Abstract
THE first step of the model of the excision repair mechanism for ultraviolet-irradiated DNA is the incision of the DNA adjacent to the pyrimidine dimer by an endonuclease (ultraviolet endonuclease)1. Such endonucleases have been purified from M. luteus2 and T4-infected E. coli3 and partially purified from uninfected E. coli4. Human cells also perform excision-repair of ultraviolet-irradiated DNA5 and ultraviolet endonuclease activity has been identified in extracts of HeLa cells6,7 and human fibroblasts7. An ultraviolet endonuclease has been purified from rat liver8. But it has not been proved that any of these enzymes are true repair endonucleases, for the proof of an enzyme's role in cellular metabolism rests on analysis of its activity in mutants4. Cells from patients with xeroderma pigmentosum (XP) seem to be excision-repair defective mutants1 and have been postulated to lack the ultraviolet endonuclease activity necessary to initiate repair9.
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DUKER, N., TEEBOR, G. Different ultraviolet DNA endonuclease activity in human cells. Nature 255, 82–84 (1975). https://doi.org/10.1038/255082a0
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DOI: https://doi.org/10.1038/255082a0
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