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存在一种控制脱氧嘧啶激酶转录的单纯疱疹病毒特异性因子的证据。

Evidence for a herpes simplex virus-specific factor controlling the transcription of deoxypyrimidine kinase.

作者信息

Leung W C

出版信息

J Virol. 1978 Aug;27(2):269-74. doi: 10.1128/JVI.27.2.269-274.1978.

DOI:10.1128/JVI.27.2.269-274.1978
PMID:211259
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC354164/
Abstract

A cistron-specific, enzyme-forming-capacity method was used to study the control of herpes simplex virus (HSV)-specific deoxypyrimidine kinase (dPyK) mRNA synthesis. A virus-specific factor was formed by a primary infecting virus, and this factor effected the transcription of dPyK mRNA of a superinfecting virus in the presence of cycloheximide, suggesting that the factor acted in "trans" and was a diffusible one. After the addition of actinomycin D to prevent further transcription and upon removal of cycloheximide, the dPyK mRNA was allowed to express into dPyK activity. A factor from HSV-1 could effect the transcription of dPyK mRNA of both HSV-1 and HSV-2. Amino acid analogs, canavanine or ethionine, inhibited the action of this factor, suggesting that a protein was involved. This protein factor was shown to belong to the alpha (or immediate-early) group of HSV-Specific polypeptides in preductively infected cells.

摘要

采用一种顺反子特异性的、形成酶能力的方法来研究单纯疱疹病毒(HSV)特异性脱氧嘧啶激酶(dPyK)mRNA合成的调控。一种病毒特异性因子由初次感染的病毒形成,并且在放线菌酮存在的情况下,该因子影响再次感染病毒的dPyK mRNA的转录,这表明该因子以“反式”作用,是一种可扩散的因子。在添加放线菌素D以阻止进一步转录并去除放线菌酮后,dPyK mRNA被允许表达为dPyK活性。来自HSV - 1的一种因子可影响HSV - 1和HSV - 2的dPyK mRNA的转录。氨基酸类似物刀豆氨酸或乙硫氨酸抑制该因子的作用,表明涉及一种蛋白质。在生产性感染的细胞中,这种蛋白质因子被证明属于HSV特异性多肽的α(或立即早期)组。

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Evidence for a herpes simplex virus-specific factor controlling the transcription of deoxypyrimidine kinase.存在一种控制脱氧嘧啶激酶转录的单纯疱疹病毒特异性因子的证据。
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本文引用的文献

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INHIBITION OF THYMIDINE KINASE FORMATION IN LM (TK-) CELLS SIMULTANEOUSLY INFECTED WITH VACCINIA AND A THYMIDINE KINASELESS VACCINIA MUTANT.在同时感染痘苗病毒和胸苷激酶缺陷型痘苗病毒突变体的LM(TK-)细胞中胸苷激酶形成的抑制作用
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