Four cloned rat cell lines (NX-1 to -4) infected with Moloney murine leukemia virus and defective in virus replication were found to be all different by viral protein and nucleic acid analyses. All four clones produced noninfectious particles and, except for NX-2, at about the same level as wild type. Compared with wild-type virions these defective particles contained larger amounts of gag precursor proteins and very little or no p30 or p15. Analysis of intracellular precursor proteins revealed that NX-2 to -4 synthesized normal Pr65gag, whereas NX-1 produced a slightly smaller precursor. Both NX-1 and NX-4 synthesized an intracellular polyprotein with a size similar to that of wild-type Pr180 gag-pol. Restriction endonuclease analysis of NX-1 to -4 cellular DNA showed that each clone contained a single integrated provirus which possessed large terminal repeat sequences at both the 5' and 3' ends. The proviruses of NX-1 to -3 appeared normal by restriction endonuclease analysis, but NX-4 provirus had a deletion of 1,700 base pairs comprising part of the polymerase region. The noninfectious particles produced by all four clones packaged Moloney viral RNAs and rat RNAs of two different sizes.
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http://dx.doi.org/10.1128/JVI.38.3.895-905.1981 | DOI Listing |
Int J Clin Exp Pathol
December 2024
School of Stomatology, Hunan University of Medicine No. 492 Jinxi South Road, Huaihua 418000, Hunan, China.
Background: B-cell specific Moloney MLV insertion site-1 (Bmi-1) belongs to the polycomb group (PcG) gene and is a transcriptional suppressor to maintain appropriate gene expression patterns during development. To investigate whether the Bmi-1 gene has a corrective effect on bone senescence induced in Bmi-1 mice through regulating the bone microenvironment.
Methods: Littermate heterozygous male and female mice (Bmi-1) were used in this study.
Cancer Med
January 2025
Faculty of Medical Sciences, Neuroscience Research Center, Lebanese University, Hadath, Lebanon.
Background: Glioblastoma (GBM) is the most common primary brain tumor in adults and has a median survival of less than 15 months. Advancements in the field of epigenetics have expanded our understanding of cancer biology and helped explain the molecular heterogeneity of these tumors. B-cell-specific Moloney murine leukemia virus insertion site-1 (Bmi-1) is a member of the highly conserved polycomb group (PcG) protein family that acts as a transcriptional repressor of multiple genes, including those that determine cell proliferation and differentiation.
View Article and Find Full Text PDFAnn Neurol
January 2025
Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA.
Virologie (Montrouge)
December 2024
Unité des Virus émergents (UVE : Aix-Marseille Univ, Università di Corsica, Corte, IRD 190, Inserm 1207, IRBA), France.
The reverse transcriptase of Moloney Murine Leukemia Virus (MMLV) is an enzyme that synthesizes DNA from an RNA template. Among reverse transcriptases, this enzyme is currently the most commonly used in molecular biology and diagnostics. Since its discovery, this viral protein has been extensively studied, shedding light on its structural and functional characteristics, and offering opportunities to optimize the catalytic performances for biotechnological applications.
View Article and Find Full Text PDFPro-viral Insertion site for the Moloney Murine Leukemia virus 1 (PIM-1) is widely involved in various biological processes and diseases, which is based on its structure and functional sites. However, the relationship between active sites and function of PIM-1 kinase remains unclear due to the lack of effective study approaches in live cells. Herein, to visualize the effect of different active sites in PIM-1 protein on its function activity and relation with PI3K/Akt/mTOR pathway, three mutant probes of EPHY which was developed previously based on fluorescence resonance energy transfer (FRET) technology to detect PIM-1 kinase activity in living cells were further constructed and transfected into cells followed by treating with PIM-1 inhibitors, ATP and PI3K inhibitor, respectively.
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