Lindahl T
Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, Herts., Great Britain.
Mutat Res. 1990 May;238(3):305-11. doi: 10.1016/0165-1110(90)90022-4.
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.
本文描述了无嘌呤/无嘧啶（AP）位点的修复过程。主要途径是由AP内切核酸酶水解损伤位点5'侧的稳定磷酸二酯键。5'末端脱氧核糖磷酸残基由一种单独的磷酸二酯酶切除，该酶似乎不是外切核酸酶。DNA聚合酶对单个缺失核苷酸残基进行修复复制并连接，从而完成切除修复过程。本文还考虑了随着时间推移，小的DNA损伤可能在长寿细胞中积累的可能性。这些损伤在化学上应是稳定的，且不应被DNA修复酶识别。
