کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9909060 | 1548430 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Transcription-coupled repair: Impact on UV-induced mutagenesis in cultured rodent cells and mouse skin tumors
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
UV-induced cyclobutane pyrimidine dimers (CPDs) are removed with accelerated speed from the transcribed strand of expressed genes in cultured mammalian cells by a process called transcription-coupled repair (TCR). It has been previously shown that this phenomenon has consequences for the molecular nature of the mutations induced by UV-light. Here, we review these data and show that TCR has not only a clear impact on UV-induced mutations in cultured mammalian cells but also on genes involved in tumor formation in the skin of UV-exposed mice. Mutations observed in the p53 gene in UV-induced squamous cell carcinoma are predominantly found at sites of dipyrimidines in the non-transcribed strand. In contrast, in UVC-irradiated Csbâ/â Chinese hamster cells and in UVB-induced tumors in the Csbâ/â mouse, almost all mutations are at positions of dipyrimidine sites in the transcribed strand of the mutated gene. Csbâ/â mice appear to be susceptible to UVB-induced skin cancer in contrast to the human CSB patients. We speculate that the UVB-induced cancer susceptibility of Csbâ/â mice is related to the absence of TCR as well as to a lack of a compensating global genome repair system for CPDs in mice.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 577, Issues 1â2, 4 September 2005, Pages 170-178
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 577, Issues 1â2, 4 September 2005, Pages 170-178
نویسندگان
Albert A. van Zeeland, Maaike P.G. Vreeswijk, Frank R. de Gruijl, Henk J. van Kranen, Harry Vrieling, Leon F.H. Mullenders,