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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Recent advances on neuronal caspases in development and neurodegeneration.
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Recent advances on neuronal caspases in development and neurodegeneration.

机译：神经元胱天蛋白酶在发育和神经变性中的最新进展。

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In view of a large and growing literature, this overview emphasizes recent advances in neuronal caspases and their role in cell death. To provide historical perspective, morphology and methods are surveyed with emphasis on early studies on interleukin converting enzyme (ICE) as a prototype for identifying zymogen subunits. The unexpected homology of ICE (caspase-1) to Caenorhabditis elegans death gene CED-3 provided early clues linking caspases to programmed cell death, and led later to discovery of bcl-2 proteins (CED-9 homologs) and 'apoptosis associated factors' (Apafs). Availability of substrates, inhibitors, and cDNAs led to identification of up to 16 caspases as a new superfamily of unique cysteine proteinases targeting Asp groups. Those acting as putative death effectors dismantle neurons by catabolism of proteins essential for survival. Caspases degrade amyloid precursor protein (APP), presenilins (PS1, PS2), tau, and huntingtin, raising questions on their role in neurodegeneration. Brain contains 'inhibitors of apoptosis proteins' (IAPs) survivin and NAIP associated also with some neuronal disorders. Apoptotic stress in neurons initiates a chain of events leading to activation of distal caspases by pathways that remain to be fully mapped. Neuronal caspases play multiple roles for initiation and execution of cell death, for morphogenesis, and in non-mitotic neurons for homeostasis. Recent studies focus on cytochrome c as pivotal in mediating conversion of procaspase-9 as a major initiator for apoptosis. Identifying signaling pathways and related events paves the way to design useful therapeutic remedies to prevent neuronal loss in disease or aging.
机译：鉴于大量且不断增长的文献，本概述着重介绍了神经元胱天蛋白酶及其在细胞死亡中的作用的最新进展。为了提供历史观点，对形态和方法进行了调查，重点研究了白介素转化酶（ICE）作为鉴定酶原亚基的原型的早期研究。 ICE（caspase-1）与秀丽隐杆线虫致死基因CED-3的意外同源性提供了将caspases与程序性细胞死亡联系起来的早期线索，后来导致发现bcl-2蛋白（CED-9同源物）和“凋亡相关因子” （Apafs）。底物，抑制剂和cDNA的可获得性导致多达16个半胱天冬酶被鉴定为针对Asp组的独特半胱氨酸蛋白酶的新超家族。那些假定的死亡效应因子通过对生存必需的蛋白质的分解代谢来分解神经元。胱天蛋白酶可降解淀粉样蛋白前体蛋白（APP），早老蛋白（PS1，PS2），tau和亨廷顿蛋白，这引发了有关它们在神经变性中作用的疑问。大脑含有与某些神经元疾病相关的“凋亡蛋白抑制剂”（survivin）和NAIP。神经元中的细胞凋亡应激会引发一系列事件，从而导致远端胱天蛋白酶激活的途径尚未完全阐明。神经元胱天蛋白酶在细胞死亡的起始和执行，形态发生以及在非有丝分裂神经元中的稳态中起着多种作用。最近的研究集中于细胞色素c在介导procaspase-9作为细胞凋亡的主要引发剂的转化中起关键作用。识别信号传导途径和相关事件为设计有用的治疗方法铺平了道路，以防止疾病或衰老中的神经元丢失。

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