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DNA修复中的5-羟甲基胞嘧啶:是新角色还是误导因素?

5-hydroxymethylcytosine in DNA repair: A new player or a red herring?

作者信息

Kantidze Omar L, Razin Sergey V

机构信息

a Institute of Gene Biology RAS , Moscow , Russia.

b LIA1066 French-Russian Joint Cancer Research Laboratory , Villejuif , France.

出版信息

Cell Cycle. 2017 Aug 18;16(16):1499-1501. doi: 10.1080/15384101.2017.1346761. Epub 2017 Jul 26.

DOI:10.1080/15384101.2017.1346761
PMID:28745936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5584847/
Abstract

Active DNA demethylation performed by ten-eleven translocation (TET) enzymes produces 5-hydroxymethylcytosines, 5-formylcytosines, and 5-carboxylcytosines. Recent observations suggest that 5-hydroxymethylcytosine is a stable epigenetic mark rather than merely an intermediate of DNA demethylation. However, the clear functional role of this new epigenetic player is elusive. The contribution of 5-hydroxymethylation to DNA repair is being discussed currently. Recently, Jiang and colleagues have demonstrated that DNA damage response-activated ATR kinase phosphorylates TET3 in mammalian cells and promotes DNA demethylation and 5-hydroxymethylcytosine accumulation. Moreover, TET3 catalytic activity is important for proper DNA repair and cell survival. Here, we discuss recent studies on the potential role of 5-hydroxymethylation in DNA repair and genome integrity maintenance.

摘要

由十一易位(TET)酶介导的主动DNA去甲基化产生5-羟甲基胞嘧啶、5-甲酰基胞嘧啶和5-羧基胞嘧啶。最近的观察结果表明,5-羟甲基胞嘧啶是一种稳定的表观遗传标记,而不仅仅是DNA去甲基化的中间体。然而,这种新的表观遗传因子的明确功能作用仍不清楚。目前正在讨论5-羟甲基化对DNA修复的贡献。最近,蒋等人证明,DNA损伤反应激活的ATR激酶在哺乳动物细胞中使TET3磷酸化,促进DNA去甲基化和5-羟甲基胞嘧啶积累。此外,TET3催化活性对于适当的DNA修复和细胞存活很重要。在此,我们讨论了关于5-羟甲基化在DNA修复和基因组完整性维持中的潜在作用的最新研究。

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