ArticleJournal of virology2002
A transactivator function of cottontail rabbit papillomavirus e2 is essential for tumor induction in rabbits.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Modeling HPV-Associated Disease and Cancer Using the Cottontail Rabbit Papillomavirus.Viruses · 2022Review
- Orf Virus-Based Therapeutic Vaccine for Treatment of Papillomavirus-Induced Tumors.Journal of virology · 2020Article
- The rabbit papillomavirus model: a valuable tool to study viral-host interactions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Cottontail Rabbit Papillomavirus E1 and E2 Proteins Mutually Influence Their Subcellular Localizations.Journal of virology · 2018Article
- BET bromodomain inhibitors show anti-papillomavirus activity in vitro and block CRPV wart growth in vivo.Antiviral research · 2018Article
- Papillomavirus-Associated Tumor Formation Critically Depends on c-Fos Expression Induced by Viral Protein E2 and Bromodomain Protein Brd4.PLoS pathogens · 2016Article
- Review
- A novel pre-clinical murine model to study the life cycle and progression of cervical and anal papillomavirus infections.PloS one · 2015Article
- A novel recombinant papillomavirus genome enabling in vivo RNA interference reveals that YB-1, which interacts with the viral regulatory protein E2, is required for CRPV-induced tumor formation in vivo.American journal of cancer research · 2014Article
- The papillomavirus E2 proteins.Virology · 2013Review
- Production of human papilloma virus type 16 e6 oncoprotein as a recombinant protein in eukaryotic cells.Iranian journal of cancer prevention · 2012Article
- Small molecule inhibitors of human papillomavirus protein - protein interactions.The open virology journal · 2011Article
- Differences in methodology, but not differences in viral strain, account for variable experimental outcomes in laboratories utilizing the cottontail rabbit papillomavirus model.Journal of virological methods · 2010Article
- Papillomavirus DNA complementation in vivo.Virus research · 2009Article
- Wounding prior to challenge substantially improves infectivity of cottontail rabbit papillomavirus and allows for standardization of infection.Journal of virological methods · 2008Article
- Replication and partitioning of papillomavirus genomes.Advances in virus research · 2008Review
- Impact of genetic changes to the CRPV genome and their application to the study of pathogenesis in vivo.Virology · 2007Article
- Recent advances in the search for antiviral agents against human papillomaviruses.Antiviral therapy · 2007Review
- Identification of the E9/E2C cDNA and functional characterization of the gene product reveal a new repressor of transcription and replication in cottontail rabbit papillomavirus.Journal of virology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of domestic rabbits with cottontail rabbit papillomavirus (CRPV) causes local papillomas which progress to carcinomas in more than 80% of cases. This animal model system therefore allows the identification of molecular mechanisms required for the induction and progression of epithelial tumors. The viral E2 protein stimulates both viral DNA replication and transcription, and these functions can be genetically separated. We introduced the respective mutations into CRPV E2 and found, in line with published data for other papillomavirus E2 proteins, that mutation of the highly conserved amino acid 37 or 73 resulted in replication-competent but transactivation-deficient E2 proteins, whereas E2 proteins with mutations at residue 39 were replication deficient and transactivation competent. The R37A, I73L, and I73A E2 mutants, showing a loss of transactivation function, and the R37K E2 mutant, which is still transactivation competent, were introduced into the whole genome of CRPV, which was then injected into the skin of rabbits. Strikingly, the ability to induce tumors within 6 weeks was abolished by each of the E2 mutations, in contrast to the tumor induction rate (93%) obtained with wild-type CRPV DNA. Two small papillomas induced by mutant E2 I73A CRPV DNA appeared as late as 12 or 24 weeks postinjection, were significantly smaller, and showed no further extension of growth. These data suggest that functionally conserved amino acids in the transactivation domain of E2 are also required for the induction and growth of epithelial tumors in rabbits infected with CRPV.
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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.