ArticleJournal of virology2004
Regulation of hepatitis B virus core promoter by transcription factors HNF1 and HNF4 and the viral X protein.
Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 98 citations in OpenAlex.
- IFI35 suppresses the transcription of hepatitis B virus cccDNA minichromosome via promoting HNF4α proteasomal degradation.Journal of biomedical science · 2026Article
- Impact of a naturally occurring hepatitis B virus genotype D-specific core-promoter mutation on viral replication.The Journal of general virology · 2026Article
- Kaempferol inhibits hepatitis B virus replicationFrontiers in cellular and infection microbiology · 2026Article
- HCC-derived SNU cell lines as model systems to study HBV life cycle.Journal of virology · 2025Article
- TRIM proteins: A 'swiss army knife' of antiviral immunity.PLoS pathogens · 2025Review
- Liver mechanosignaling as a natural anti-hepatitis B virus mechanism.Nature communications · 2024Article
- Deubiquitinase OTUD5 promotes hepatitis B virus replication by removing K48-linked ubiquitination of HBV core/precore and upregulates HNF4ɑ expressions by inhibiting the ERK1/2/mitogen-activated protein kinase pathway.Cellular and molecular life sciences : CMLS · 2023Article
- Fibroblast Growth Factor 11 Inhibits Hepatitis B Virus Gene Expression Through FXRα Suppression.Journal of microbiology (Seoul, Korea) · 2023Article
- Pathogenicity and virulence of Hepatitis B virus.Virulence · 2022Review
- Review
- (-)-Lariciresinol Isolated from the Roots ofMolecules (Basel, Switzerland) · 2022Article
- Review
- GATA binding protein 4 promotes the expression and transcription of hepatitis B virus by facilitating hepatocyte nuclear factor 4 alpha in vitro.Virology journal · 2021Article
- Review
- Silencing hepatitis B virus covalently closed circular DNA: The potential of an epigenetic therapy approach.World journal of gastroenterology · 2021Review
- [Role of the liver-enriched transcription factor binding site mutation in the C promoter region of hepatitis B virus genome for HBx-enhanced hepatitis B virus replication].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- The Functional and Antiviral Activity of Interferon Alpha-Inducible IFI6 Against Hepatitis B Virus Replication and Gene Expression.Frontiers in immunology · 2021Article
- Hepatocyte Growth Factor-Dependent Antiviral Activity of Activated cdc42-Associated Kinase 1 Against Hepatitis B Virus.Frontiers in microbiology · 2021Article
- Biological Characterization of Hepatitis B virus Genotypes: Their Role in Viral Replication and Antigen Expression.Frontiers in microbiology · 2021Article
- Establishment of a novel hepatitis B virus culture system using immortalized human hepatocytes.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) core promoter contains a binding site for nuclear receptors. A natural double mutation in this binding site, which changes nucleotide (nt) 1765 from A to T and nt 1767 from G to A, selectively abolishes the binding of several nuclear receptors without affecting that of HNF4. This double mutation also creates a binding site for the transcription factor HNF1 and changes two amino acids in the overlapping X protein sequence. In this study, we have examined the roles of HNF1, HNF4, and the X protein in the regulation of the core promoter activities in Huh7 hepatoma cells. Our results indicate that HNF4 could stimulate the expression of the precore RNA and the core RNA from the core promoter of both the wild-type (WT) HBV and the double mutant, although its effect on the former was more prominent. In contrast, HNF1, which did not affect the WT core promoter, suppressed the precore RNA expression of the double mutant. Further analysis using HBV genomic constructs, with and without the ability to express the X protein, indicates that the X protein did not affect the HNF4 activity on the core promoter and affected the HNF1 activity on the core promoter of only the double mutant. Thus, our results indicate that the phenotypic differences of HBV WT and double-mutant core promoters are at least partially due to the differential activities of HNF1, HNF4, and the X protein on these two promoters.
Indexed as
Identifiers
What OpenQuestion holds
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.