Abstract
The major pathway for the removal of oxidative base damage is the DNA base excision repair pathway, found in prokaryotes and eukaryotes (1). In this pathway, oxidized DNA bases are removed by specific DNA glycosylases, leaving apurinic/apyrimidinic (AP) sites in the DNA (1,2). AP sites can also arise spontaneously in DNA through depurination (3) and, being devoid of genetic information, can be both cytotoxic and mutagenic lesions (4–6). Several DNA glycosylases have been found that convert a variety of damaged nucleotide residues to AP sites by removing deaminated, oxidized, or alkylated bases from DNA. Uracil, either misincorporated in place of thymine or resulting from deamination of cytosine, is removed by a specific glycosylase, uracil-DNA glycosylase, found in prokaryotes and eukaryotes (1,4).
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Sandigursky, M., Franklin, W.A. (2000). Detection of DNA Deoxyribophosphodiesterase Activity. In: Vaughan, P. (eds) DNA Repair Protocols. Methods in Molecular Biology™, vol 152. Humana Press. https://doi.org/10.1385/1-59259-068-3:39
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DOI: https://doi.org/10.1385/1-59259-068-3:39
Publisher Name: Humana Press
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