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猿猴病毒40大T抗原编码序列中不到40%是转化所必需的。

Less than 40% of the simian virus 40 large T-antigen-coding sequence is required for transformation.

作者信息

Sompayrac L, Danna K J

出版信息

Mol Cell Biol. 1984 Aug;4(8):1661-3. doi: 10.1128/mcb.4.8.1661-1663.1984.

DOI:10.1128/mcb.4.8.1661-1663.1984
PMID:6092929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC368965/
Abstract

F8dl is a simian virus 40 early-region deletion mutant that lacks the simian virus 40 DNA sequences between 0.168 and 0.424 map units. Despite this large deletion, cloned F8dl DNA transforms Fisher rat F111 cells and BALB/3T3 clone A31 mouse cells as efficiently as does cloned simian virus 40 wild-type DNA. These results indicate that less than 40% of the large T-antigen-coding sequence is required for efficient transformation.

摘要

F8dl是一种猿猴病毒40早期区域缺失突变体，它缺少猿猴病毒40在0.168至0.424图谱单位之间的DNA序列。尽管有如此大的缺失，克隆的F8dl DNA转化Fisher大鼠F111细胞和BALB/3T3克隆A31小鼠细胞的效率与克隆的猿猴病毒40野生型DNA一样高。这些结果表明，高效转化所需的大T抗原编码序列不到40%。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ae/368965/805cabfd09db/molcellb00150-0242-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ae/368965/cdb9cc7a6fa1/molcellb00150-0242-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ae/368965/805cabfd09db/molcellb00150-0242-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ae/368965/cdb9cc7a6fa1/molcellb00150-0242-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80ae/368965/805cabfd09db/molcellb00150-0242-b.jpg

相似文献

1
Less than 40% of the simian virus 40 large T-antigen-coding sequence is required for transformation.猿猴病毒40大T抗原编码序列中不到40%是转化所必需的。
Mol Cell Biol. 1984 Aug;4(8):1661-3. doi: 10.1128/mcb.4.8.1661-1663.1984.
2
Simian virus 40 sequences between 0.168 and 0.424 map units are not required for abortive transformation.猿猴病毒40在0.168至0.424个图距单位之间的序列对于流产性转化并非必需。
J Virol. 1983 May;46(2):475-80. doi: 10.1128/JVI.46.2.475-480.1983.
3
The simian virus 40 sequences between 0.169 and 0.423 map units are not essential to immortalize early-passage rat embryo cells.猿猴病毒40在0.169至0.423个图谱单位之间的序列对于永生化早期传代大鼠胚胎细胞并非必需。
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Simian virus 40 large T-antigen point mutants that are defective in viral DNA replication but competent in oncogenic transformation.猿猴病毒40大T抗原点突变体，其在病毒DNA复制方面存在缺陷，但在致癌转化方面具有能力。
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Genetic and biochemical analysis of transformation-competent, replication-defective simian virus 40 large T antigen mutants.具有转化能力的复制缺陷型猿猴病毒40大T抗原突变体的遗传与生化分析
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Conversion through homologous recombination of the gene encoding Simian virus 40 115,000-molecular-weight super T antigen to a gene encoding a normal-size large T antigen variant.通过同源重组将编码猿猴病毒40 115,000分子量超级T抗原的基因转化为编码正常大小大T抗原变体的基因。
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The t-unique coding domain is important to the transformation maintenance function of the simian virus 40 small t antigen.t独特编码结构域对猿猴病毒40小t抗原的转化维持功能很重要。
Mol Cell Biol. 1986 Apr;6(4):1172-8. doi: 10.1128/mcb.6.4.1172-1178.1986.

引用本文的文献

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Overproduction of protein p53 contributes to simian virus 40-mediated transformation.蛋白质p53的过度产生有助于猿猴病毒40介导的转化。
Mol Cell Biol. 1986 Oct;6(10):3531-6. doi: 10.1128/mcb.6.10.3531-3536.1986.
2
The simian virus 40 sequences between 0.169 and 0.423 map units are not essential to immortalize early-passage rat embryo cells.猿猴病毒40在0.169至0.423个图谱单位之间的序列对于永生化早期传代大鼠胚胎细胞并非必需。
Mol Cell Biol. 1985 May;5(5):1191-4. doi: 10.1128/mcb.5.5.1191-1194.1985.
3
The large tumor antigen of simian virus 40 encodes at least two distinct transforming functions.

本文引用的文献

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Simian virus 40 deletion mutants that transform with reduced efficiency.转化效率降低的猿猴病毒40缺失突变体。
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Cleavage of structural proteins during the assembly of the head of bacteriophage T4.在噬菌体T4头部组装过程中结构蛋白的切割
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A new technique for the assay of infectivity of human adenovirus 5 DNA.一种检测人腺病毒5型DNA感染性的新技术。
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