Biosignal Research Center, Organization of Advanced Science and Technology, Kobe University, Kobe, Hyogo 657-8501, Japan.
Mutat Res. 2010 Mar 1;685(1-2):29-37. doi: 10.1016/j.mrfmmm.2009.08.004. Epub 2009 Aug 12.
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 cancer-prone 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.
核苷酸切除修复在哺乳动物基因组中发挥着关键作用，可以抑制突变和癌变的发生，这些突变和癌变可能是由各种遗传毒性物质诱导的 DNA 损伤引起的，如紫外线和化学化合物。该 DNA 修复途径的一个关键过程是损伤识别，它通过多个步骤完成，包括受损 DNA 结合因子 XPC 和 UV-DDB 的协同作用，这两种因子都与一种易患人类癌症的遗传疾病——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多种水平的精细调控，包括转录激活、翻译后修饰、复合物形成以及通过泛素化的蛋白质降解。
