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人类硫氧还蛋白网络的氧化还原调节

Redox regulation of human thioredoxin network.

作者信息

Kondo Norihiko, Nakamura Hajime, Masutani Hiroshi, Yodoi Junji

机构信息

Department of Biological Responses, Institute for Virus Research, Kyoto University, Translational Research Center Kyoto University Hospital, Kyoto, Japan.

出版信息

Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1881-90. doi: 10.1089/ars.2006.8.1881.

DOI:10.1089/ars.2006.8.1881
PMID:16987040
Abstract

Oxidative stresses are largely mediated by intracellular protein oxidations by reactive oxygen species (ROS). Host cells are equipped with antioxidants that scavenge ROS. The cellular reduction/oxidation (redox) balance is maintained by ROS and antioxidants. Accumulating evidence suggests that the redox balance plays an important role in cellular signaling through the redox modification of cysteine residues in various important components of the signal transduction pathway. Thioredoxin (TRX) is a small protein playing important roles in cellular responses, including cell growth, cell cycle, gene expression, and apoptosis, to maintain the redox circumstance. Moreover, many recent papers have shown that the redox regulation by TRX is deeply involved in the pathogenesis of various oxidative stress-associated disorders. This review focuses on TRX and its related molecules, and discusses the role of TRX-dependent redox regulation in oxidative stress-induced signal transduction.

摘要

氧化应激很大程度上由活性氧(ROS)介导的细胞内蛋白质氧化作用引起。宿主细胞配备有清除ROS的抗氧化剂。细胞的还原/氧化(redox)平衡由ROS和抗氧化剂维持。越来越多的证据表明,氧化还原平衡通过对信号转导途径中各种重要成分的半胱氨酸残基进行氧化还原修饰,在细胞信号传导中发挥重要作用。硫氧还蛋白(TRX)是一种小蛋白,在维持氧化还原环境的细胞反应(包括细胞生长、细胞周期、基因表达和细胞凋亡)中发挥重要作用。此外,最近许多论文表明,TRX的氧化还原调节与各种氧化应激相关疾病的发病机制密切相关。本综述聚焦于TRX及其相关分子,并探讨TRX依赖性氧化还原调节在氧化应激诱导的信号转导中的作用。

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