ArticleJournal of virology2012
p53 degradation activity, expression, and subcellular localization of E6 proteins from 29 human papillomavirus genotypes.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 91 citations in OpenAlex.
- Post-translational control of IL-1β via the human papillomavirus type 16 E6 oncoprotein: a novel mechanism of innate immune escape mediated by the E3-ubiquitin ligase E6-AP and p53.PLoS pathogens · 2013Trial
- Molecular insights and therapeutic innovations in low-risk human papillomavirus-associated cutaneous wart.Molecular biology reports · 2026Review
- High-risk HPV E6 induces an aneuploidy-prone chromosome congression defect through destabilization of CENP-E.Journal of virology · 2026Article
- Review
- Article
- Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Role of human papillomavirus (HPV) variants and host genetic susceptibility in cervical carcinogenesis.Archives of microbiology · 2026Review
- Article
- Article
- Cervical Cancer in the Era of HPV: Translating Molecular Mechanisms into Preventive Public Health Action.International journal of molecular sciences · 2025Review
- Translational regulation of human papillomavirus mRNAs in carcinogenesis: old questions and new insights.Frontiers in cell and developmental biology · 2025Review
- Why HPV16? Why, now, HPV42? How the discovery of HPV42 in rare cancers provides an opportunity to challenge our understanding about the transition between health and disease for common members of the healthy microbiota.FEMS microbiology reviews · 2024Review
- Alternative splicing in the genome of HPV and its regulation.Frontiers in cellular and infection microbiology · 2024Review
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Human papillomavirus infection, cervical cancer and the less explored role of trace elements.Biological trace element research · 2023Review
- Differences in integration frequencies and APOBEC3 profiles of five high-risk HPV types adheres to phylogeny.Tumour virus research · 2022Article
- Activating transcription factor 3 mediates apoptotic functions through a p53-independent pathway in human papillomavirus 18 infected HeLa cells.Virus genes · 2022Article
- Non-human primate papillomavirus E6-mediated p53 degradation reveals ancient evolutionary adaptation of carcinogenic phenotype to host niche.PLoS pathogens · 2022Article
- An enhanced triple fluorescence flow-cytometry-based assay shows differential activation of the Notch signaling pathway by human papillomavirus E6 proteins.Scientific reports · 2022Article
- High-Risk Human Papillomavirus Oncogenic E6/E7 mRNAs Splicing Regulation.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Human papillomaviruses (HPVs) are the etiological agents of cervical cancer and other human malignancies. HPVs are classified into high- and low-risk genotypes according to their association with cancer. Host cell transformation by high-risk HPVs relies in part on the ability of the viral E6 protein to induce the degradation of p53. We report the development of a cellular assay that accurately quantifies the p53 degradation activity of E6 in vivo, based on the fusion of p53 to Renilla luciferase (RLuc-p53). This assay was used to measure the p53 degradation activities of E6 proteins from 29 prevalent HPV types and variants of HPV type 16 (HPV16) and HPV33 by determining the amount of E6 expression vector required to reduce by half the levels of RLuc-p53 (50% effective concentration [EC₅₀]). These studies revealed an unexpected variability in the p53 degradation activities of different E6 proteins, even among active types whose EC₅₀s span more than 2 log units. Differences in activity were greater between types than between variants and did not correlate with differences in the intracellular localization of E6, with most being predominantly nuclear. Protein and mRNA expression of the 29 E6 proteins was also examined. For 16 high-risk types, spliced transcripts that encode shorter E6*I proteins of variable sizes and abundances were detected. Mutation of the splice donor site in five different E6 proteins increased their p53 degradation activity, suggesting that mRNA splicing can limit the activity of some high-risk E6 types. The quantification of p53 degradation in vivo represents a novel tool to systematically compare the oncogenic potentials of E6 proteins from different HPV types and variants.
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Registered trials
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