【复制和修复过程中mCpG位点突变的替代机制】。

Q3 Medicine
E S Shilkin, D V Petrova, D O Zharkov, A V Makarova
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引用次数: 0

摘要

CpG位点的5-甲基-2'-脱氧胞苷(mC)在表观遗传学基因调控、细胞分化和致癌作用中起着关键作用。尽管mC对正常细胞功能很重要,但CpG二核苷酸是已知的诱变热点。mC的脱氨基作用产生T,导致C→T过渡。然而,最近的几项研究证明了C的表观遗传学修饰对DNA聚合酶和切除修复酶的保真度和效率的影响。综述了表明CpG位点存在脱氨基非依赖性诱变机制的现有数据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Alternative Mechanisms of Mutagenesis at mCpG Sites during Replication and Repair].

5-Methyl-2'-deoxycytidine (mC) at CpG sites plays a key role in the epigenetic gene regulation, cell differentiation, and carcinogenesis. Despite the importance of mC for normal cell function, CpG dinucleotides are known as mutagenesis hotspots. Deamination of mC yields T, causing C→T transitions. However, several recent studies demonstrated the effect of epigenetic modifications of C on the fidelity and efficiency of DNA polymerases and excision repair enzymes. The review summarizes the available data that indicate the existence of deamination-independent mechanisms of mutagenesis at CpG sites.

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来源期刊
Molekulyarnaya Biologiya
Molekulyarnaya Biologiya Medicine-Medicine (all)
CiteScore
0.70
自引率
0.00%
发文量
131
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