Transcription-coupled nucleotide excision repair: New insights revealed by genomic approaches.
Transcription-coupled nucleotide excision repair: New insights revealed by genomic approaches.
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DOI：
10.1016/j.dnarep.2021.103126
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发表时间：
2021-07
期刊：
影响因子：
3.8
通讯作者：
Mao P
中科院分区：
文献类型：
--
作者：
Duan M;Speer RM;Ulibarri J;Liu KJ;Mao P
RNA聚合酶II（Pol II）的延伸受到包括DNA损伤在内的许多因素的影响。大的损伤，如紫外线（UV）辐射引起的病变，阻止Pol II和抑制基因转录，并可能导致基因组不稳定和细胞死亡。细胞激活转录偶联核苷酸切除修复（TC-NER），以消除Pol II阻碍损伤并允许转录恢复。人类的TC-NER起始由Cockayne综合征B组（CS B）蛋白介导，该蛋白与停滞的Pol II结合并促进修复机制的组装。鉴于TC-NER途径的复杂性及其在转录和修复之间的界面上的独特功能，需要新的方法来深入了解该机制。基因组方法的进展提供了一个重要的机会，研究如何启动TC-NER后，损伤诱导的Pol II失速，什么因素参与了这一过程。在这篇综述中，我们讨论了全基因组DNA损伤图谱揭示的新的TC-NER机制和高通量筛选确定的新的TC-NER因子。由于TC-NER进行链特异性修复突变损伤，我们还讨论了这种修复途径如何导致癌症基因组中的突变链不对称性。
Elongation of RNA polymerase II (Pol II) is affected by many factors including DNA damage. Bulky damage, such as lesions caused by ultraviolet (UV) radiation, arrests Pol II and inhibits gene transcription, and may lead to genome instability and cell death. Cells activate transcription-coupled nucleotide excision repair (TC-NER) to remove Pol II-impeding damage and allow transcription resumption. TC-NER initiation in humans is mediated by Cockayne syndrome group B (CSB) protein, which binds to the stalled Pol II and promotes assembly of the repair machinery. Given the complex nature of the TC-NER pathway and its unique function at the interface between transcription and repair, new approaches are required to gain in-depth understanding of the mechanism. Advances in genomic approaches provide an important opportunity to investigate how TC-NER is initiated upon damage-induced Pol II stalling and what factors are involved in this process. In this Review, we discuss new mechanisms of TC-NER revealed by genome-wide DNA damage mapping and new TC-NER factors identified by high-throughput screening. As TC-NER conducts strand-specific repair of mutagenic damage, we also discuss how this repair pathway causes mutational strand asymmetry in the cancer genome.
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影响因子：
4.5
作者：
Gaillard H;Tous C;Botet J;González-Aguilera C;Quintero MJ;Viladevall L;García-Rubio ML;Rodríguez-Gil A;Marín A;Ariño J;Revuelta JL;Chávez S;Aguilera A
通讯作者：
Aguilera A
影响因子：
64.5
作者：
Haradhvala NJ;Polak P;Stojanov P;Covington KR;Shinbrot E;Hess JM;Rheinbay E;Kim J;Maruvka YE;Braunstein LZ;Kamburov A;Hanawalt PC;Wheeler DA;Koren A;Lawrence MS;Getz G
通讯作者：
Getz G
DOI：
10.1073/pnas.1614430113
发表时间：
2016-10-11
影响因子：
11.1
作者：
Hu, Jinchuan;Lieb, Jason D.;Adar, Sheera
通讯作者：
Adar, Sheera
影响因子：
16
作者：
Li CL;Golebiowski FM;Onishi Y;Samara NL;Sugasawa K;Yang W
通讯作者：
Yang W
影响因子：
8.8
作者：
Boeing S;Williamson L;Encheva V;Gori I;Saunders RE;Instrell R;Aygün O;Rodriguez-Martinez M;Weems JC;Kelly GP;Conaway JW;Conaway RC;Stewart A;Howell M;Snijders AP;Svejstrup JQ
通讯作者：
Svejstrup JQ