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1
Differential inhibition of host protein synthesis in L cells infected with RNA - temperature-sensitive mutants of vesicular stomatitis virus.水泡性口炎病毒RNA温度敏感突变体感染的L细胞中宿主蛋白合成的差异抑制
J Virol. 1976 May;18(2):550-8. doi: 10.1128/JVI.18.2.550-558.1976.
2
Temperature-sensitive mutants of vesicular stomatitis virus: synthesis of virus-specific proteins.水泡性口炎病毒的温度敏感突变体:病毒特异性蛋白质的合成
J Virol. 1971 May;7(5):651-62. doi: 10.1128/JVI.7.5.651-662.1971.
3
Further studies of the RNA synthesis phenotype selected during persistent infection with vesicular stomatitis virus.对水泡性口炎病毒持续感染期间选择的RNA合成表型的进一步研究。
Virology. 1984 Jul 15;136(1):211-20. doi: 10.1016/0042-6822(84)90260-5.
4
RNA synthesis in temperature-sensitive mutants of vesicular stomatitis virus.水泡性口炎病毒温度敏感突变体中的RNA合成
J Virol. 1973 Sep;12(3):570-8. doi: 10.1128/JVI.12.3.570-578.1973.
5
Location of the transcription defect in group I temperature-sensitive mutants of vesicular stomatitis virus.水泡性口炎病毒I组温度敏感突变体中转录缺陷的定位
J Virol. 1974 Jan;13(1):28-35. doi: 10.1128/JVI.13.1.28-35.1974.
6
Enhanced mutability associated with a temperature-sensitive mutant of vesicular stomatitis virus.与水疱性口炎病毒温度敏感突变体相关的增强的变异性。
J Virol. 1981 Aug;39(2):377-89. doi: 10.1128/JVI.39.2.377-389.1981.
7
Temperature-sensitive defect of vesicular stomatitis virus in complementation group II.水泡性口炎病毒在互补组II中的温度敏感性缺陷
J Virol. 1977 Mar;21(3):913-23. doi: 10.1128/JVI.21.3.913-923.1977.
8
Dominance of temperature-sensitive phenotypes. I. Studies of the mechanism of inhibition of the growth of wild-type vesicular stomatitis virus.温度敏感表型的显性。I. 野生型水疱性口炎病毒生长抑制机制的研究。
Virology. 1986 Nov;155(1):225-35. doi: 10.1016/0042-6822(86)90182-0.
9
Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription.抑制感染水疱性口炎病毒的小鼠L细胞中核糖核酸的积累需要病毒核糖核酸转录。
Biochemistry. 1980 Feb 19;19(4):804-10. doi: 10.1021/bi00545a029.
10
Vesicular stomatitis virus mRNA and inhibition of translation of cellular mRNA--is there a P function in vesicular stomatitis virus?水泡性口炎病毒mRNA与细胞mRNA翻译的抑制——水泡性口炎病毒中存在P功能吗?
J Virol. 1981 May;38(2):504-17. doi: 10.1128/JVI.38.2.504-517.1981.

引用本文的文献

1
New mRNAs are preferentially translated during vesicular stomatitis virus infection.在水疱性口炎病毒感染期间,新的信使核糖核酸(mRNA)被优先翻译。
J Virol. 2008 Mar;82(5):2286-94. doi: 10.1128/JVI.01761-07. Epub 2007 Dec 19.
2
Preferential translation of vesicular stomatitis virus mRNAs is conferred by transcription from the viral genome.水泡性口炎病毒mRNA的优先翻译是由病毒基因组转录赋予的。
J Virol. 2006 Dec;80(23):11733-42. doi: 10.1128/JVI.00971-06. Epub 2006 Sep 27.
3
Migration of vesicular stomatitis virus glycoprotein to the nucleus of infected cells.水泡性口炎病毒糖蛋白向受感染细胞细胞核的迁移。
Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8268-73. doi: 10.1073/pnas.93.16.8268.
4
Sphingolipids and glycoproteins are differentially trafficked to the Chlamydia trachomatis inclusion.鞘脂和糖蛋白被不同地转运至沙眼衣原体包涵体。
J Cell Biol. 1996 Jul;134(2):363-74. doi: 10.1083/jcb.134.2.363.
5
Role of mRNA competition in regulating translation: further characterization of mRNA discriminatory initiation factors.mRNA竞争在调节翻译中的作用:mRNA识别起始因子的进一步表征
Proc Natl Acad Sci U S A. 1983 Feb;80(3):663-7. doi: 10.1073/pnas.80.3.663.
6
Two transcription products of the vesicular stomatitis virus genome may control L-cell protein synthesis.水泡性口炎病毒基因组的两种转录产物可能控制L细胞的蛋白质合成。
J Virol. 1983 Feb;45(2):618-26. doi: 10.1128/JVI.45.2.618-626.1983.
7
Effect of intracellular vesicular stomatitis virus mRNA concentration on the inhibition of host cell protein synthesis.细胞内水泡性口炎病毒mRNA浓度对宿主细胞蛋白质合成抑制作用的影响。
J Virol. 1983 Jan;45(1):206-14. doi: 10.1128/JVI.45.1.206-214.1983.
8
Translational control of vesicular stomatitis virus protein synthesis: isolation of an mRNA-sequestering particle.水疱性口炎病毒蛋白质合成的翻译控制:一种mRNA隔离颗粒的分离
J Virol. 1982 Dec;44(3):932-8. doi: 10.1128/JVI.44.3.932-938.1982.
9
Novel phenotype of RNA synthesis expressed by vesicular stomatitis virus isolated from persistent infection.从持续性感染中分离出的水疱性口炎病毒所表达的RNA合成新表型。
J Virol. 1982 Oct;44(1):167-74. doi: 10.1128/JVI.44.1.167-174.1982.
10
Regulation of protein synthesis in vesicular stomatitis virus-infected mouse L-929 cells by decreased protein synthesis initiation factor 2 activity.通过降低蛋白质合成起始因子2的活性来调节水疱性口炎病毒感染的小鼠L-929细胞中的蛋白质合成
J Virol. 1982 Mar;41(3):781-91. doi: 10.1128/JVI.41.3.781-791.1982.

本文引用的文献

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BIOLOGIC PROPERTIES OF TWO PLAQUE VARIANTS OF VESICULAR STOMATITIS VIRUS (INDIANA SEROTYPE).水泡性口炎病毒(印第安纳血清型)两种蚀斑变体的生物学特性
J Immunol. 1963 Jul;91:112-22.
2
Interferon production and inhibition of host synthesis in cells infected with vesicular stomatitis virus.水泡性口炎病毒感染细胞中干扰素的产生及对宿主合成的抑制作用。
J Virol. 1970 Oct;6(4):476-84. doi: 10.1128/JVI.6.4.476-484.1970.
3
Action of interferon: kinetics and differential effects on viral functions.干扰素的作用:动力学及对病毒功能的差异影响
J Virol. 1970 Oct;6(4):421-9. doi: 10.1128/JVI.6.4.421-429.1970.
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Studies on the intracellular synthesis of reovirus-specified proteins.呼肠孤病毒特异性蛋白质的细胞内合成研究。
Virology. 1970 Jul;41(3):501-18. doi: 10.1016/0042-6822(70)90171-6.
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Protein synthesis in Newcastle disease virus-infected chicken embryo cells.新城疫病毒感染的鸡胚细胞中的蛋白质合成
J Virol. 1974 Apr;13(4):788-800. doi: 10.1128/JVI.13.4.788-800.1974.
6
Persistent noncytocidal vesicular stomatitis virus infections mediated by defective T particles that suppress virion transcriptase.由抑制病毒粒子转录酶的缺陷型T颗粒介导的持续性非杀细胞性水疱性口炎病毒感染。
Proc Natl Acad Sci U S A. 1974 Aug;71(8):2956-60. doi: 10.1073/pnas.71.8.2956.
7
Transcription and replication of vesicular stomatitis virus: effects of temperature-sensitive mutations in complementation group IV.水泡性口炎病毒的转录与复制:互补群IV中温度敏感突变的影响
J Virol. 1974 Apr;13(4):922-30. doi: 10.1128/JVI.13.4.922-930.1974.
8
Cell killing by viruses. I. Comparison of cell-killing, plaque-forming, and defective-interfering particles of vesicular stomatitis virus.病毒导致的细胞杀伤。I. 水疱性口炎病毒的细胞杀伤、噬斑形成及缺陷干扰颗粒的比较
Virology. 1974 Feb;57(2):321-38. doi: 10.1016/0042-6822(74)90172-x.
9
Location of the transcription defect in group I temperature-sensitive mutants of vesicular stomatitis virus.水泡性口炎病毒I组温度敏感突变体中转录缺陷的定位
J Virol. 1974 Jan;13(1):28-35. doi: 10.1128/JVI.13.1.28-35.1974.
10
RNA synthesis of vesicular stomatitis virus. V. Interactions between transcription and replication.水泡性口炎病毒的RNA合成。V.转录与复制之间的相互作用。
J Virol. 1973 Dec;12(6):1395-400. doi: 10.1128/JVI.12.6.1395-1400.1973.

水泡性口炎病毒RNA温度敏感突变体感染的L细胞中宿主蛋白合成的差异抑制

Differential inhibition of host protein synthesis in L cells infected with RNA - temperature-sensitive mutants of vesicular stomatitis virus.

作者信息

McAllister P E, Wagner R R

出版信息

J Virol. 1976 May;18(2):550-8. doi: 10.1128/JVI.18.2.550-558.1976.

DOI:10.1128/JVI.18.2.550-558.1976
PMID:178896
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC515581/
Abstract

The response of mouse L cells to infection with wild-type (wt) and temperature-sensitive (ts) mutants of vesicular stomatitis virus was monitored by sodium dodecyl sulfate-polyacrylamide gel electrophoresis to delineate the synthesis of host cell and viral proteins. Experiments utilized transcriptase mutants of complementation group I (ts114 and ts13), a group IV mutant (ts44) that is restricted in total RNA synthesis (RNA-1) but not in primary transcription, and a group II mutant (ts52) variably restricted in RNA synthesis (RNA +/-). L cells infected with ts mutants at permissive temperature exhibited the wt response of progressive inhibition of host cell protein synthesis accompanied by accumulation of all five viral proteins. Mutant ts44 (IV) also switched off cell protein synthesis at restrictive temperature and accumulated all five viral proteins, but with disproportionate ratios of N and G proteins. At restrictive temperature, cells infected with group I ts mutants failed to accumulate any viral protein and did not exhibit significant reduction in host cell protein synthesis. These data suggest that vesicular stomatitis virus inhibits cell protein synthesis at a stage of viral infection after transcription and possibly translation but preceding replication of progeny viral RNA.

摘要

通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳监测小鼠L细胞对水泡性口炎病毒野生型(wt)和温度敏感型(ts)突变体感染的反应,以描绘宿主细胞和病毒蛋白的合成情况。实验使用了互补组I的转录酶突变体(ts114和ts13)、在总RNA合成(RNA-1)中受限但在初级转录中不受限的IV组突变体(ts44)以及在RNA合成(RNA +/-)中可变受限的II组突变体(ts52)。在允许温度下用ts突变体感染的L细胞表现出野生型反应,即宿主细胞蛋白合成逐渐受到抑制,同时所有五种病毒蛋白积累。突变体ts44(IV)在限制温度下也关闭了细胞蛋白合成并积累了所有五种病毒蛋白,但N和G蛋白的比例不均衡。在限制温度下用I组ts突变体感染的细胞未能积累任何病毒蛋白,宿主细胞蛋白合成也未出现显著减少。这些数据表明,水泡性口炎病毒在病毒感染的转录和可能的翻译之后但在子代病毒RNA复制之前的阶段抑制细胞蛋白合成。