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首页> 外文期刊>Current topics in membranes >Oxidative Modification of Ca~(2+)Channels,Ryanodine Receptors, and the Sarco/Endoplasmic Reticulum Ca~(2+)-ATPase
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Oxidative Modification of Ca~(2+)Channels,Ryanodine Receptors, and the Sarco/Endoplasmic Reticulum Ca~(2+)-ATPase

机译:Ca〜(2+)通道,Ryanodine受体和Sarco /内质网Ca〜(2 +)-ATPase的氧化修饰

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摘要

This paper reviews our current knowledge on the oxidative modifications of mem-brane proteins implicated in Ca~(2+)transport. The high sensitivity of some Ca~(2+)handling proteins, such as the L-type voltage-gated channel, the ryanodine re-ceptor, and the sarco/endoplasmic reticulum Ca~(2+)-ATPase (SERCA) to oxidativemodifications renders them important targets for oxidative regulation/modulationendowing a crosstalk between redox signaling and calcium transients in the cell.The main focus of this review is to correlate either loss or gain of protein functionunder conditions of oxidative stress to selective, potentially reversible, modifica-tions of specific amino acids. Among those special emphasis will be placed onS-nitrosation, S-glutathiolation, disulfide formation, and Tyr nitration, as poten-tial mechanism of redox-dependent signaling in the cell.
机译:本文综述了我们目前对涉及Ca〜(2+)转运的膜蛋白的氧化修饰的认识。某些Ca〜(2+)处理蛋白(如L型电压门控通道,雷诺丁受体和肌浆网/内质网Ca〜(2 +)-ATPase(SERCA))对氧化修饰具有很高的敏感性由于氧化还原信号和细胞内钙瞬变之间存在串扰,因此使它们成为氧化调节/调节的重要靶标。本综述的主要重点是将氧化应激条件下蛋白质功能的丧失或获得与选择性的,可能可逆的修饰相关联。特定氨基酸。作为细胞中氧化还原依赖性信号转导的潜在机制,将特别强调S-亚硝化,S-谷氨酰胺化,二硫键形成和Tyr硝化。

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