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单纯疱疹病毒感染或转化细胞后合成的宿主细胞DNA的低甲基化。

Hypomethylation of host cell DNA synthesized after infection or transformation of cells by herpes simplex virus.

作者信息

Macnab J C, Adams R L, Rinaldi A, Orr A, Clark L

机构信息

MRC Institute of Virology, Glasgow, United Kingdom.

出版信息

Mol Cell Biol. 1988 Apr;8(4):1443-8. doi: 10.1128/mcb.8.4.1443-1448.1988.

DOI:10.1128/mcb.8.4.1443-1448.1988
PMID:2837642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC363301/
Abstract

Infection of rat embryo cells with herpes simplex virus type 2 caused undermethylation of host cell DNA synthesized during infection. DNA made prior to infection was not demethylated, but some of its degradation products, including methyl dCMP, were incorporated into viral DNA. The use of mutant virus showed that some viral DNA synthesis appears to be required for the inhibition of methylation. Inhibition of methylation cannot be explained by an absence of DNA methyltransferase as the activity of this enzyme did not change during the early period of infection. Inhibition of host cell DNA methylation may be an important step in the transformation of cells by herpesviruses, and various transformed cell lines tested showed reduced levels of DNA methylation.

摘要

用2型单纯疱疹病毒感染大鼠胚胎细胞会导致感染期间合成的宿主细胞DNA发生甲基化不足。感染前合成的DNA未发生去甲基化,但其一些降解产物,包括甲基脱氧胞苷单磷酸,被整合到病毒DNA中。使用突变病毒表明,抑制甲基化似乎需要一些病毒DNA的合成。甲基化的抑制不能用DNA甲基转移酶的缺失来解释,因为该酶的活性在感染早期并未改变。宿主细胞DNA甲基化的抑制可能是疱疹病毒使细胞发生转化的一个重要步骤,并且测试的各种转化细胞系显示出DNA甲基化水平降低。

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本文引用的文献

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Enzymatic methylation of DNA and poly(dG-dC) X poly(dG-dC) modified by 4-acetoxyaminoquinoline-1-oxide, the ultimate carcinogen of 4-nitroquinoline-1-oxide.DNA和经4-乙酰氧基氨基喹啉-1-氧化物(4-硝基喹啉-1-氧化物的最终致癌物)修饰的聚(dG-dC)×聚(dG-dC)的酶促甲基化作用
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