ArticleJournal of virology2004
Roles of the E6 and E7 proteins in the life cycle of low-risk human papillomavirus type 11.
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 50 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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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
50 citing papers in PubMed, 113 citations in OpenAlex.
- Integrating non-coding RNA profiling with HPV genotyping for cervical cancer risk stratification and early detection.Molecular biology reports · 2026Review
- Development of a novel prognostic assessment tool for recurrent respiratory papillomatosis.BMC medicine · 2026Article
- Clinical, virological, and immunohistochemical features of laryngeal papilloma with low-risk human papillomavirus infection: insights from a 13-year institutional cohort.World journal of surgical oncology · 2026Article
- PATHOMORPHOLOGY OF VERRUCAE: A CLINICOPATHOLOGIC STUDY.Annals of Ibadan postgraduate medicine · 2024Article
- Human Viral Oncoproteins and Ubiquitin-Proteasome System.Global medical genetics · 2024Review
- VEGF as a Key Actor in Recurrent Respiratory Papillomatosis: A Narrative Review.Current issues in molecular biology · 2024Review
- Expression profile of long noncoding RNAs and comprehensive analysis of lncRNA-cisTF-DGE regulation in condyloma acuminatum.BMC medical genomics · 2024Article
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- HPV E6 inhibits E6AP to regulate epithelial homeostasis by modulating keratinocyte differentiation commitment and YAP1 activation.PLoS pathogens · 2023Article
- Human papillomavirus type 16 E6 induces cell competition.PLoS pathogens · 2022Article
- HPV and Recurrent Respiratory Papillomatosis: A Brief Review.Life (Basel, Switzerland) · 2021Review
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- Human Papillomavirus and Cellular Pathways: Hits and Targets.Pathogens (Basel, Switzerland) · 2021Review
- Persistent Human Papillomavirus Infection.Viruses · 2021Review
- Modeling and Molecular Dynamics of the 3D Structure of the HPV16 E7 Protein and Its Variants.International journal of molecular sciences · 2021Article
- MHC Phosphopeptides: Promising Targets for Immunotherapy of Cancer and Other Chronic Diseases.Molecular & cellular proteomics : MCP · 2021Review
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- Human PapillomavirusPathogens (Basel, Switzerland) · 2020Article
- HPV Oncoproteins and the Ubiquitin Proteasome System: A Signature of Malignancy?Pathogens (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Many important functions have been attributed to the high-risk human papillomavirus (HPV) E6 and E7 proteins, including binding and degradation of p53 as well as interacting with Rb proteins. In contrast, the physiological roles of the low-risk E6 and E7 proteins remain unclear. Previous studies demonstrated that the high-risk E6 and E7 proteins also play roles in the productive life cycle by facilitating the maintenance of viral episomes (J. T. Thomas, W. G. Hubert, M. N. Ruesch, and L. A. Laimins, Proc. Natl. Acad. Sci. USA 96:8449-8454, 1999). In order to determine whether low-risk E6 or E7 is similarly necessary for the stable maintenance of episomes, HPV type 11 (HPV-11) genomes that contained translation termination mutations in E6 or E7 were constructed. Upon transfection into normal human keratinocytes, genomes in which E6 function was abolished were unable to be maintained episomally. Transfection of genomes containing substitution mutations in amino acids conserved in high- and low-risk HPV types suggested that multiple protein domains are involved in this process. Examination of cells transfected with HPV-11 genomes in which E7 function was inhibited were found to exhibit a more complex phenotype. At the second passage following transfection, mutant genomes were maintained as episomes but at significantly reduced levels than in cells transfected with the wild-type HPV-11 genome. Upon further passage in culture, however, the episomal forms of these E7 mutant genomes quickly disappeared. These findings identify important new functions for the low-risk E6 and E7 proteins in the episomal maintenance of low-risk HPV-11 genomes and suggest that they may act in a manner similar to that observed for the high-risk proteins.
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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.