从 DNA 中切除一种耐裂解的氧化脱碱基损伤。
Excision of a lyase-resistant oxidized abasic lesion from DNA.
机构信息
Department of Chemistry, Johns Hopkins University, 3400 North Charles Street, Baltimore, Maryland 21218, USA.
出版信息
Chem Res Toxicol. 2010 Apr 19;23(4):766-70. doi: 10.1021/tx9003984.
Abstract
The C2'-oxidized abasic lesion (C2-AP) is produced in DNA that is subjected to oxidative stress. The lesion disrupts replication and gives rise to mutations that are dependent upon the identity of the upstream nucleotide. Ape1 incises C2-AP, but the 5'-phosphorylated fragment is not a substrate for the lyase activity of DNA polymerase beta. Excision of the lesion is achieved by strand displacement synthesis in the presence of flap endonuclease during which C2-AP and the 3'-adjacent nucleotide are replaced. The oxidized abasic lesion is also a substrate for the bacterial UvrABC nucleotide excision repair system. These data suggest that the redundant nature of DNA repair systems provides a means for removing a lesion that resists excision by short patch base excision repair.
摘要
C2'-氧化脱碱基损伤（C2-AP）是在经受氧化应激的 DNA 中产生的。该损伤会破坏复制并导致依赖于上游核苷酸身份的突变。Ape1 切割 C2-AP，但 5'-磷酸化片段不是 DNA 聚合酶β的裂解酶活性的底物。在带有侧翼核酸内切酶的链置换合成的存在下，通过切除损伤来实现，在此过程中，C2-AP 和 3'-相邻核苷酸被取代。氧化脱碱基损伤也是细菌 UvrABC 核苷酸切除修复系统的底物。这些数据表明，DNA 修复系统的冗余性质为去除抵抗短补丁碱基切除修复的损伤提供了一种手段。
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