人类核苷酸切除修复中核酸内切酶活性的调控。
Regulation of endonuclease activity in human nucleotide excision repair.
机构信息
Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794-3400, USA.
出版信息
DNA Repair (Amst). 2011 Jul 15;10(7):722-9. doi: 10.1016/j.dnarep.2011.04.022. Epub 2011 May 17.
Abstract
Nucleotide excision repair (NER) is a DNA repair pathway that is responsible for removing a variety of lesions caused by harmful UV light, chemical carcinogens, and environmental mutagens from DNA. NER involves the concerted action of over 30 proteins that sequentially recognize a lesion, excise it in the form of an oligonucleotide, and fill in the resulting gap by repair synthesis. ERCC1-XPF and XPG are structure-specific endonucleases responsible for carrying out the incisions 5' and 3' to the damage respectively, culminating in the release of the damaged oligonucleotide. This review focuses on the recent work that led to a greater understanding of how the activities of ERCC1-XPF and XPG are regulated in NER to prevent unwanted cuts in DNA or the persistence of gaps after incision that could result in harmful, cytotoxic DNA structures.
摘要
核苷酸切除修复（NER）是一种 DNA 修复途径，负责从 DNA 中去除由有害的紫外线、化学致癌剂和环境诱变剂引起的各种损伤。NER 需要超过 30 种蛋白质的协同作用，这些蛋白质依次识别损伤，以寡核苷酸的形式切除它，并通过修复合成填充由此产生的缺口。ERCC1-XPF 和 XPG 是负责分别在损伤的 5' 和 3' 端进行切口的结构特异性内切酶，最终导致损伤的寡核苷酸的释放。这篇综述重点介绍了最近的工作，这些工作使我们对 NER 中 ERCC1-XPF 和 XPG 的活性如何受到调节有了更深入的了解，以防止在 DNA 中产生不必要的切割，或在切口后保持缺口，这可能导致有害的、细胞毒性的 DNA 结构。
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