Repair of deaminated bases in DNA 1 2 1Guest Editor: Miral Dizdaroglu 2This article is part of a series of reviews on “Oxidative DNA Damage and Repair.” The full list of papers may be found on the homepage of the journal.

摘要: Deamination of DNA bases can occur spontaneously, generating highly mutagenic lesions such as uracil, hypoxanthine, and xanthine. When cells are under oxidative stress that is induced either by oxidizing agents or mitochondrial dysfunction, additional deamination products 5-hydroxymethyluracil (5-HMU) 5-hydroxyuracil (5-OH-Ura) formed. The cellular level these increased substantially when exposed to damaging agent, ionizing radiation, redox reagents, nitric oxide, others. repair predominantly through the base excision (BER) pathway, a major pathway initiated lesion specific glycosylases. In BER, removed combined action glycosylase an AP endonuclease, leaving behind one-base gap. gapped product then further repaired sequential polymerase ligase. glycosylases recognize 5-OH-Ura, 5-HMU (derived from 5-methylcytosine) T/G mismatch 5-methylcytosine/G pair) present in most cells. Many have been cloned well characterized. yeast mammalian cells, hypoxanthine efficiently methylpurine N-glycosylase, it thought BER might be important for hypoxanthine. contrast, no xanthine has identified Escherichia coli, enzyme activity initiates endonuclease V. Endonuclease V hydrolyzes second phosphodiester bond 3' lesion. It hypothesized cleaved alternative (AER) requires participation 5' 3'-5' exonuclease remove damaged base. process completed actions sequence homologs all kingdoms, conceivable also