DNA糖基化酶修复氧化胞嘧啶损伤。

Atsushi Katafuchi, Aya Matsuo, Hiroaki Terato, Yoshihiko Ohyama, Hiroshi Ide
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引用次数: 4

摘要

5-羟基尿嘧啶(HOU)和5-羟基胞嘧啶(HOC)是胞嘧啶的主要氧化损伤,具有致突变潜力。因此,需要从DNA中去除HOU和HOC以避免突变。本研究通过DNA聚合酶反应合成了含有HOU和HOC的寡核苷酸底物,并检测了DNA糖基化酶。与尿嘧啶(U)相比,Ung对HOU的活性极低。相比之下,hSMUG1以相当的效率切除HOU和U。Ung和hSMUG1不切除HOC。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Repair of oxidative cytosine damage by DNA glycosylases.

5-Hydroxyuracil (HOU) and 5-hydroxycytosine (HOC) are major oxidative lesions of cytosine with mutagenic potentials. Therefore, HOU and HOC need to be removed from DNA to avoid mutation. In this study, oligonucleotide substrates containing HOU and HOC were synthesized by DNA polymerase reactions and tested for DNA glycosylases. Ung exhibited an extremely low activity for HOU as compared to uracil (U). In contrast, hSMUG1 excised HOU and U with a comparable efficiency. Ung and hSMUG1 did not excise HOC.

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