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Titlebook: DNA Repair Protocols; Prokaryotic Systems Pat Vaughan Book 2000 Humana Press 2000

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https://doi.org/10.1007/978-3-642-68106-6r single nucleotide changes and small insertions and deletions. The method is a more simple, nontoxic alternative to the chemical cleavage of the mismatch (CCM) method (.) and as such, the techniques proceed along similar lines; heteroduplex formation then mismatch cleavage then electrophoresis to v
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Repair of A/G and A/8-oxoG Mismatches by MutY Adenine DNA Glycosylaseable products of oxidative DNA damage. The formation of GO in DNA, if not repaired, can lead to misincorporation of A opposite to the GO lesion and result in G:C to T:A transversions (.–.). In ., a family of enzymes, MutY, MutM, and MutT, is involved in defending against the mutagenic effects of GO
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Assays for the Repair of Oxidative Damage by Formamidopyrimidine Glycosylase (Fpg) and 8-)Oxoguanines and may play an important role in the pathogenesis of aging (.). Among ROS, the hydroxyl radical is highly reactive, producing a variety of purine- and pyrimidine-derived lesions in DNA (.,.). A major pathway of hydroxyl radical-induced DNA damage involves attack on the C8 position of purines to p
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Detection of DNA Deoxyribophosphodiesterase Activityathway, oxidized DNA bases are removed by specific DNA glycosylases, leaving apurinic/apyrimidinic (AP) sites in the DNA (.,.). AP sites can also arise spontaneously in DNA through depurination (.) and, being devoid of genetic information, can be both cytotoxic and mutagenic lesions (.–.). Several D
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