this review, we discuss events that underlie the commitment-to-die in nerve growth factor-deprivation-induced death of sympathetic neurons. Findings in this model system implicate the mitochondrion as an important site of regulation for the commitment-to-die in the presence or absence of caspase inhibition. (C) 2002 Societe francaise de biochimie et biologic moleculaire / Editions scientifiques et medicales Elsevier SAS. All rights reserved.