ArticlePLoS pathogens2009
PLK1 down-regulates parainfluenza virus 5 gene expression.
Article in PLoS pathogens, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- PLK3 facilitates replication of swine influenza virus by phosphorylating viral NP protein.Emerging microbes & infections · 2023Article
- Master mitotic kinases regulate viral genome delivery during papillomavirus cell entry.Nature communications · 2023Article
- Identification of Molecular Markers Related to Immune Infiltration in Patients with Severe Asthma: A Comprehensive Bioinformatics Analysis Based on the Human Bronchial Epithelial Transcriptome.Disease markers · 2022Article
- The Nucleocapsid of Paramyxoviruses: Structure and Function of an Encapsidated Template.Viruses · 2021Review
- Evolutionary history of cotranscriptional editing in the paramyxoviral phosphoprotein gene.Virus evolution · 2021Review
- Global phosphoproteomic analysis of Ebola virions reveals a novel role for VP35 phosphorylation-dependent regulation of genome transcription.Cellular and molecular life sciences : CMLS · 2020Article
- Regulation of Mumps Virus Replication and Transcription by Kinase RPS6KB1.Journal of virology · 2020Article
- Influenza Virus Infections and Cellular Kinases.Viruses · 2019Review
- The switch between acute and persistent paramyxovirus infection caused by single amino acid substitutions in the RNA polymerase P subunit.PLoS pathogens · 2019Article
- Polo-like-kinase 1 is a proviral host factor for hepatitis B virus replication.Hepatology (Baltimore, Md.) · 2017Article
- Identification of Polo-like kinases as potential novel drug targets for influenza A virus.Scientific reports · 2017Article
- Human IFIT1 Inhibits mRNA Translation of Rubulaviruses but Not Other Members of the Paramyxoviridae Family.Journal of virology · 2016Article
- Interactions of Prototype Foamy Virus Capsids with Host Cell Polo-Like Kinases Are Important for Efficient Viral DNA Integration.PLoS pathogens · 2016Article
- Mumps Virus Nucleoprotein Enhances Phosphorylation of the Phosphoprotein by Polo-Like Kinase 1.Journal of virology · 2016Article
- Regulation of Viral RNA Synthesis by the V Protein of Parainfluenza Virus 5.Journal of virology · 2015Article
- Review
- Article
- Paramyxovirus activation and inhibition of innate immune responses.Journal of molecular biology · 2013Review
- Phosphorylation of measles virus nucleoprotein affects viral growth by changing gene expression and genomic RNA stability.Journal of virology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The paramyxoviruses are a family of negative-sense RNA viruses that includes many important human and animal pathogens. Paramyxovirus RNA synthesis requires the viral phosphoprotein (P) and the large (L) protein. Phosphorylation of P is thought to regulate viral gene expression, though direct proof remains elusive. Recently, we reported that phosphorylation of a specific residue (Ser157) of the P protein of parainfluenza virus 5 (PIV5), a prototypical paramyxovirus, correlates with decreased viral gene expression and cytokine expression in infected cells. Here, we show that: Polo-like kinase 1 (PLK1), a serine/theronine kinase that plays a critical role in regulating the cell cycle, interacts with PIV5 P through the S157 residue; PLK1 inhibition increases viral gene expression; PLK1 over-expression inhibits viral gene expression; and PLK1 directly phosphorylates P in vitro, indicating that PLK1 down-regulates viral gene expression by phosphorylating P. Furthermore, we have determined the PLK1 phosphorylation site on P and found that mutant recombinant PIV5 whose P proteins cannot either bind to or be phosphorylated by PLK1 have similar phenotypes. Increased viral gene expression in PIV5 with mutations in the PLK1 binding/phosphorylation sites correlates with increased induction of cell death and cytokine expression, suggesting that PIV5 limits its viral gene expression to avoid these host effects. It is possible that targeting PLK1 will enhance host innate immune responses, leading to a novel strategy of clearing paramyxovirus infections quickly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.