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DNA abasic sites (AP sites, apurinic/apyrimidinic sites) are locations in DNA where either a purine or a pyrimidine base has been lost, leaving the deoxyribose backbone intact but missing the nucleobase[1][3][9]. They arise spontaneously or as repair intermediates following removal of damaged nucleobases by DNA glycosylases as part of the base excision repair pathway[3][9][10]. AP sites are highly abundant endogenous DNA lesions, estimated to occur thousands of times per cell per day under physiological conditions[1][3]. If not efficiently repaired—primarily by AP endonucleases such as APE1—they can lead to mutations (especially during DNA replication), single-strand and double-strand breaks, and chromosomal instability, contributing to carcinogenesis, neurodegeneration, and aging[2][3][5][6][9]. Abasic sites are not considered druggable therapeutic targets themselves, but are important biological markers for DNA damage and repair capacity, and their formation or processing can be modulated indirectly by drugs affecting DNA repair enzymes[2][3][10].
Not applicable (abasic sites are DNA lesions, not proteins or receptors acted on directly by drugs)
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