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DNA repair. The bases for Cockayne syndrome.DNA修复。科凯恩综合征的基础。
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UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome.紫外线损伤会导致具有着色性干皮病D型(XP-D)和科凯恩综合征综合特征患者的细胞中出现不受控制的DNA断裂。
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Cells from XP-D and XP-D-CS patients exhibit equally inefficient repair of UV-induced damage in transcribed genes but different capacity to recover UV-inhibited transcription.来自着色性干皮病D型(XP-D)和XP-D补体缺陷型(XP-D-CS)患者的细胞在转录基因中对紫外线诱导损伤的修复效率同样低下,但恢复紫外线抑制转录的能力不同。
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The organization of replication and transcription.复制与转录的组织形式。
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Action of DNA repair endonuclease ERCC1/XPF in living cells.DNA修复核酸内切酶ERCC1/XPF在活细胞中的作用。
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Molecular mechanism of nucleotide excision repair.核苷酸切除修复的分子机制。
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Transcription response and nucleotide excision repair.
Mutat Res. 1998 Nov 12;409(2):59-64. doi: 10.1016/s0921-8777(98)00048-2.
9
Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair.着色性干皮病C组蛋白复合体是全基因组核苷酸切除修复的起始因子。
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10
Yeast RNA polymerase II transcription in vitro is inhibited in the presence of nucleotide excision repair: complementation of inhibition by Holo-TFIIH and requirement for RAD26.在核苷酸切除修复存在的情况下,体外酵母RNA聚合酶II转录受到抑制:全酶TFIIH对抑制作用的互补及RAD26的需求。
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细胞核中局部紫外线诱导的DNA损伤会导致局部转录抑制。

Local UV-induced DNA damage in cell nuclei results in local transcription inhibition.

作者信息

Moné M J, Volker M, Nikaido O, Mullenders L H, van Zeeland A A, Verschure P J, Manders E M, van Driel R

机构信息

Swammerdam Institute for Life Sciences, BioCentrum Amsterdam, University of Amsterdam, Plantage Muidergracht 12, 1018 TV Amsterdam, The Netherlands.

出版信息

EMBO Rep. 2001 Nov;2(11):1013-7. doi: 10.1093/embo-reports/kve224.

DOI:10.1093/embo-reports/kve224
PMID:11713193
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1084123/
Abstract

UV-induced DNA damage causes cells to repress RNA synthesis and to initiate nucleotide excision repair (NER). NER and transcription are intimately linked processes. Evidence has been presented that, in addition to damaged genes, undamaged loci are transcriptionally inhibited. We investigated whether RNA synthesis from undamaged genes is affected by the presence of UV damage elsewhere in the same nucleus, using a novel technique to UV irradiate only part of a nucleus. We show that the basal transcription/repair factor TFIIH is recruited to the damaged nuclear area, partially depleting the undamaged nuclear area. Remarkably, this sequestration has no effect on RNA synthesis. This result was obtained for cells that are able to carry out NER and for cells deficient in NER. We conclude that cross talk between NER and transcription occurs only over short distances in nuclei of living cells.

摘要

紫外线诱导的DNA损伤会导致细胞抑制RNA合成并启动核苷酸切除修复(NER)。NER和转录是紧密相连的过程。已有证据表明,除了受损基因外,未受损的基因座也会受到转录抑制。我们使用一种仅对细胞核的一部分进行紫外线照射的新技术,研究了来自未受损基因的RNA合成是否会受到同一细胞核中其他位置紫外线损伤的影响。我们发现,基础转录/修复因子TFIIH会被招募到受损的核区域,从而使未受损的核区域部分耗尽。值得注意的是,这种隔离对RNA合成没有影响。无论是能够进行NER的细胞还是NER缺陷的细胞,都得到了这一结果。我们得出结论,在活细胞的细胞核中,NER和转录之间的相互作用仅在短距离内发生。