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• W2029928269 abstract "In the thirty-third Cold Spring Harbor Symposium, mycolleagues and I reported on our demonstration of Repair replication of DNA in vivo (Hanawalt et al. 1969).We began with the cautious statement, It has been postulated that damaged DNA in bacteria and in some othercellular systems is subject to repair by a mechanism thatinvolves the replacement of the defective single-strandregions with a short stretch of oligonucleotide utilizingthe complementary base pairing information in the intactstrand. That symposium was held just a few years following the discovery of excision repair in Escherichiacoli (Boyce and Howard-Flanders 1964; Pettijohn andHanawalt 1964; Setlow and Carrier 1964). At that meeting, we also learned of an endonuclease activity in extracts of T4-bacteriophage-infected E. coli that incisesUV-irradiated DNA (Takagi et al. 1969). The responsibleenzyme, later designated T4 endoV, was to figure prominently in our research in subsequent years as a highly specific and sensitive probe for UV-induced cyclobutanepyrimidine dimers (CPDs) (Ganesan 1973; van Zeelandet al. 1981; Bohr et al. 1985). The fledgeling DNA repairfield received an important stimulus that same year withthe discovery that repair replication is defective in cellsfrom victims of the rare autosomal recessive hereditarydisease, xeroderma pigmentosum (XP), characterized bysevere sensitivity to sunlight and a several thousandfoldincrease in cutaneous cancers (Cleaver 1968). For manyyears thereafter, it has been considered that nucleotideexcision repair (NER) is of importance primarily for dealing with UV-induced DNA photoproducts—a view reinforced by the fact that the incidence of internal cancers inXP patients is not remarkably enhanced..." @default.
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• W2029928269 date "2000-01-01" @default.
• W2029928269 modified "2023-09-25" @default.
• W2029928269 title "Regulation of Nucleotide Excision Repair in Bacteria and Mammalian Cells" @default.
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• W2029928269 doi "https://doi.org/10.1101/sqb.2000.65.183" @default.
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