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蛋白质谷胱甘肽化在神经退行性疾病发病机制中的作用。

Protein Glutathionylation in the Pathogenesis of Neurodegenerative Diseases.

机构信息

Soonchunhyang Institute of Medi-Bio Science, Soonchunhyang University, Cheonan 31151, Republic of Korea.

Department of Medical Biotechnology, Soonchunhyang University, Asan 31538, Republic of Korea.

出版信息

Oxid Med Cell Longev. 2017;2017:2818565. doi: 10.1155/2017/2818565. Epub 2017 Dec 31.

DOI:10.1155/2017/2818565
PMID:29456785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5804111/
Abstract

Protein glutathionylation is a redox-mediated posttranslational modification that regulates the function of target proteins by conjugating glutathione with a cysteine thiol group on the target proteins. Protein glutathionylation has several biological functions such as regulation of metabolic pathways, calcium homeostasis, signal transduction, remodeling of cytoskeleton, inflammation, and protein folding. However, the exact role and mechanism of glutathionylation during irreversible oxidative stress has not been completely defined. Irreversible oxidative damage is implicated in a number of neurological disorders. Here, we discuss and highlight the most recent findings and several evidences for the association of glutathionylation with neurodegenerative diseases and the role of glutathionylation of specific proteins in the pathogenesis of neurodegenerative diseases. Understanding the important role of glutathionylation in the pathogenesis of neurodegenerative diseases may provide insights into novel therapeutic interventions.

摘要

蛋白质谷胱甘肽化是一种氧化还原介导的翻译后修饰,通过将谷胱甘肽与靶蛋白上的半胱氨酸巯基缀合,调节靶蛋白的功能。蛋白质谷胱甘肽化具有多种生物学功能,如调节代谢途径、钙稳态、信号转导、细胞骨架重塑、炎症和蛋白质折叠。然而,在不可逆氧化应激过程中,谷胱甘肽化的确切作用和机制尚未完全确定。不可逆氧化损伤与许多神经退行性疾病有关。在这里,我们讨论并强调了最近的发现以及谷胱甘肽化与神经退行性疾病相关的一些证据,并探讨了特定蛋白质的谷胱甘肽化在神经退行性疾病发病机制中的作用。了解谷胱甘肽化在神经退行性疾病发病机制中的重要作用,可能为新的治疗干预提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cda/5804111/62c38a7a0d50/OMCL2017-2818565.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cda/5804111/62c38a7a0d50/OMCL2017-2818565.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6cda/5804111/62c38a7a0d50/OMCL2017-2818565.001.jpg

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