Nucleotide excision repair in humans.
Nucleotide excision repair in humans.
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DOI：
10.1016/j.dnarep.2015.09.003
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发表时间：
2015-12
期刊：
影响因子：
3.8
通讯作者：
Spivak G
中科院分区：
文献类型：
--
作者：
Spivak G
Setlow、Howard-Flanders、Hanawalt和他们的同事在20世纪60年代早期对DNA损伤切除和修复复制的证明，构成了核苷酸切除修复（NER）的普遍存在途径的发现。NER中的一系列步骤在从单细胞细菌到复杂的哺乳动物和植物的生物体中是相似的，并且包括识别破坏DNA双螺旋的损伤、加合物或结构，去除含有破坏性损伤的短寡核苷酸，合成复制相对未受损链的修复补丁，以及连接，以将DNA恢复到其原始形式。近20年后发现的NER的转录偶联修复（TCR）子途径致力于从活跃转录基因的模板DNA链中去除损伤。在这篇综述中，我将概述NER在人类中所涉及的基本因素和复合物，并将评论影响这一重要过程的效率的其他因素和代谢过程。
The demonstration of DNA damage excision and repair replication by Setlow, Howard-Flanders, Hanawalt and their colleagues in the early 1960s, constituted the discovery of the ubiquitous pathway of nucleotide excision repair (NER). The serial steps in NER are similar in organisms from unicellular bacteria to complex mammals and plants, and involve recognition of lesions, adducts or structures that disrupt the DNA double helix, removal of a short oligonucleotide containing the offending lesion, synthesis of a repair patch copying the opposite undamaged strand, and ligation, to restore the DNA to its original form. The transcription-coupled repair (TCR) subpathway of NER, discovered nearly two decades later, is dedicated to the removal of lesions from the template DNA strands of actively transcribed genes. In this review I will outline the essential factors and complexes involved in NER in humans, and will comment on additional factors and metabolic processes that affect the efficiency of this important process.