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诱导17千道尔顿t蛋白改变的猿猴病毒40缺失突变体的致癌性

Oncogenicity of simian virus 40 deletion mutants that induce altered 17-kilodalton t-proteins.

作者信息

Lewis A M, Martin R G

出版信息

Proc Natl Acad Sci U S A. 1979 Sep;76(9):4299-302. doi: 10.1073/pnas.76.9.4299.

Abstract

Plaque-purified viable simian virus 40 deletion mutants containing deletions between map positions 0.54 and 0.59 induced tumors in 21--92% of LSH hamsters inoculated during the first 24 hr of life. HinfI restriction endonuclease digestion patterns of the genomes of virions rescued from the tumor cells and the distribution of simian virus 40 early proteins in these cells associated tumor induction with the inoculated mutants. These results imply that the DNA sequences comprising that portion of the early simian virus 40 genome between map positions 0.54 and 0.59 are not essential for simian virus 40 oncogenicity.

摘要

在出生后最初24小时内接种的LSH仓鼠中,含有0.54至0.59图谱位置之间缺失的噬菌斑纯化的活猴病毒40缺失突变体在21%至92%的仓鼠中诱发了肿瘤。从肿瘤细胞中拯救出的病毒粒子基因组的HinfI限制性内切酶消化模式以及这些细胞中猴病毒40早期蛋白的分布表明肿瘤诱导与接种的突变体有关。这些结果意味着,组成猴病毒40早期基因组图谱位置0.54至0.59之间那部分的DNA序列对猴病毒40的致癌性并非必不可少。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2c/411561/64975fc1fc1a/pnas00009-0149-a.jpg

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