碱基切除修复
碱基切除修复（Base excision repair，BER）是细胞修复受损DNA的一种机制，主要用来修补大小较小、对DNA双股螺旋结构影响较小的损伤，包括脱氨、被烷基化或氧化的碱基，如8-羟基鸟嘌呤（8-oxoG）、7-甲基鸟苷、黄嘌呤与尿嘧啶等[1][2]。大小较大、影响DNA结构较大的损伤（如紫外线造成的胸腺嘧啶二聚体）则是由核苷酸切除修复（NER）途径修补[3]。细菌[4]、古菌[5]与真核生物皆有碱基切除修复的机制。
BER的过程首先由DNA糖基酶移除损伤的碱基，形成AP位点，随后AP核酸内切酶将此位点的磷酸二酯键切除，造成DNA单股断裂，接着再由DNA聚合酶合成缺失的碱基（与一般DNA复制的过程一样有DNA夹参与），可能仅合成单一缺失的碱基后由DNA连接酶完成修补（短补丁修复；short-patch BER），也可能合成2-10个核苷酸以取代下游的若干的核苷酸，由Flap核酸内切酶将旧有的核苷酸切除后，再由DNA连接酶完成修补（长补丁修复；long-patch BER）[6]，两途径的选择由DNA损伤种类、细胞周期、细胞分化状态与物种种类等因素决定[7]。
参考文献
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