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Detection and Quantitation of Uracil DNA Glycosylase Activity

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DNA Repair Protocols

Part of the book series: Methods in Molecular Biology™ ((MIMB,volume 152))

Abstract

One of the main determining factors for maintaining the informational integrity of the DNA genomes in all organisms is the efficiency of repair of DNA lesions. DNArepair mechanisms have evolved to counteract the deleterious effects of DNA damage. One such repair mechanism is Base Excision Repair (BER). BER is a repair process initiated by a class of enzymes called glycosylases. These enzymes catalyze the hydrolysis of the N-glycosidic bond, thereby liberating the damaged or inappropriate base and generating an abasic site, which is subsequently acted upon by apurinic/apyrimidinic endonucleases (AP endonucleases). Repair synthesis is then completed by DNA polymerase and DNA ligase (reviewed in ref. 1).

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References

  1. Sancar, A. (1996) DNA excision repair. Annu. Rev. Biochem. 65, 43–81.

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  2. Lindahl, T. (1974) An N-glycosidase from Escherichia coli that releases free uracil from DNA containing deaminated cytosine residues. Proc. Natl. Acad. Sci.USA 71, 3649–3653.

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© 2000 Humana Press Inc.

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O’Grady, G.M. (2000). Detection and Quantitation of Uracil DNA Glycosylase Activity. In: Vaughan, P. (eds) DNA Repair Protocols. Methods in Molecular Biology™, vol 152. Humana Press. https://doi.org/10.1385/1-59259-068-3:33

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  • DOI: https://doi.org/10.1385/1-59259-068-3:33

  • Publisher Name: Humana Press

  • Print ISBN: 978-0-89603-643-7

  • Online ISBN: 978-1-59259-068-1

  • eBook Packages: Springer Protocols

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