ArticlePLoS pathogens2017
Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 21 citations in OpenAlex.
- Activation-induced cytidine deaminase (AID) suppresses the activity of HBV EnhII/CP by downregulating FANCE expression.Virus genes · 2026Article
- Study Protocol for a Randomized Controlled Trial of Multisensory Early Oral Administration of Human Milk (M-MILK) for Very Preterm Infants: Enhancing Stress Regulation, Neurodevelopment, and Oral Feeding Skills.Biological research for nursing · 2026Article
- Early Life Stress, DNA Methylation of NR3C1 and HSD11B2 , and Oral Feeding Skill Development in Preterm Infants : A Pilot Study.Advances in neonatal care : official journal of the National Association of Neonatal Nurses · 2025Article
- Epigenetics Embedding of Oral Feeding Skill Development in Preterm Infants: A Study Protocol.Advances in neonatal care : official journal of the National Association of Neonatal Nurses · 2024Article
- Epigenetic modification of hepatitis B virus infection and related hepatocellular carcinoma.Virulence · 2024Review
- Foxa deficiency restricts hepatitis B virus biosynthesis through epigenic silencing.Journal of virology · 2024Article
- Ten-eleven translocation (Tet) methylcytosine dioxygenase-dependent viral DNA demethylation mediatesJournal of virology · 2024Article
- Selective effect of β-catenin on nuclear receptor-dependent hepatitis B virus transcription and replication.Virology · 2022Article
- Article
- Restoration of a functional antiviral immune response to chronic HBV infection by reducing viral antigen load: if not sufficient, is it necessary?Emerging microbes & infections · 2021Review
- Mechanisms of DNA Methylation in Virus-Host Interaction in Hepatitis B Infection: Pathogenesis and Oncogenetic Properties.International journal of molecular sciences · 2021Review
- Inhibiting roles of FOXA2 in liver cancer cell migration and invasion by transcriptionally suppressing microRNA-103a-3p and activating the GREM2/LATS2/YAP axis.Cytotechnology · 2021Article
- Relative DNA Methylation and Demethylation Efficiencies during Postnatal Liver Development Regulate Hepatitis B Virus Biosynthesis.Journal of virology · 2021Article
- Modulation of hepatitis B virus pregenomic RNA stability and splicing by histone deacetylase 5 enhances viral biosynthesis.PLoS pathogens · 2020Article
- Single Hepatocyte Hepatitis B Virus Transcriptional Landscape in HIV Coinfection.The Journal of infectious diseases · 2020Article
- 2-Amino-4-(1-piperidine) pyridine exhibits inhibitory effect on colon cancer through suppression of FOXA2 expression.3 Biotech · 2019Article
- Host functions used by hepatitis B virus to complete its life cycle: Implications for developing host-targeting agents to treat chronic hepatitis B.Antiviral research · 2018Review
- FOXA2 promotes the proliferation, migration and invasion, and epithelial mesenchymal transition in colon cancer.Experimental and therapeutic medicine · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The FoxA family of pioneer transcription factors regulates hepatitis B virus (HBV) transcription, and hence viral replication. Hepatocyte-specific FoxA-deficiency in the HBV transgenic mouse model of chronic infection prevents the transcription of the viral DNA genome as a result of the failure of the developmentally controlled conversion of 5-methylcytosine residues to cytosine during postnatal hepatic maturation. These observations suggest that pioneer transcription factors such as FoxA, which mark genes for expression at subsequent developmental steps in the cellular differentiation program, mediate their effects by reversing the DNA methylation status of their target genes to permit their ensuing expression when the appropriate tissue-specific transcription factor combinations arise during development. Furthermore, as the FoxA-deficient HBV transgenic mice are viable, the specific developmental timing, abundance and isoform type of pioneer factor expression must permit all essential liver gene expression to occur at a level sufficient to support adequate liver function. This implies that pioneer transcription factors can recognize and mark their target genes in distinct developmental manners dependent upon, at least in part, the concentration and affinity of FoxA for its binding sites within enhancer and promoter regulatory sequence elements. This selective marking of cellular genes for expression by the FoxA pioneer factor compared to HBV may offer the opportunity for the specific silencing of HBV gene expression and hence the resolution of chronic HBV infections which are responsible for approximately one million deaths worldwide annually due to liver cirrhosis and hepatocellular carcinoma.
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