ArticleScientific reports2017
Glycogen synthase kinase 3β inhibitors prevent hepatitis C virus release/assembly through perturbation of lipid metabolism.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026Review
- Identification of glycogen synthase kinase 3alpha/beta as a host factor required for HBV transcription using high-throughput screening.Hepatology (Baltimore, Md.) · 2025Article
- Multi-protomics analysis identified host cellular pathways perturbed by tick-borne encephalitis virus infection.Nature communications · 2024Article
- Chicken Glycogen Synthase Kinase 3β Suppresses Innate Immune Responses and Enhances Avian Leukosis Virus Replication in DF-1 Cells.Microbiology spectrum · 2023Article
- Review
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- Lithium salts as a treatment for COVID-19: Pre-clinical outcomes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Review
- Domain 2 of Hepatitis C Virus Protein NS5A Activates Glucokinase and Induces Lipogenesis in Hepatocytes.International journal of molecular sciences · 2022Article
- Article
- Article
- The Role of GSK-3 in Cancer Immunotherapy: GSK-3 Inhibitors as a New Frontier in Cancer Treatment.Cells · 2020Review
- Lithium's antiviral effects: a potential drug for CoViD-19 disease?International journal of bipolar disorders · 2020Review
- Review
- Lithium and coronaviral infections. A scoping review.F1000Research · 2020Article
- GSK3β Plays a Negative Role During White Spot Syndrome Virus (WSSV) Infection by Regulating NF-κB Activity in ShrimpFrontiers in immunology · 2020Article
- Glycogen synthase kinase 3ß participates in late stages of Dengue virus-2 infection.Memorias do Instituto Oswaldo Cruz · 2020Article
- HCV Pit Stop at the Lipid Droplet: Refuel Lipids and Put on a Lipoprotein Coat before Exit.Cells · 2019Review
- Discovery and characterization of a novel HCV inhibitor targeting the late stage of HCV life cycle.Antiviral therapy · 2019Article
- Glycogen Synthase Kinase 3β Enhances Hepatitis C Virus Replication by Supporting miR-122.Frontiers in microbiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Direct acting antivirals against hepatitis C virus (HCV) have markedly improved cure rates in the past few years. However, they are expensive, with only few targeting host cell factors, and affecting virus assembly and release. Huh7.5 cells infected with a JFH-1 clone of HCV were treated with two different glycogen synthase kinase (GSK3)-β inhibitors; AR-A014418 and lithium chloride. Intra- and extracellular HCV virions and specific infectivity was determined using real-time RT-PCR and TCID50, and changes in lipid production were identified by enzyme-linked immunoassay and mass spectrometry analyses. Similarly, effect on two HCV replicon cells were identified by the luciferase activity. Although there was limited effect on virus replication in Huh7.5 cells and replicons, Huh7.5 cells treated with GSK3β inhibitors produced significantly less viral particles in comparison to untreated cells. In addition, the treated cells synthesized significantly lower amounts of ApoB and trapped the ApoE lipoproteins in the cells. In conclusion, our study suggests that GSK3β plays a pivotal role in HCV virion assembly and release mediated in part through inhibition of apolipoprotein synthesis.
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