ArticleJournal of virology1994
Identification of factor-binding sites in the duck hepatitis B virus enhancer and in vivo effects of enhancer mutations.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Characterization of nucleosome positioning in hepadnaviral covalently closed circular DNA minichromosomes.Journal of virology · 2012Article
- Zinc finger proteins designed to specifically target duck hepatitis B virus covalently closed circular DNA inhibit viral transcription in tissue culture.Journal of virology · 2008Article
- Identification and characterization of avihepadnaviruses isolated from exotic anseriformes maintained in captivity.Journal of virology · 2005Article
- Avian and Mammalian hepadnaviruses have distinct transcription factor requirements for viral replication.Journal of virology · 2002Article
- Hepatitis B virus biology.Microbiology and molecular biology reviews : MMBR · 2000Review
- In vivo effects of mutations in woodchuck hepatitis virus enhancer II.Journal of virology · 1998Article
- A functional hepatocyte nuclear factor 3 binding site is a critical component of the duck hepatitis B virus major surface antigen promoter.Journal of virology · 1996Article
- The HNF1/HNF4-dependent We2 element of woodchuck hepatitis virus controls viral replication and can activate the N-myc2 promoter.Journal of virology · 1996Article
- Gfi-1 encodes a nuclear zinc finger protein that binds DNA and functions as a transcriptional repressor.Molecular and cellular biology · 1996Article
- Cellular factors controlling the activity of woodchuck hepatitis virus enhancer II.Journal of virology · 1996Article
- Sequence-selective carbohydrate-DNA interaction: dimeric and monomeric forms of the calicheamicin oligosaccharide interfere with transcription factor function.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Illegitimate replication of linear hepadnavirus DNA through nonhomologous recombination.Journal of virology · 1995Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hepatitis B viruses (hepadnaviruses) can cause chronic, productive infections of hepatocytes. Analyses of the enhancers and promoters of these viruses in cell lines have suggested a requirement of these elements for liver-enriched transcription factors. In this study, a minimum of seven factor-binding sites on the duck hepatitis B virus enhancer were detected by DNase I footprinting using duck liver nuclear extracts. Among the sites that were tentatively identified were one C/EBP-, one HNF1-, and two HNF3-binding sites. Mutations of the HNF1- and HNF3-like sites, which eliminated factor binding, as assessed by both DNase I footprinting and competitive gel shift assays, were evaluated for their effects on enhancer activity. Using a construct in which human growth hormone was expressed from the viral enhancer and core gene promoter, we found that all of the mutations, either alone or in combination, reduced expression two- to fourfold in LMH chicken hepatoma cells. The mutations in the HNF1 site and one of the HNF3 sites, when inserted into the intact viral genome, also suppressed virus RNA synthesis in primary hepatocyte cultures. Virus carrying the latter HNF3 mutation was also examined for its ability to infect and replicate in ducks. No significant inhibition of virus replication was observed in a short-term assay; however, virus with the HNF3 mutation was apparently unable to grow in the pancreas, a second site of duck hepatitis B virus replication in the duck.
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