Regulation of damage recognition in mammalian global genomic nucleotide excision repair
Regulation of damage recognition in mammalian global genomic nucleotide excision repair
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DOI：
10.1016/j.mrfmmm.2009.08.004
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发表时间：
2010-03-01
影响因子：
2.3
通讯作者：
Sugasawa, Kaoru
中科院分区：
文献类型：
--
作者：
Sugasawa, Kaoru
在哺乳动物基因组中，核苷酸切除修复在抑制突变和致癌方面发挥着至关重要的作用，这些突变和致癌可以由多种遗传毒性物质引起的DNA损伤引起，如紫外线和化合物。DNA修复途径的一个关键过程，损伤识别，是通过多个步骤完成的，包括受损的DNA结合因子XPC和UV-DDB的协同作用，这两个因子都与人类一种易患癌症的遗传性疾病--着色性干皮病有关。越来越多的证据表明，这些损伤识别因子的表达和功能受到不同水平的精细调控，包括转录激活、翻译后修饰、复合体形成和泛素化导致的蛋白质降解。(C)2009爱思唯尔B.V.保留所有权利。
Nucleotide excision repair operating throughout the mammalian genome plays a crucial role in the suppression of mutagenesis and carcinogenesis, which can arise from DNA lesions induced by a wide variety of genotoxic agents, such as ultraviolet light and chemical compounds. A key process of this DNA repair pathway, damage recognition, is accomplished through multiple steps including concerted actions of the damaged DNA binding factors XPC and UV-DDB, both of which are implicated in a human cancerprone genetic disorder, xeroderma pigmentosum. Accumulating evidence indicates that the expression and functions of these damage recognition factors are subject to exquisite regulation at diverse levels, including transcriptional activation, post-translational modification, complex formation, and protein degradation through ubiquitination. (C) 2009 Elsevier B.V. All rights reserved.