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紫外线照射对水疱性口炎病毒L蛋白和NS蛋白的影响:对宿主细胞关闭机制的启示

Alteration of vesicular stomatitis virus L and NS proteins by uv irradiation: implications for the mechanism of host cell shut-off.

作者信息

Whitaker-Dowling P, Youngner J S

机构信息

Department of Microbiology, Biochemistry and Molecular Biology, School of Medicine, University of Pittsburgh, Pennsylvania 15261.

出版信息

Virology. 1988 May;164(1):171-5. doi: 10.1016/0042-6822(88)90633-2.

DOI:10.1016/0042-6822(88)90633-2
PMID:2834868
Abstract

When purified, [35S]methionine-labeled vesicular stomatitis virus (VSV) was exposed to ultraviolet light, an irradiation-induced change in the viral proteins was detected by SDS-polyacrylamide gel electrophoresis and immunoblotting. With dose of uv irradiation in the same range as that required to inactivate VSV leader RNA, a loss occurred in the bands corresponding to the L and NS proteins concomitant with the appearance of several new bands of radioactivity throughout the gel. This alteration of viral proteins correlated with the loss of ability of the virus to inhibit host macromolecular synthesis. In light of these results, the role that has been ascribed to the VSV leader RNA in VSV-mediated host shut-off needs to be reevaluated.

摘要

纯化后的[35S]甲硫氨酸标记的水疱性口炎病毒(VSV)经紫外线照射后,通过SDS-聚丙烯酰胺凝胶电泳和免疫印迹法检测到病毒蛋白的辐射诱导变化。当紫外线照射剂量与使VSV前导RNA失活所需剂量相当时,对应于L和NS蛋白的条带出现缺失,同时整个凝胶中出现几条新的放射性条带。病毒蛋白的这种改变与病毒抑制宿主大分子合成能力的丧失相关。鉴于这些结果,VSV前导RNA在VSV介导的宿主关闭中所起的作用需要重新评估。

相似文献

1
Alteration of vesicular stomatitis virus L and NS proteins by uv irradiation: implications for the mechanism of host cell shut-off.紫外线照射对水疱性口炎病毒L蛋白和NS蛋白的影响:对宿主细胞关闭机制的启示
Virology. 1988 May;164(1):171-5. doi: 10.1016/0042-6822(88)90633-2.
2
Dominance of temperature-sensitive phenotypes. II. Vesicular stomatitis virus mutants from a persistent infection interfere with shut-off of host protein synthesis by wild-type virus.温度敏感表型的优势。II. 来自持续性感染的水泡性口炎病毒突变体干扰野生型病毒对宿主蛋白合成的阻断。
Virology. 1987 Jun;158(2):407-13. doi: 10.1016/0042-6822(87)90212-1.
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Persistence of vesicular stomatitis virus in cloned interleukin-2-dependent natural killer cell lines.水泡性口炎病毒在克隆的白细胞介素-2依赖型自然杀伤细胞系中的持续性
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Role of de novo protein synthesis in target cells recognized by cytotoxic T lymphocytes specific for vesicular stomatitis virus.从头合成蛋白质在被水泡性口炎病毒特异性细胞毒性T淋巴细胞识别的靶细胞中的作用。
J Virol. 1991 Dec;65(12):6856-61. doi: 10.1128/JVI.65.12.6856-6861.1991.
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Ultraviolet-irradiated vesicular stomatitis virus and defective-interfering particles are similar non-specific inhibitors of virus infection.紫外线照射的水疱性口炎病毒和缺陷干扰颗粒是类似的病毒感染非特异性抑制剂。
J Gen Virol. 1982 Jun;60(Pt 2):327-33. doi: 10.1099/0022-1317-60-2-327.
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Resolution of multiple complexes of phosphoprotein NS with nucleocapsid protein N of vesicular stomatitis virus.水泡性口炎病毒磷蛋白NS与核衣壳蛋白N的多个复合物的解析
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The functional domains of the phosphoprotein (NS) of vesicular stomatitis virus (Indiana serotype).水疱性口炎病毒(印第安纳血清型)磷蛋白(NS)的功能结构域。
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Vaccinia virus stimulates the growth of vesicular stomatitis virus at the level of protein synthesis in mouse L cells.痘苗病毒在小鼠L细胞的蛋白质合成水平上刺激水疱性口炎病毒的生长。
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Order of transcription of genes of vesicular stomatitis virus.水泡性口炎病毒基因的转录顺序
Proc Natl Acad Sci U S A. 1976 Feb;73(2):442-6. doi: 10.1073/pnas.73.2.442.
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Location of the binding domains for the RNA polymerase L and the ribonucleocapsid template within different halves of the NS phosphoprotein of vesicular stomatitis virus.水泡性口炎病毒NS磷蛋白不同区域内RNA聚合酶L和核糖核蛋白模板结合域的定位
Proc Natl Acad Sci U S A. 1987 Aug;84(16):5655-9. doi: 10.1073/pnas.84.16.5655.

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Effect of vesicular stomatitis virus matrix protein on host-directed translation in vivo.
水泡性口炎病毒基质蛋白对体内宿主导向翻译的影响。
J Virol. 1994 Jan;68(1):555-60. doi: 10.1128/JVI.68.1.555-560.1994.
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Vesicular stomatitis virus infection induces a nuclear DNA-binding factor specific for the interferon-stimulated response element.水泡性口炎病毒感染可诱导一种对干扰素刺激反应元件具有特异性的核DNA结合因子。
J Virol. 1995 Jul;69(7):4173-81. doi: 10.1128/JVI.69.7.4173-4181.1995.
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Viral transcription is necessary and sufficient for vesicular stomatitis virus to inhibit maturation of small nuclear ribonucleoproteins.水泡性口炎病毒抑制小核核糖核蛋白成熟,病毒转录是必要且充分的条件。
J Virol. 1989 Oct;63(10):4172-80. doi: 10.1128/JVI.63.10.4172-4180.1989.