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氧化还原应激

Stress on redox.

作者信息

Bánhegyi Gábor, Benedetti Angelo, Csala Miklós, Mandl József

机构信息

Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, 1444 Budapest, POB 260, Hungary.

出版信息

FEBS Lett. 2007 Jul 31;581(19):3634-40. doi: 10.1016/j.febslet.2007.04.028. Epub 2007 Apr 24.

Abstract

Redox imbalance in the endoplasmic reticulum lumen is the most frequent cause of endoplasmic reticulum stress and consequent apoptosis. The mechanism involves the impairment of oxidative protein folding, the accumulation of unfolded/misfolded proteins in the lumen and the initiation of the unfolded protein response. The participation of several redox systems (glutathione, ascorbate, FAD, tocopherol, vitamin K) has been demonstrated in the process. Recent findings have attracted attention to the possible mechanistic role of luminal pyridine nucleotides in the endoplasmic reticulum stress. The aim of this minireview is to summarize the luminal redox systems and the redox sensing mechanisms of the endoplasmic reticulum.

摘要

内质网腔中的氧化还原失衡是内质网应激及随后细胞凋亡最常见的原因。其机制涉及氧化蛋白折叠受损、腔内未折叠/错误折叠蛋白的积累以及未折叠蛋白反应的启动。在此过程中已证实几种氧化还原系统(谷胱甘肽、抗坏血酸、黄素腺嘌呤二核苷酸、生育酚、维生素K)参与其中。最近的研究结果引起了人们对内质网应激中腔内含吡啶核苷酸可能的机制作用的关注。这篇小型综述的目的是总结内质网的腔内氧化还原系统和氧化还原感应机制。

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