ArticleJournal of virology2003
Phosphorylated serine residues and an arginine-rich domain of the moloney murine leukemia virus p12 protein are required for early events of viral infection.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Essential functions of inositol hexakisphosphate (IP6) in murine leukemia virus replication.mBio · 2024Article
- Murine leukemia virus (MLV) P50 protein induces cell transformation via transcriptional regulatory function.Retrovirology · 2023Article
- BET-Independent Murine Leukemia Virus Integration Is RetargetedMicrobiology spectrum · 2022Article
- Moloney Murine Leukemia Virus p12 Is Required for Histone Loading onto Retroviral DNAs.Journal of virology · 2021Article
- Dynein Light-Chain Dynlrb2 Is Essential for Murine Leukemia Virus Traffic and Nuclear Entry.Journal of virology · 2021Article
- Post-Translational Modifications of Retroviral HIV-1 Gag Precursors: An Overview of Their Biological Role.International journal of molecular sciences · 2021Review
- IQGAP1 Negatively Regulates HIV-1 Gag Trafficking and Virion Production.Cell reports · 2020Article
- Article
- Murine leukemia virus p12 tethers the capsid-containing pre-integration complex to chromatin by binding directly to host nucleosomes in mitosis.PLoS pathogens · 2018Article
- Tetherin Inhibits Cell-Free Virus Dissemination and Retards Murine Leukemia Virus Pathogenesis.Journal of virology · 2017Article
- Phosphorylation Requirement of Murine Leukemia Virus p12.Journal of virology · 2016Article
- Repression of the Chromatin-Tethering Domain of Murine Leukemia Virus p12.Journal of virology · 2016Article
- Dynein Regulators Are Important for Ecotropic Murine Leukemia Virus Infection.Journal of virology · 2016Article
- ESCRT Requirements for Murine Leukemia Virus Release.Viruses · 2016Article
- The N-terminus of murine leukaemia virus p12 protein is required for mature core stability.PLoS pathogens · 2014Article
- Clonotypic composition of the CD4+ T cell response to a vectored retroviral antigen is determined by its speed.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- RNA:DNA hybrids are a novel molecular pattern sensed by TLR9.The EMBO journal · 2014Article
- Viral DNA tethering domains complement replication-defective mutations in the p12 protein of MuLV Gag.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- p12 tethers the murine leukemia virus pre-integration complex to mitotic chromosomes.PLoS pathogens · 2012Article
- The gammaretroviral p12 protein has multiple domains that function during the early stages of replication.Retrovirology · 2012Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutational analyses of the p12 Gag phosphoprotein of Moloney murine leukemia virus have demonstrated its participation in both virus assembly and the early stages of infection. The molecular mechanisms by which p12 functions in these events are still poorly understood. We performed studies to examine the significance of p12 phosphorylation in the viral life cycle. Alanine substitutions were introduced at the potential phosphorylation sites in p12, and the resulting mutants were tested for replication. Mutant viruses with changes at S61 and S78 were severely impaired, whereas the other mutant viruses were viable. S61 was shown to be required for normal levels of phosphorylation of p12 in vivo. These defective mutant viruses showed no apparent alteration to Gag protein processing or reduction in the yield of virions after transient transfection, but the mutants failed to form circular viral DNAs in acutely infected cells. Sequence analysis of revertant clones derived from S(61,65)A mutant virus revealed two classes: one group with a single mutation at a residue adjacent to S61 and another group with mutations introducing new positive charges surrounding S61. In vivo [32P]orthophosphate labeling indicated that the rescue of the S(61,65)A mutant virus did not result in a significant increase in the phosphorylation level of p12. Alanine substitutions of an arginine-rich stretch near S61 (at R-66, -68, -70, and -71) resulted in the same phenotype as the S(61,65)A mutant virus. The restored function of S(61,65)A mutant virus by second or third site mutations may result from a structural change or the addition of positively charged residues in the arginine-rich region.
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