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碱基切除修复,一种受翻译后修饰调控的途径。

Base Excision Repair, a Pathway Regulated by Posttranslational Modifications.

作者信息

Carter Rachel J, Parsons Jason L

机构信息

North West Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom.

North West Cancer Research Centre, Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom

出版信息

Mol Cell Biol. 2016 May 2;36(10):1426-37. doi: 10.1128/MCB.00030-16. Print 2016 May 15.

Abstract

Base excision repair (BER) is an essential DNA repair pathway involved in the maintenance of genome stability and thus in the prevention of human diseases, such as premature aging, neurodegenerative diseases, and cancer. Protein posttranslational modifications (PTMs), including acetylation, methylation, phosphorylation, SUMOylation, and ubiquitylation, have emerged as important contributors in controlling cellular BER protein levels, enzymatic activities, protein-protein interactions, and protein cellular localization. These PTMs therefore play key roles in regulating the BER pathway and are consequently crucial for coordinating an efficient cellular DNA damage response. In this review, we summarize the presently available data on characterized PTMs of key BER proteins, the functional consequences of these modifications at the protein level, and also the impact on BER in vitro and in vivo.

摘要

碱基切除修复(BER)是一种重要的DNA修复途径,参与维持基因组稳定性,从而预防人类疾病,如早衰、神经退行性疾病和癌症。蛋白质翻译后修饰(PTM),包括乙酰化、甲基化、磷酸化、SUMO化和泛素化,已成为控制细胞BER蛋白水平、酶活性、蛋白质-蛋白质相互作用和蛋白质细胞定位的重要因素。因此,这些PTM在调节BER途径中起关键作用,进而对于协调有效的细胞DNA损伤反应至关重要。在本综述中,我们总结了目前关于关键BER蛋白特征性PTM的现有数据、这些修饰在蛋白质水平上的功能后果,以及对体外和体内BER的影响。

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