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小鼠非病毒血症Mov亚系中的内源性莫洛尼白血病病毒在原病毒基因组中存在缺陷。

Endogenous Moloney leukemia virus in nonviremic Mov substrains of mice carries defects in the proviral genome.

作者信息

Schnieke A, Stuhlmann H, Harbers K, Chumakov I, Jaenisch R

出版信息

J Virol. 1983 Feb;45(2):505-13. doi: 10.1128/JVI.45.2.505-513.1983.

Abstract

Substrains of mice carrying Moloney murine leukemia virus as a Mendelian gene (Mov locus) have been derived previously. Some of these strains, i.e., Mov-3 and Mov-9, develop viremia, whereas others, i.e., Mov-2, Mov-7, and Mov-10, do not regularly activate virus. We previously have molecularly cloned the respective Mov loci and shown that proviral clones derived from the different viral loci were either infectious (Mov-3, Mov-9) or failed to induce infectious virus (Mov-2, Mov-7, Mov-10) in a transfection assay. To analyze the sites affecting infectivity of the latter clones, complementation assays, in vitro recombinations, and marker rescue experiments were performed. Our results show that the three endogenous Moloney murine leukemia virus clones derived from Mov-2, Mov-7, and Mov-10 carry different mutations in the gag-pol region of the proviral genome. No inhibitory effect of flanking mouse sequences on provirus infectivity was observed.

摘要

携带莫洛尼鼠白血病病毒作为孟德尔基因(Mov位点)的小鼠亚系此前已被培育出来。其中一些品系,即Mov-3和Mov-9,会发生病毒血症,而其他品系,即Mov-2、Mov-7和Mov-10,则不会定期激活病毒。我们之前已经对各自的Mov位点进行了分子克隆,并表明在转染试验中,源自不同病毒位点的前病毒克隆要么具有感染性(Mov-3、Mov-9),要么无法诱导感染性病毒(Mov-2、Mov-7、Mov-10)。为了分析影响后一种克隆感染性的位点,我们进行了互补试验、体外重组和标记拯救实验。我们的结果表明,源自Mov-2、Mov-7和Mov-10的三个内源性莫洛尼鼠白血病病毒克隆在前病毒基因组的gag-pol区域携带不同的突变。未观察到侧翼小鼠序列对前病毒感染性的抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d0e/256443/523a922a99de/jvirol00149-0033-a.jpg

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