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间歇性低氧期间蛋白质的翻译后修饰

Post-translational modification of proteins during intermittent hypoxia.

作者信息

Kumar Ganesh K, Prabhakar Nanduri R

机构信息

The Center for Systems Biology, Department of Medicine, University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA.

出版信息

Respir Physiol Neurobiol. 2008 Dec 10;164(1-2):272-6. doi: 10.1016/j.resp.2008.05.017.

Abstract

Post-translational modification (PTM) is one of the mechanisms by which protein function is regulated by chronic hypoxia. This article presents an overview of recent findings on PTM of proteins induced by chronic intermittent hypoxia (CIH) which is experienced by humans with sleep disordered breathing resulting in autonomic abnormalities. The analysis of PTM of proteins involves electrophoretic separation of tissue or cellular proteins followed by immunolabeling using antibodies specific to native and post-translationally modified forms. Recent results demonstrate that CIH, depending on the pattern, duration and severity of hypoxia, alters the state of phosphorylation of a subset of proteins associated with transcriptional factor activation, signaling pathways and neurotransmitter synthesis via activation of appropriate enzymatic machinery that catalyzes specific phosphorylation reactions. Investigation pertaining to PTMs associated with CIH is at its infant stage and future application of high throughput proteomics techniques are necessary to unravel other important PTMs associated with various critical metabolic and signaling pathways that are activated by intermittent hypoxia.

摘要

翻译后修饰(PTM)是慢性缺氧调节蛋白质功能的机制之一。本文概述了由慢性间歇性缺氧(CIH)诱导的蛋白质翻译后修饰的最新研究结果,患有睡眠呼吸障碍的人类会经历这种慢性间歇性缺氧,进而导致自主神经异常。蛋白质翻译后修饰的分析包括对组织或细胞蛋白质进行电泳分离,然后使用针对天然形式和翻译后修饰形式的特异性抗体进行免疫标记。最近的结果表明,根据缺氧的模式、持续时间和严重程度,慢性间歇性缺氧会通过激活催化特定磷酸化反应的适当酶机制,改变与转录因子激活、信号通路和神经递质合成相关的一部分蛋白质的磷酸化状态。与慢性间歇性缺氧相关的翻译后修饰研究尚处于起步阶段,未来需要应用高通量蛋白质组学技术来揭示与间歇性缺氧激活的各种关键代谢和信号通路相关的其他重要翻译后修饰。

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