ArticleThe Journal of biological chemistry2015
Dysregulation of retinoic acid receptor diminishes hepatocyte permissiveness to hepatitis B virus infection through modulation of sodium taurocholate cotransporting polypeptide (NTCP) expression.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- A key role for the exoribonuclease XRN1 in regulating the hepatitis B viral transcriptome.iScience · 2026Article
- The Evolution of Cell Culture Systems to Study Hepatitis B Virus Pathogenesis and Antiviral Susceptibility.Viruses · 2025Review
- Development of anFrontiers in pharmacology · 2025Article
- Targeting NTCP for liver disease treatment: A promising strategy.Journal of pharmaceutical analysis · 2024Review
- The Interactions between Cells and Viruses.International journal of molecular sciences · 2024Article
- ATP5B Is an Essential Factor for Hepatitis B Virus Entry.International journal of molecular sciences · 2022Article
- Novel Neplanocin A Derivatives as Selective Inhibitors of Hepatitis B Virus with a Unique Mechanism of Action.Antimicrobial agents and chemotherapy · 2022Article
- Fungal Secondary Metabolite Exophillic Acid Selectively Inhibits the Entry of Hepatitis B and D Viruses.Viruses · 2022Article
- The kinesin KIF4 mediates HBV/HDV entry through the regulation of surface NTCP localization and can be targeted by RXR agonists in vitro.PLoS pathogens · 2022Article
- Regulation of the HBV Entry Receptor NTCP and its Potential in Hepatitis B Treatment.Frontiers in molecular biosciences · 2022Review
- Review
- Envelope Proteins of Hepatitis B Virus: Molecular Biology and Involvement in Carcinogenesis.Viruses · 2021Review
- Advances in HBV infection and replication systems in vitro.Virology journal · 2021Review
- The role of the retinoid receptor, RAR/RXR heterodimer, in liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- Hepatitis D Virus Entry Inhibitors Based on Repurposing Intestinal Bile Acid Reabsorption Inhibitors.Viruses · 2021Article
- Circadian control of hepatitis B virus replication.Nature communications · 2021Article
- Selective hepatitis B and D virus entry inhibitors from the group of pentacyclic lupane-type betulin-derived triterpenoids.Scientific reports · 2020Article
- Hepatitis B Virus Entry into Cells.Cells · 2020Review
- Non-nucleoside hepatitis B virus polymerase inhibitors identified by an in vitro polymerase elongation assay.Journal of gastroenterology · 2020Article
- Identification of SARS-CoV-2 Cell Entry Inhibitors by Drug Repurposing UsingFrontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium taurocholate cotransporting polypeptide (NTCP) is an entry receptor for hepatitis B virus (HBV) and is regarded as one of the determinants that confer HBV permissiveness to host cells. However, how host factors regulate the ability of NTCP to support HBV infection is largely unknown. We aimed to identify the host signaling that regulated NTCP expression and thereby permissiveness to HBV. Here, a cell-based chemical screening method identified that Ro41-5253 decreased host susceptibility to HBV infection. Pretreatment with Ro41-5253 inhibited the viral entry process without affecting HBV replication. Intriguingly, Ro41-5253 reduced expression of both NTCP mRNA and protein. We found that retinoic acid receptor (RAR) regulated the promoter activity of the human NTCP (hNTCP) gene and that Ro41-5253 repressed the hNTCP promoter by antagonizing RAR. RAR recruited to the hNTCP promoter region, and nucleotides -112 to -96 of the hNTCP was suggested to be critical for RAR-mediated transcriptional activation. HBV susceptibility was decreased in pharmacologically RAR-inactivated cells. CD2665 showed a stronger anti-HBV potential and disrupted the spread of HBV infection that was achieved by continuous reproduction of the whole HBV life cycle. In addition, this mechanism was significant for drug development, as antagonization of RAR blocked infection of multiple HBV genotypes and also a clinically relevant HBV mutant that was resistant to nucleoside analogs. Thus, RAR is crucial for regulating NTCP expression that determines permissiveness to HBV infection. This is the first demonstration showing host regulation of NTCP to support HBV infection.
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