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首页> 外文期刊>Biochemistry >Long Patch Base Excision Repair Compensates for DNA Polymerase β Inactivation by the C4′-Oxidized Abasic Site
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Long Patch Base Excision Repair Compensates for DNA Polymerase β Inactivation by the C4′-Oxidized Abasic Site

机译：长补丁碱基切除修复通过C4'-氧化的碱基位点补偿DNA聚合酶β的失活

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摘要

The C40n-oxidized abasic site (C4-AP), which is produced by a variety of damaging agents, hasnsignificant consequences for DNA. The lesion is highly mutagenic and reactive, resulting in interstrand cross-nlinks. The base excision repair of DNA containing independently generated C4-AP was examined. C4-AP isnincised byApe1 ∼12-fold less efficiently than an apurinic/apyrimidinic lesion.DNA polymerase β induces thenβ-elimination of incised C4-AP in ternary complexes, duplexes, and single-stranded substrate. However,nexcision from a ternary complex is most rapid. In addition, the lesion inactivates the enzyme afternapproximately seven turnovers on average by reacting with one or more lysine residues in the lyase activensite. Unlike 50n-(2-phosphoryl-1,4-dioxobutane), which very efficiently irreversibly inhibits DNA polymerasenβ, the lesion is readily removed by strand displacement synthesis conducted by the polymerase in conjunctionnwith flap endonuclease 1. DNA repair inhibition by C4-AP may be a partial cause of the cytotoxicity of drugsnthat produce this lesion.
机译：由各种破坏剂产生的C40n氧化的碱基（C4-AP）对DNA的影响不大。病变高度诱变和反应性，导致链间交联。检查了含有独立生成的C4-AP的DNA的碱基切除修复。 C4-AP的Ape1增效效率比紫杉醇/嘧啶的增效效率低约12倍.DNA聚合酶β诱导三元复合物，双链体和单链底物中切割的C4-AP的β消除。然而，三元复合物的切除是最快的。另外，通过与裂解酶活性位点中的一个或多个赖氨酸残基反应，病变平均平均约七次失活后使酶失活。与50n-（2-磷酰基-1,4-二氧丁烷）非常有效地不可逆地抑制DNA聚合酶nβ不同，通过结合变位内切核酸酶1的聚合酶进行的链置换合成，可以轻松去除病变。可能是造成此病灶的药物细胞毒性的部分原因。

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