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跨越核苷酸切除修复阈。

Navigating the nucleotide excision repair threshold.

机构信息

Department of Pathology and Laboratory Medicine, Weill Cornell Medical College and Weill Cornell Graduate School of Medical Sciences, New York, New York 10065, USA.

出版信息

J Cell Physiol. 2010 Sep;224(3):585-9. doi: 10.1002/jcp.22205.

DOI:10.1002/jcp.22205
PMID:20458729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2897951/
Abstract

Nucleotide excision repair (NER) is the primary DNA repair pathway that removes helix-distorting DNA strand damage induced by ultraviolet light irradiation or chemical carcinogens to ensure genome integrity. While the core NER proteins that carry out damage recognition, excision, and repair reactions have been identified and extensively characterized, and the NER pathway has been reconstituted in vitro, the regulatory pathways that govern the threshold levels of NER have not been fully elucidated. This mini-review focuses on recently discovered transcriptional and post-translational mechanisms that specify the capacity of NER, and suggests the potential implications of modulating NER activity in cancer prevention and therapeutic intervention.

摘要

核苷酸切除修复 (NER) 是一种主要的 DNA 修复途径,可去除由紫外线照射或化学致癌物引起的扭曲 DNA 链损伤,以确保基因组的完整性。尽管已经鉴定并广泛描述了执行损伤识别、切除和修复反应的核心 NER 蛋白,并且已经在体外重建了 NER 途径,但调节 NER 阈值水平的调控途径尚未完全阐明。本篇综述重点介绍了最近发现的转录和翻译后机制,这些机制特异性地规定了 NER 的能力,并提出了调节 NER 活性在癌症预防和治疗干预中的潜在意义。

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本文引用的文献

1
Two-step recognition of DNA damage for mammalian nucleotide excision repair: Directional binding of the XPC complex and DNA strand scanning.哺乳动物核苷酸切除修复中DNA损伤的两步识别:XPC复合物的定向结合与DNA链扫描
Mol Cell. 2009 Nov 25;36(4):642-53. doi: 10.1016/j.molcel.2009.09.035.
2
CUL4A abrogation augments DNA damage response and protection against skin carcinogenesis.CUL4A缺失增强DNA损伤反应并抵御皮肤癌发生。
Mol Cell. 2009 May 14;34(4):451-60. doi: 10.1016/j.molcel.2009.04.020.
3
The role of the retinoblastoma/E2F1 tumor suppressor pathway in the lesion recognition step of nucleotide excision repair.视网膜母细胞瘤/E2F1肿瘤抑制通路在核苷酸切除修复的损伤识别步骤中的作用。
DNA Repair (Amst). 2009 Jul 4;8(7):795-802. doi: 10.1016/j.dnarep.2009.03.003. Epub 2009 Apr 18.
4
UV-DDB-dependent regulation of nucleotide excision repair kinetics in living cells.活细胞中紫外线损伤DNA结合蛋白(UV-DDB)依赖的核苷酸切除修复动力学调控
DNA Repair (Amst). 2009 Jun 4;8(6):767-76. doi: 10.1016/j.dnarep.2009.02.004. Epub 2009 Mar 21.
5
Regulating post-translational modifications of the eukaryotic replication clamp PCNA.调控真核生物复制夹增殖细胞核抗原的翻译后修饰
DNA Repair (Amst). 2009 Apr 5;8(4):461-9. doi: 10.1016/j.dnarep.2009.01.006. Epub 2009 Feb 13.
6
Circadian oscillation of nucleotide excision repair in mammalian brain.哺乳动物大脑中核苷酸切除修复的昼夜节律振荡。
Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2864-7. doi: 10.1073/pnas.0812638106. Epub 2009 Jan 21.
7
The p38 mitogen-activated protein kinase augments nucleotide excision repair by mediating DDB2 degradation and chromatin relaxation.p38丝裂原活化蛋白激酶通过介导损伤特异性DNA结合蛋白2的降解和染色质松弛来增强核苷酸切除修复。
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The CRL4Cdt2 ubiquitin ligase targets the degradation of p21Cip1 to control replication licensing.CRL4Cdt2泛素连接酶靶向降解p21Cip1以控制复制许可。
Genes Dev. 2008 Sep 15;22(18):2507-19. doi: 10.1101/gad.1703708.
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PCNA-dependent regulation of p21 ubiquitylation and degradation via the CRL4Cdt2 ubiquitin ligase complex.通过CRL4Cdt2泛素连接酶复合体,PCNA依赖的p21泛素化和降解调控
Genes Dev. 2008 Sep 15;22(18):2496-506. doi: 10.1101/gad.1676108.
10
CDK inhibitor p21 is degraded by a proliferating cell nuclear antigen-coupled Cul4-DDB1Cdt2 pathway during S phase and after UV irradiation.细胞周期蛋白依赖性激酶抑制剂p21在S期及紫外线照射后,通过增殖细胞核抗原偶联的Cul4-DDB1-Cdt2途径被降解。
J Biol Chem. 2008 Oct 24;283(43):29045-52. doi: 10.1074/jbc.M806045200. Epub 2008 Aug 14.