| Literature DB >> 1692969 |
Abstract
The repair of apurinic/apyrimidinic (AP) sites is described. The major pathway involves hydrolysis of the stable phosphodiester bond on the 5' side of the lesion by an AP endonuclease. The 5' terminal deoxyribose-phosphate residue is excised by a separate phosphodiesterase which does not appear to be an exonuclease. Repair replication of the single missing nucleotide residue by a DNA polymerase and ligation complete the excision-repair process. The possibility that minor DNA lesions may accumulate with time in long-lived cells is considered. Such lesions should be chemically stable and should not be recognized by DNA-repair enzymes.Entities:
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Year: 1990 PMID: 1692969 DOI: 10.1016/0165-1110(90)90022-4
Source DB: PubMed Journal: Mutat Res ISSN: 0027-5107 Impact factor: 2.433