线粒体 ATP 合酶的氧化还原调节。
Redox regulation of mitochondrial ATP synthase.
机构信息
Sheng-Bing Wang is at the Division of Cardiology, Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD 21224, USA.
出版信息
Trends Cardiovasc Med. 2013 Jan;23(1):14-8. doi: 10.1016/j.tcm.2012.08.005.
Abstract
Reversible cysteine oxidative post-translational modifications (Ox-PTMs) represent an important mechanism to regulate protein structure and function. In mitochondria, redox reactions can modulate components of the electron transport chain (ETC), the F(1)F(0)-ATP synthase complex, and other matrix proteins/enzymes. Emerging evidence has linked Ox-PTMs to mitochondrial dysfunction and heart failure, highlighting some potential therapeutic avenues. Ox-PTMs can modify a variety of amino acid residues, including cysteine, and have the potential to modulate the function of a large number of proteins. Among this group, there is a selected subset of amino acid residues that can function as redox switches. These unique sites are proposed to monitor the cell's oxidative balance through their response to the various Ox-PTMs. In this review, the role of Ox-PTMs in the regulation of the F(1)F(0)-ATP synthase complex is discussed in the context of heart failure and its possible clinical treatment.
摘要
可逆半胱氨酸氧化翻译后修饰（Ox-PTMs）是调节蛋白质结构和功能的重要机制。在线粒体中，氧化还原反应可以调节电子传递链（ETC）、F(1)F(0)-ATP 合酶复合物和其他基质蛋白/酶的组成部分。新出现的证据将 Ox-PTMs 与线粒体功能障碍和心力衰竭联系起来，突出了一些潜在的治疗途径。Ox-PTMs 可以修饰包括半胱氨酸在内的多种氨基酸残基，并且有可能调节大量蛋白质的功能。在这组中，有一组选定的氨基酸残基可以作为氧化还原开关。这些独特的位点通过对各种 Ox-PTMs 的反应来监测细胞的氧化平衡。在这篇综述中，讨论了 Ox-PTMs 在心力衰竭及其可能的临床治疗中对 F(1)F(0)-ATP 合酶复合物调节的作用。
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