Effect of DNA lesions on transcription elongation

Effect of DNA lesions on transcription elongation
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DOI:
10.1016/s0300-9084(99)80046-7
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发表时间:
1999-01-01
期刊:
影响因子:
3.9
通讯作者:
Hanawalt, PC
Hanawalt, PC
中科院分区:
生物学3区
文献类型:
--
作者:
Tornaletti, S;Hanawalt, PC

文献摘要

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相似文献

某些类型的细胞DNA损伤已被证明会干扰复制和转录的基本交易。不仅聚合酶的易位在病变部位被阻止,而且结合的蛋白也可能妨碍修复酶对病变的识别。在转录方面,一种被称为转录偶联修复(transcriptcoupled repair, TCR)的切除修复亚通路已被证明可以作用于细菌、酵母、哺乳动物细胞和许多其他生物体中表达基因的转录链中的病变。哺乳动物细胞中的某些基因(如CSA和CSB)与TCR有独特的关联,而其他基因(如XPC-HR23和XPE)已被证明在核苷酸切除修复的全球基因组途径中起作用,但在TCR中不起作用。为了了解TCR的机制,了解RNA聚合酶延伸复合物如何与受损的DNA模板相互作用是很重要的。本文探讨了不同病变和不同RNA聚合酶系统的关系。(C)法国生物化学和生物分子研究所/爱思唯尔,巴黎。
Some types of damage to cellular DNA have been shown to interfere with the essential transactions of replication and transcription. Not only may the translocation of the polymerase be arrested at the site of the lesion but the bound protein may encumber recognition of the lesion by repair enzymes. In the case of transcription a subpathway of excision repair, termed transcription-coupled repair (TCR) has been shown to operate on lesions in the transcribed strands of expressed genes in bacteria, yeast, mammalian cells and a number of other organisms. Certain genes in mammalian cells (e.g., CSA and CSB) have been uniquely implicated in TCR while others (e.g., XPC-HR23 and XPE) have been shown to operate in the global genomic pathway of nucleotide excision repair, but not in TCR. In order to understand the mechanism of TCR it is important to learn how an RNA polymerase elongation complex interacts with a damaged DNA template. That relationship is explored for different lesions and different RNA polymerase systems in this article. (C) Societe francaise de biochimie et biologie moleculaire / Elsevier, Paris.