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Oncogene. 2002 Sep 26;21(43):6614-23. doi: 10.1038/sj.onc.1205912.
2
Model for the initiation of ionizing radiation-induced apoptosis in lymphoid cells by complex DNA double-strand breaks.
Int J Radiat Biol. 2002 Jun;78(6):467-74. doi: 10.1080/09553000110120346.
3
Induction of gene amplification as a gain-of-function phenotype of mutant p53 proteins.基因扩增的诱导作为突变型p53蛋白的功能获得性表型。
Cancer Res. 2002 Jun 1;62(11):3264-70.
4
Processing of nucleopeptides mimicking the topoisomerase I-DNA covalent complex by tyrosyl-DNA phosphodiesterase.酪氨酸-DNA磷酸二酯酶对模拟拓扑异构酶I-DNA共价复合物的核肽的处理
Nucleic Acids Res. 2002 Mar 1;30(5):1198-204. doi: 10.1093/nar/30.5.1198.
5
Increased frequency of DNA deletions in pink-eyed unstable mice carrying a mutation in the Werner syndrome gene homologue.携带沃纳综合征基因同源物突变的粉眼不稳定小鼠中DNA缺失频率增加。
Carcinogenesis. 2002 Jan;23(1):213-6. doi: 10.1093/carcin/23.1.213.
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The tyrosyl-DNA phosphodiesterase Tdp1 is a member of the phospholipase D superfamily.酪氨酰-DNA磷酸二酯酶Tdp1是磷脂酶D超家族的成员之一。
Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12009-14. doi: 10.1073/pnas.211429198. Epub 2001 Sep 25.
7
Pathways for repair of topoisomerase I covalent complexes in Saccharomyces cerevisiae.酿酒酵母中拓扑异构酶I共价复合物的修复途径。
Genes Cells. 2001 Aug;6(8):677-87. doi: 10.1046/j.1365-2443.2001.00452.x.
8
A human topoisomerase I cleavage complex is recognized by an additional human topisomerase I molecule in vitro.在体外，人拓扑异构酶I切割复合物可被另一个人拓扑异构酶I分子识别。
Nucleic Acids Res. 2001 Aug 1;29(15):3195-203. doi: 10.1093/nar/29.15.3195.
9
RET rearrangements in radiation-induced papillary thyroid carcinomas: high prevalence of topoisomerase I sites at breakpoints and microhomology-mediated end joining in ELE1 and RET chimeric genes.辐射诱导的甲状腺乳头状癌中的RET重排：断点处拓扑异构酶I位点的高发生率以及ELE1和RET嵌合基因中的微同源性介导的末端连接
Genomics. 2001 Apr 15;73(2):149-60. doi: 10.1006/geno.2000.6434.
10
Topoisomerase I-mediated cytotoxicity of N-methyl-N'-nitro-N-nitrosoguanidine: trapping of topoisomerase I by the O6-methylguanine.N-甲基-N'-硝基-N-亚硝基胍的拓扑异构酶I介导的细胞毒性：O6-甲基鸟嘌呤对拓扑异构酶I的捕获
Cancer Res. 2001 Jan 1;61(1):53-8.

人拓扑异构酶I切割复合物在体外通过p53刺激的类重组反应进行修复。

Human topoisomerase I cleavage complexes are repaired by a p53-stimulated recombination-like reaction in vitro.

作者信息

Stephan Holger, Grosse Frank, Søe Kent

机构信息

Institute of Molecular Biotechnology, Department of Biochemistry, Beutenbergstrasse 11, D-07745 Jena, Germany.

出版信息

Nucleic Acids Res. 2002 Dec 1;30(23):5087-93. doi: 10.1093/nar/gkf659.

DOI:10.1093/nar/gkf659
PMID:12466531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC137972/
Abstract

Several studies have shown that human topoisomerase I (htopoI) cleaves in the vicinity of various DNA lesions and thereby forms covalent intermediates known as 'cleavage complexes'. Such complexes are detrimental to cells if they are not repaired. Therefore, it is generally accepted that repair pathways must exist for such lesions. We have demonstrated that a htopoI cleavage complex can be recognized by a second topoisomerase I molecule and thereby perform a so-called htopoI 'double cleavage' in vitro. In addition, we found that the double cleavage reaction was stimulated by p53. Here we show that the double cleavage reaction results in the removal of the original htopoI cleavage complex and the generation of a single-stranded gap of approximately 13 nt. This gap supports a sequence-dependent DNA recombination reaction mediated by the second htopoI molecule. Furthermore, we show that p53 strongly stimulates the recombination reaction. We suggest that this reaction may represent a novel p53-dependent topoisomerase I-induced recombination repair (TIRR) pathway for htopoI cleavage complexes.

摘要

多项研究表明，人类拓扑异构酶I（htopoI）在各种DNA损伤附近进行切割，从而形成被称为“切割复合物”的共价中间体。如果这些复合物不被修复，对细胞是有害的。因此，人们普遍认为必然存在针对此类损伤的修复途径。我们已经证明，一个htopoI切割复合物能够被第二个拓扑异构酶I分子识别，从而在体外进行所谓的htopoI“双重切割”。此外，我们发现双重切割反应受到p53的刺激。在此我们表明，双重切割反应导致原始htopoI切割复合物的去除，并产生一个约13个核苷酸的单链缺口。这个缺口支持由第二个htopoI分子介导的序列依赖性DNA重组反应。此外，我们表明p53强烈刺激重组反应。我们认为，该反应可能代表一种针对htopoI切割复合物的新型p53依赖性拓扑异构酶I诱导的重组修复（TIRR）途径。