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小鼠微小病毒(一种细小病毒)DNA的细胞周期依赖性复制。

Cell cycle-dependent replication of the DNA of minute virus of mice, a parvovirus.

作者信息

Wolter S, Richards R, Armentrout R W

出版信息

Biochim Biophys Acta. 1980 May 30;607(3):420-31. doi: 10.1016/0005-2787(80)90152-5.

Abstract

The formation of double-stranded viral DNA was examined in synchronized cells infected with minute virus of mice in early G1 phase. In the infected cells, a minimum of 50-100 copies of the input single-stranded DNA have been converted to a double-stranded form by mid S phase. In well-synchronized cells, the amount of double-stranded form by mid A phase. In well-synchronized cells, the amount of double-stranded viral DNA detected during G1 is on the order of a few copies per cell or less. When cells are infected in the presence of the thymidine analog, 5-bromodeoxyuridine, viral DNA synthesis is inhibited. However, 5-bromodeoxyuridine does not inhibit host DNA synthesis nor does it prevent replication of viral DNA if added to the infected cells in late S phase. Viral DNA replication first becomes resistant to 5-bromodeoxyuridine inhibition at the beginning of S phase. As 5-bromodeoxyuridine appears to specifically block early steps in viral DNA synthesis but not the subsequent replication of the DNA, the conversion of the input viral genome to a double-stranded form which undergoes further replication appears to be a S phase-specific event.

摘要

在处于G1早期阶段被小鼠微小病毒感染的同步化细胞中,研究了双链病毒DNA的形成。在被感染的细胞中,到S期中期时,至少50 - 100份输入的单链DNA已转化为双链形式。在同步良好的细胞中,到A期中期时双链形式的量。在同步良好的细胞中,在G1期检测到的双链病毒DNA的量约为每个细胞几份或更少。当细胞在胸苷类似物5-溴脱氧尿苷存在的情况下被感染时,病毒DNA合成受到抑制。然而,5-溴脱氧尿苷不抑制宿主DNA合成,并且如果在S期后期添加到被感染细胞中,它也不会阻止病毒DNA的复制。病毒DNA复制在S期开始时首先变得对5-溴脱氧尿苷抑制有抗性。由于5-溴脱氧尿苷似乎特异性地阻断病毒DNA合成的早期步骤,但不阻断随后的DNA复制,输入的病毒基因组转化为双链形式并进行进一步复制似乎是一个S期特异性事件。

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