Abstract
There is convincing evidence that the structure of chromatin may influence both the induction and processing of DNA damage within various parts of the genome that exhibit diverse molecular structures and activities. For a variety of lesions it has been shown that nucleotide excision repair (NER) takes place preferentially in transcriptionally active DNA (Mullenders and Smith 1994). Cyclobutane pyrimidine dimers (CPD) induced by ultraviolet (UV) light as well as DNA adducts induced by chemical carcinogens such as benzo(a)pyrene diol epoxide, aflatoxin B1 and psoralen are more rapidly repaired in transcriptionally active housekeeping genes than in inactive tissue specific genes, ribosomal genes, regions of noncoding DNA, or the genome overall (Bohr et al. 1985; Mellon et al. 1986; Venema et al. 1990; Ruven et al. 1993). However, from the analysis of repair of other bulky lesions in specific sequences in both rodent and human cells it has become clear that not all bulky lesions are preferentially repaired in active genes and that there are no simple rules predicting whether a given lesion is repaired preferentially or not (Mullenders and Smith 1994).
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Mullenders, L.H.F., van Hoffen, A., Vreeswijk, M.P.G., Ruven, HJ., Vrieling, H., van Zeeland, A.A. (1997). UItraviolet-Induced Photolesions: Repair and Mutagenesis. In: Müller-Hermelink, H.K., Neumann, HG., Dekant, W. (eds) Risk and Progression Factors in Carcinogenesis. Recent Results in Cancer Research, vol 143. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60393-8_7
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DOI: https://doi.org/10.1007/978-3-642-60393-8_7
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