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人类c-myc癌基因领域中的紫外线损伤与修复

UV damage and repair in the domain of the human c-myc oncogene.

作者信息

Bianchi N O, Bianchi M S, Alitalo K, De La Chapelle A

机构信息

IMBICE, La Plata, Argentina.

出版信息

DNA Cell Biol. 1991 Mar;10(2):125-32. doi: 10.1089/dna.1991.10.125.

DOI:10.1089/dna.1991.10.125
PMID:2003876
Abstract

We have used a modification of the Southern hybridization method to analyze the removal of UV-induced pyrimidine cyclobutane dimers from the domain of the c-myc oncogene. The study was performed in human COLO320HSR cells, which exhibit a 30- to 40-fold amplification of c-myc that is maintained in a marker chromosome as a homogeneously staining region. Intron 2 and the region upstream from the gene showed better dimer removal than intron 1 or the region downstream from the c-myc gene. Regions showing less repair coincide with regions that are hotspots for mutations and chromosome translocations. Therefore, it is proposed that the inefficiency of DNA repair may play an important role in the origin of c-myc rearrangements.

摘要

我们采用了改良的Southern杂交方法,来分析c-myc癌基因区域中紫外线诱导的嘧啶环丁烷二聚体的去除情况。该研究在人COLO320HSR细胞中进行,这些细胞中c-myc基因呈现30至40倍的扩增,并作为一个均匀染色区保留在一条标记染色体上。与内含子1或c-myc基因下游区域相比,内含子2和基因上游区域的二聚体去除效果更好。修复较少的区域与突变和染色体易位的热点区域重合。因此,有人提出DNA修复效率低下可能在c-myc重排的起源中起重要作用。

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Evolutionary consequences of nonrandom damage and repair of chromatin domains.染色质结构域非随机损伤与修复的进化后果。
J Mol Evol. 1992 Aug;35(2):156-80. doi: 10.1007/BF00183227.