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1
Analysis of minimal functions of simian virus 40. 3. Evidence for "host cell repair" of oncogenicity and infectivity of UV-irradiated simian virus 40.猴病毒40最小功能的分析。3. 紫外线照射的猴病毒40致癌性和感染性“宿主细胞修复”的证据。
J Virol. 1974 Jan;13(1):36-41. doi: 10.1128/JVI.13.1.36-41.1974.
2
Analysis of minimal functions of simian virus 40. II. Enhancement of oncogenic transformation in vitro by UV irradiation.猴病毒40的最小功能分析。II.紫外线照射对体外致癌转化的增强作用。
J Virol. 1973 Dec;12(6):1265-71. doi: 10.1128/JVI.12.6.1265-1271.1973.
3
Enhancement of SV40 transformation by treatment of C3H2K cells with UV light and caffeine. II. The effects of multiplicity of infection, cell phase, and time with caffeine.用紫外线和咖啡因处理C3H2K细胞增强SV40转化作用。II.感染复数、细胞周期以及咖啡因处理时间的影响
Virology. 1976 Jul 15;72(2):480-5. doi: 10.1016/0042-6822(76)90176-8.
4
Analysis of minimal functions of simian virus 40. I. Oncogenic transformation of Syrian hamster kidney cells in vitro by photodynamically inactivated SV40.猿猴病毒40的最小功能分析。I. 光动力灭活的SV40对叙利亚仓鼠肾细胞的体外致癌转化。
Int J Cancer. 1973 Sep 15;12(2):524-31. doi: 10.1002/ijc.2910120224.
5
Properties of simian virus 40 rescued from cell lines transformed by ultraviolet-irradiated simian virus 40.从经紫外线照射的猴病毒40转化的细胞系中拯救出的猴病毒40的特性。
J Virol. 1969 Nov;4(5):585-95. doi: 10.1128/JVI.4.5.585-595.1969.
6
Carcinogens enhance survival of UV-irradiated simian virus 40 in treated monkey kidney cells: induction of a recovery pathway?致癌物可提高经处理的猴肾细胞中紫外线照射的猿猴病毒40的存活率:是否诱导了一种恢复途径?
Proc Natl Acad Sci U S A. 1978 Jan;75(1):346-50. doi: 10.1073/pnas.75.1.346.
7
Investigations on oncogenic transformation, induction of DNA-synthesis and t-antigen formation by UV-irradiated simian virus (SV-) 40.紫外线照射的猿猴病毒(SV-)40 致癌转化、DNA 合成诱导及 T 抗原形成的研究
Z Med Mikrobiol Immunol. 1969;155(2):123-32. doi: 10.1007/BF02123856.
8
The effect of caffeine on the ultraviolet light induction of SV40 virus from transformed hamster cells.
Virology. 1976 Sep;73(2):468-75. doi: 10.1016/0042-6822(76)90408-6.
9
Enhancement of SV40 transformation by treatment of C3H2K cells with UV light and caffeine. I. Combined effect of UV light and caffeine.用紫外线和咖啡因处理C3H2K细胞增强SV40转化作用。I. 紫外线和咖啡因的联合效应。
Virology. 1975 Aug;66(2):568-78. doi: 10.1016/0042-6822(75)90229-9.
10
Variation in oncogenic and transforming potential of PARA (defective SV40)-adenovirus 7.PARA(缺陷型SV40)-腺病毒7致癌及转化潜能的变异
Virology. 1972 Mar;47(3):849-53. doi: 10.1016/0042-6822(72)90579-x.

引用本文的文献

1
Analysis of minimal functions of simian virus 40. IV. Oncogenic transformation of syrian hamster kidney cells in vitro by beta-propiolactone inactivated sv40.猿猴病毒40的最小功能分析。IV. β-丙内酯灭活的猿猴病毒40对叙利亚仓鼠肾细胞的体外致癌转化作用
Arch Gesamte Virusforsch. 1974;45(4):301-8.
2
Plaque formation with simian virus 40: enhancement by dimethyl sulfoxide.猿猴病毒40的噬菌斑形成:二甲基亚砜的增强作用
J Virol. 1974 Dec;14(6):1607-10. doi: 10.1128/JVI.14.6.1607-1610.1974.
3
Effect of beta-propiolactone inactivation of polyoma virus on viral functions.β-丙内酯对多瘤病毒的灭活作用对病毒功能的影响。
J Virol. 1974 Oct;14(4):840-5. doi: 10.1128/JVI.14.4.840-845.1974.
4
Production of plasminogen activator by human and hamster cells infected with human cytomegalovirus.人巨细胞病毒感染的人和仓鼠细胞产生纤溶酶原激活剂。
J Virol. 1979 Aug;31(2):415-9. doi: 10.1128/JVI.31.2.415-419.1979.

本文引用的文献

1
INFECTION OF HUMAN AND SIMIAN TISSUE CULTURES WITH ROUS SARCOMA VIRUS.劳斯肉瘤病毒对人和猴组织培养物的感染
Proc Natl Acad Sci U S A. 1964 Jul;52(1):53-9. doi: 10.1073/pnas.52.1.53.
2
INTERACTION OF NUCLEIC ACIDS, I. PHYSICAL BINDING OF THYMINE, ADENINE, STEROIDS, AND AROMATIC HYDROCARBONS TO NUCLEIC ACIDS.核酸的相互作用,I. 胸腺嘧啶、腺嘌呤、类固醇和芳香烃与核酸的物理结合
Proc Natl Acad Sci U S A. 1964 Jan;51(1):17-24. doi: 10.1073/pnas.51.1.17.
3
Radiological evidence for partial genetic homology between bacteriophage and host bacteria.噬菌体与宿主细菌之间部分基因同源性的放射学证据。
Virology. 1955 Nov;1(4):347-76. doi: 10.1016/0042-6822(55)90030-1.
4
Evidence for dark-reactivation of ultraviolet light damage in mouse L cells.小鼠L细胞中紫外线损伤暗修复的证据。
Radiat Res. 1967 May;31(1):121-38.
5
Hydroxyurea: differential lethal effects on cultured mammalian cells during the cell cycle.羟基脲:在细胞周期中对培养的哺乳动物细胞的差异性致死效应。
Science. 1965 Dec 24;150(3704):1729-31. doi: 10.1126/science.150.3704.1729.
6
Inhibition of host cell reactivation in phage T1 by caffeine.
Biochem Biophys Res Commun. 1964;14:340-6. doi: 10.1016/s0006-291x(64)80007-3.
7
The interaction of caffeine with ultra-violet-light-irradiated DNA.咖啡因与紫外线照射的DNA之间的相互作用。
Int J Radiat Biol Relat Stud Phys Chem Med. 1970;17(4):395-9. doi: 10.1080/09553007014550481.
8
DNA repair.DNA修复
Annu Rev Biochem. 1968;37:175-200. doi: 10.1146/annurev.bi.37.070168.001135.
9
[Degradation by the host cell of DNA of lambda bacteriophage irradiated by ultraviolet rays].[宿主细胞对紫外线照射的λ噬菌体DNA的降解作用]
Mutat Res. 1967 May-Jun;4(3):241-52. doi: 10.1016/0027-5107(67)90019-x.
10
Ultraviolet photobiology of Kilham rat virus and the absolute ultraviolet photosensitivities of other animal viruses: influence of DNA strandedness, molecular weight, and host-cell repair.
Virology. 1972 Aug;49(2):368-78. doi: 10.1016/0042-6822(72)90489-8.

猴病毒40最小功能的分析。3. 紫外线照射的猴病毒40致癌性和感染性“宿主细胞修复”的证据。

Analysis of minimal functions of simian virus 40. 3. Evidence for "host cell repair" of oncogenicity and infectivity of UV-irradiated simian virus 40.

作者信息

Seemayer N H, Defendi V

出版信息

J Virol. 1974 Jan;13(1):36-41. doi: 10.1128/JVI.13.1.36-41.1974.

DOI:10.1128/JVI.13.1.36-41.1974
PMID:4359429
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC355255/
Abstract

The in vitro transforming capacity of simian virus 40 (SV40) for Syrian hamster cells is highly resistant to inactivation by UV light in comparison to infectivity. In the same cell system, we demonstrated a "host cell repair mechanism" sensitive to caffeine which is, to a large extent, responsible for the high resistance to UV inactivation of the transforming capacity of SV40. The survival of infectivity of UV-irradiated SV40 in CV-1 cells was also sensitive to caffeine, again indicating host cell repair. On the other hand, depression of normal cell DNA synthesis by hydroxyurea during the first 24 h postinfection only modestly reduced, and to a similar extent, the transforming capacity of UV-irradiated and nonirradiated SV40.

摘要

与感染性相比,猿猴病毒40(SV40)对叙利亚仓鼠细胞的体外转化能力对紫外线灭活具有高度抗性。在同一细胞系统中,我们证明了一种对咖啡因敏感的“宿主细胞修复机制”,这种机制在很大程度上导致了SV40转化能力对紫外线灭活的高抗性。紫外线照射的SV40在CV-1细胞中的感染性存活也对咖啡因敏感,再次表明存在宿主细胞修复。另一方面,在感染后最初24小时内,羟基脲对正常细胞DNA合成的抑制仅适度降低了紫外线照射和未照射的SV40的转化能力,且降低程度相似。