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多瘤病毒早期缺失突变体的DNA序列

DNA sequences of polyoma virus early deletion mutants.

作者信息

Smolar N, Griffin B E

出版信息

J Virol. 1981 Jun;38(3):958-67. doi: 10.1128/JVI.38.3.958-967.1981.

DOI:10.1128/JVI.38.3.958-967.1981
PMID:6264166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC171234/
Abstract

The DNA sequences of four "early" viable deletion mutants of polyoma virus have been determined. Two of these (dl-8 and dl-23) are mutants with deletions in the region of the genome that codes for parts of both large and middle T-antigens, and two (dl-6 and dl-28) are mutants with deletions around the viral origin of replication. The former mutants have altered transformation properties relative to wild-type virus, and dl-8 appears to be replication deficient (B. E. Griffin and C. Maddock, J. Virol. 31:645-656, 1979). Sequences are discussed in terms of the altered phenotypes observed for the various mutants, the DNA structures and protein sequences that are affected by the deletions, and how these might affect the biological properties of the mutants.

摘要

已测定了多瘤病毒四个“早期”存活缺失突变体的DNA序列。其中两个(dl-8和dl-23)是基因组中编码大T抗原和中T抗原部分区域发生缺失的突变体,另外两个(dl-6和dl-28)是病毒复制起点周围发生缺失的突变体。相对于野生型病毒,前一类突变体具有改变的转化特性,并且dl-8似乎复制缺陷(B.E.格里芬和C.马多克,《病毒学杂志》31:645 - 656,1979年)。根据观察到的各种突变体的表型改变、受缺失影响的DNA结构和蛋白质序列以及这些可能如何影响突变体的生物学特性来讨论序列。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ba/171234/57b4c394ceb6/jvirol00006-0165-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ba/171234/57b4c394ceb6/jvirol00006-0165-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3ba/171234/57b4c394ceb6/jvirol00006-0165-a.jpg

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1
DNA sequences of polyoma virus early deletion mutants.多瘤病毒早期缺失突变体的DNA序列
J Virol. 1981 Jun;38(3):958-67. doi: 10.1128/JVI.38.3.958-967.1981.
2
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Early mutants of polyoma virus (dl8 and dl23) with altered transformation properties: is polyoma virus middle T antigen a transforming gene product?具有改变的转化特性的多瘤病毒早期突变体(dl8和dl23):多瘤病毒中T抗原是一种转化基因产物吗?
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New classes of viable deletion mutants in the early region of polyoma virus.多瘤病毒早期区域新的可行缺失突变体类别。
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6
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Host-virus interactions critical for cellular transformation by polyoma virus and SV40.宿主-病毒相互作用对多瘤病毒和SV40诱导细胞转化至关重要。
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Polyoma virus: some considerations on its transforming genes.多瘤病毒:关于其转化基因的一些思考
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Independent contributions of polyomavirus middle T and small T to the regulation of early and late gene expression and DNA replication.多瘤病毒中T抗原和小T抗原对早期和晚期基因表达及DNA复制调控的独立作用。

本文引用的文献

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Transformation of rat embryo fibroblasts by cloned polyoma virus DNA fragments containing only part of the early region.仅包含早期区域一部分的克隆多瘤病毒DNA片段对大鼠胚胎成纤维细胞的转化作用。
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Antibodies against a nonapeptide of polyomavirus middle T antigen: cross-reaction with a cellular protein(s).针对多瘤病毒中T抗原九肽的抗体:与一种细胞蛋白的交叉反应
J Virol. 1983 Dec;48(3):709-20. doi: 10.1128/JVI.48.3.709-720.1983.
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Deletion mapping of a short polyoma virus middle T antigen segment important for transformation.对转化至关重要的短多瘤病毒中T抗原片段的缺失图谱分析。
J Virol. 1983 Apr;46(1):284-7. doi: 10.1128/JVI.46.1.284-287.1983.
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mlt Mutants of polyoma virus.多瘤病毒的mlt突变体
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具有改变的转化特性的多瘤病毒早期突变体(dl8和dl23):多瘤病毒中T抗原是一种转化基因产物吗?
Cold Spring Harb Symp Quant Biol. 1980;44 Pt 1,:271-83. doi: 10.1101/sqb.1980.044.01.031.
4
Coding capacity of a 35 percent fragment of the polyoma virus genome is sufficient to initiate and maintain cellular transformation.多瘤病毒基因组35%片段的编码能力足以启动并维持细胞转化。
Proc Natl Acad Sci U S A. 1980 Jun;77(6):3278-82. doi: 10.1073/pnas.77.6.3278.
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Middle T antigen as primary inducer of full expression of the phenotype of transformation by polyoma virus.中T抗原作为多瘤病毒转化表型完全表达的主要诱导因子。
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Nucleotide sequence of the Salmonella typhimurium origin of DNA replication.鼠伤寒沙门氏菌DNA复制起点的核苷酸序列。
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Regulatory mutants of polyoma virus defective in DNA replication and the synthesis of early proteins.在DNA复制和早期蛋白质合成方面存在缺陷的多瘤病毒调节突变体。
Cell. 1980 Jun;20(2):401-9. doi: 10.1016/0092-8674(80)90626-1.
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Viable deletion mutant in the medium and large T-antigen-coding sequences of the polyoma virus genome.多瘤病毒基因组中中等大小T抗原编码序列的活缺失突变体。
J Virol. 1980 Mar;33(3):1215-20. doi: 10.1128/JVI.33.3.1215-1220.1980.
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The polyoma virus 100K large T-antigen is not required for the maintenance of transformation.多瘤病毒100K大T抗原对于维持转化并非必需。
Virology. 1980 Feb;101(1):217-32. doi: 10.1016/0042-6822(80)90497-3.
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Coding potential and regulatory signals of the polyoma virus genome.多瘤病毒基因组的编码潜能和调控信号
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