ArticleJournal of virology2010
Polo-like kinase 1 is involved in hepatitis C virus replication by hyperphosphorylating NS5A.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.Pathogens (Basel, Switzerland) · 2024Review
- PLK3 facilitates replication of swine influenza virus by phosphorylating viral NP protein.Emerging microbes & infections · 2023Article
- Polo-like kinase-1 mediates hepatitis C virus-induced cell migration, a drug target for liver cancer.Life science alliance · 2023Article
- Subversion of a protein-microRNA signaling pathway by hepatitis C virus.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Master mitotic kinases regulate viral genome delivery during papillomavirus cell entry.Nature communications · 2023Article
- PLK1-ELAVL1/HuR-miR-122 signaling facilitates hepatitis C virus proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Sequential Phosphorylation of Hepatitis C Virus NS5A Protein Requires the ATP-Binding Domain of NS3 Helicase.Journal of virology · 2022Article
- Sequential Phosphorylation of the Hepatitis C Virus NS5A Protein Depends on NS3-Mediated Autocleavage between NS3 and NS4A.Journal of virology · 2020Article
- Stress proteins: the biological functions in virus infection, present and challenges for target-based antiviral drug development.Signal transduction and targeted therapy · 2020Review
- Phenotypic analysis of mutations at residue 146 provides insights into the relationship between NS5A hyperphosphorylation and hepatitis C virus genome replication.The Journal of general virology · 2020Article
- Influenza Virus Infections and Cellular Kinases.Viruses · 2019Review
- Characterization of a Threonine-Rich Cluster in Hepatitis C Virus Nonstructural Protein 5A and Its Contribution to Hyperphosphorylation.Journal of virology · 2018Article
- Sequential S232/S235/S238 Phosphorylation of the Hepatitis C Virus Nonstructural Protein 5A.Journal of virology · 2018Article
- Hydrophobic Derivatives of Glycopeptide Antibiotics as Inhibitors of Protein Kinases.Biochemistry. Biokhimiia · 2018Article
- 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
- Serine 235 Is the Primary NS5A Hyperphosphorylation Site Responsible for Hepatitis C Virus Replication.Journal of virology · 2017Article
- Human Choline Kinase-α Promotes Hepatitis C Virus RNA Replication through Modulation of Membranous Viral Replication Complex Formation.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
- Phosphoproteomics Identified an NS5A Phosphorylation Site Involved in Hepatitis C Virus Replication.The Journal of biological chemistry · 2016Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) replication involves many viral and host factors. Here, we employed a lentivirus-based RNA interference (RNAi) screening approach to search for possible cellular factors. By using a kinase-phosphatase RNAi library and an HCV replicon reporter system, we identified a serine-threonine kinase, Polo-like kinase 1 (Plk1), as a potential host factor regulating HCV replication. Knockdown of Plk1 reduced both HCV RNA replication and nonstructural (NS) protein production in both HCV replicon cells and HCV-infected cells while it did not significantly affect host cellular growth or cell cycle. Overexpression of Plk1 in the knockdown cells rescued HCV replication. Interestingly, the ratio between the hyperphosphorylated form (p58) and the basal phosphorylated form (p56) of NS5A was lower in the Plk1 knockdown cells and Plk1 kinase inhibitor-treated cells than in the control groups. Further studies showed that Plk1 could be immunoprecipitated together with NS5A. Both proteins partially colocalized in the perinuclear region. Furthermore, Plk1 could phosphorylate NS5A to both the p58 and p56 forms in an in vitro assay system; the phosphorylation efficiency was comparable to that of the reported casein kinase. Taken together, this study shows that Plk1 is an NS5A phosphokinase and thereby indirectly regulates HCV RNA replication. Because of the differential effects of Plk1 on HCV replication and host cell growth, Plk1 could potentially serve as a target for anti-HCV therapy.
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