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小鼠微小病毒DNA的左端和右端起源在体内指导附加体扩增和整合的能力上有所不同。

The left-end and right-end origins of minute virus of mice DNA differ in their capacity to direct episomal amplification and integration in vivo.

作者信息

Corsini J, Cotmore S F, Tattersall P, Winocour E

机构信息

Math and Science Department, Chadron State College, Chadron, Nebraska 69337, USA.

出版信息

Virology. 2001 Sep 15;288(1):154-63. doi: 10.1006/viro.2001.1076.

Abstract

Previously it was shown that a 53-nucleotide viral replication origin, derived from the left-end (3') telomere of minute virus of mice (MVM) DNA, directed integration of infecting MVM genomes into an Epstein-Barr virus (EBV)-based episome in cell culture. Integration depended upon the presence, in the episome, of a functional origin sequence which could be nicked by NS1, the viral initiator protein. Here we extend our studies to the genomic right-end (5') origin and report that three 131- to 135-nucleotide right-end origin sequences failed to target MVM episomal integration even though the same sequences were functional in NS1-driven DNA replication assays in vitro. Additionally, we observed amplification of episomal DNA in response to MVM infection in cell lines harboring episomes which directed integration, but not in cell lines containing episomes which did not direct integration, including those with inserts of the MVM right-end origin.

摘要

先前的研究表明,一个53个核苷酸的病毒复制起点,源自小鼠微小病毒(MVM)DNA的左端(3')端粒,可在细胞培养中将感染性MVM基因组整合到基于爱泼斯坦-巴尔病毒(EBV)的附加体中。整合依赖于附加体中存在一个功能性起点序列,该序列可被病毒起始蛋白NS1切割。在此,我们将研究扩展到基因组右端(5')起点,并报告三个131至135个核苷酸的右端起点序列未能靶向MVM附加体整合,尽管相同序列在体外NS1驱动的DNA复制试验中具有功能。此外,我们观察到,在携带可指导整合的附加体的细胞系中,MVM感染会导致附加体DNA扩增,但在含有不能指导整合的附加体的细胞系中则不会,包括那些插入了MVM右端起点的细胞系。

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