Abstract
Human cells contain singular DNA repair pathways to excise critical lesions from DNA (Lindahl, 1982; Teebor and Frenkel, 1983; Friedberg, 1985, Strauss, 1985). Two major excision repair pathways have been identified. In nucleotide excision repair, the DNA adduct is released within an oligonucleotide after sequential action of an undetermined number of enzymes. In contrast, in base excision repair, the DNA adduct is released in the initial enzymatic step of the pathway. This reaction is catalyzed by a DNA glycosylase which cleaves the base-sugar glycosyl bond. Human cells may contain a family of DNA glycosylases each of which may be responsible for the removal of a specific modified base. Thus, the uracil DNA glycoslase removes uracil from DNA. Uracil may arise in DNA by the deamination of cytidine residues (Hayatsu, 1977) or by the incorporation of 5′dUMP during DNA synthesis (Bessman, et al., 1958). The former, by definition, would be a mutagenic event if left unrepaired. Uracil excision results in the formation of an apyrimidinic site in DNA. That site is incised by the apurinic/apyrimidinic acid (AP) endonuclease to form a single strand break. Subsequent catalysis by a DNA polymerase and DNA ligase would be minimal requirements for the completion of base excision repair.
Keywords
- Nucleotide Excision Repair
- Base Excision Repair
- Crude Cell Extract
- Normal Human Fibroblast
- Normal Human Cell
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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© 1989 Plenum Press, New York
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Sirover, M.A., Seal, G., Vollberg, T.M., Cool, B.L., Brech, K., Karp, S.J. (1989). Detection of Unique Antigenic Lesions in the Uracil DNA Glycosylase from Bloom’s Syndrome. In: Lambert, M.W., Laval, J. (eds) DNA Repair Mechanisms and Their Biological Implications in Mammalian Cells. NATO ASI Series, vol 182. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1327-4_36
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DOI: https://doi.org/10.1007/978-1-4684-1327-4_36
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