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一种含有缺陷型莫洛尼鼠白血病病毒基因组的小鼠细胞系的分离与鉴定。

Isolation and characterization of a mouse cell line containing a defective Moloney murine leukemia virus genome.

作者信息

Besmer P, Fan H, Paskind M, Baltimore D

出版信息

J Virol. 1979 Mar;29(3):1023-34. doi: 10.1128/JVI.29.3.1023-1034.1979.

Abstract

A culture of mouse cells containing a 1,000-nucleotide deletion mutant of Moloney murine leukemia virus has been isolated. The deletion did not affect the size or function of the 21S mRNA that encodes the env gene products. Both the deleted RNA and the 21S mRNA were recovered in polyribosomes. Cells containing the deleted virus made no detectable Pr180gag-pol. Pr65gag synthesis with also absent, but a 45,000-molecular-weight gag gene product was found that might be encoded by the deleted genome. Biosynthesis of Pr80env proceeded normally in these cells; the intracellular precursor was cleaved and migrated to the cell surface as gp70. The cells could not be superinfected by homologous Moloney murine leukemia virus presumably because of surface restriction due to the gp70. Although the cells express the Moloney murine leukemia virus gp70 on their surface, they will not make pseudotypes after infection with vesicular stomatitis virus implying that Pr65gag may play a critical role in pseudotype formation. Induction of endogenous virus expression in the cells carrying the deletion mutant generated an N-tropic murine leukemia virus that can fuse XC cells. This may represent a recombinant between the deletion mutant and an endogenous virus.

摘要

已分离出一种含有莫洛尼鼠白血病病毒1000个核苷酸缺失突变体的小鼠细胞培养物。该缺失不影响编码env基因产物的21S mRNA的大小或功能。缺失的RNA和21S mRNA都在多核糖体中被回收。含有缺失病毒的细胞未检测到Pr180gag-pol。Pr65gag的合成也不存在,但发现了一种45000分子量的gag基因产物,可能由缺失的基因组编码。Pr80env的生物合成在这些细胞中正常进行;细胞内前体被切割并以gp70的形式迁移到细胞表面。这些细胞不能被同源莫洛尼鼠白血病病毒超感染,可能是由于gp70导致的表面限制。尽管这些细胞在其表面表达莫洛尼鼠白血病病毒gp70,但在用水泡性口炎病毒感染后它们不会形成假型,这意味着Pr65gag可能在假型形成中起关键作用。在携带缺失突变体的细胞中诱导内源性病毒表达产生了一种能融合XC细胞的N型嗜性鼠白血病病毒。这可能代表缺失突变体与内源性病毒之间的重组体。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ea2b/353263/580a0611141e/jvirol00183-0207-a.jpg

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