Abstract
EXCISION repair plays a vital role in the recovery of human cells from ultraviolet irradiation1, but it does not remove all lesions from DNA, even when they are as potent as cyclobutane pyrimidine dimers. In fact, only about 50% to 75% of the dimers produced by low fluences of ultraviolet light are excised and the remainder persist in the DNA for at least 24 to 48 h2–4. We have investigated why some but not all dimers are excised. Our conclusion is that dimers, and possibly other ultraviolet photoproducts, persist in tracts of DNA which are rendered refractory to excision repair by a ‘mask’ of protein.
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WILKINS, R., HART, R. Preferential DNA Repair in Human Cells. Nature 247, 35–36 (1974). https://doi.org/10.1038/247035a0
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DOI: https://doi.org/10.1038/247035a0
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