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首页> 外文期刊>Biochemistry >Role of Nucleotide Excision Repair Proteins in Oxidative DNA Damage Repair: an Updating
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Role of Nucleotide Excision Repair Proteins in Oxidative DNA Damage Repair: an Updating

机译：核苷酸切除修复蛋白在氧化性DNA损伤修复中的作用：更新。

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摘要

DNA repair is a crucial factor in maintaining a low steady-state level of oxidative DNA damage. Base excision repair (BER) has an important role in preventing the deleterious effects of oxidative DNA damage, but recent evidence points to the involvement of several repair pathways in this process. Oxidative damage may arise from endogenous and exogenous sources and may target nuclear and mitochondrial DNA as well as RNA and proteins. The importance of preventing mutations associated with oxidative damage is shown by a direct association between defects in BER (i.e. MYH DNA glycosylase) and colorectal cancer, but it is becoming increasingly evident that damage by highly reactive oxygen species plays also central roles in aging and neurodegeneration. Mutations in genes of the nucleotide excision repair (NER) pathway are associated with diseases, such as xeroderma pigmentosum and Cockayne syndrome, that involve increased skin cancer risk and/or developmental and neurological symptoms. In this review we will provide an updating of the current evidence on the involvement of NER factors in the control of oxidative DNA damage and will attempt to address the issue of whether this unexpected role may unlock the difficult puzzle of the pathogenesis of these syndromes.
机译：DNA修复是维持低水平的氧化性DNA损伤的关键因素。碱基切除修复（BER）在防止氧化性DNA损伤的有害作用中起着重要作用，但是最近的证据表明该过程涉及多种修复途径。氧化损伤可能来自内源性和外源性，并可能靶向核和线粒体DNA以及RNA和蛋白质。 BER缺陷（即MYH DNA糖基化酶）与结直肠癌之间的直接联系表明了预防与氧化损伤相关的突变的重要性，但是越来越明显的是，高活性氧对损伤的影响在衰老和神经退行性变中也起着核心作用。 。核苷酸切除修复（NER）途径的基因突变与疾病相关，例如皮肤干燥性色素病和Cockayne综合征，这些疾病涉及增加的皮肤癌风险和/或发育和神经症状。在这篇综述中，我们将提供有关NER因子参与控制氧化性DNA损伤的最新证据，并试图解决这一意外作用是否可能解开这些综合征发病机理的难题。

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