ArticleJournal of virology2005
Examination of the pRb-dependent and pRb-independent functions of E7 in vivo.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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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
42 citing papers in PubMed, 72 citations in OpenAlex.
- Inactivation of the RB1 and PTPN14 tumor suppressors cooperatively enables the carcinogenic activity of the human papillomavirus E7 oncoprotein.bioRxiv : the preprint server for biology · 2026Article
- Review
- A safe and potentiated multi-type HPV L2-E7 nanoparticle vaccine with combined prophylactic and therapeutic activity.NPJ vaccines · 2024Article
- HPV18 E7 inhibits LATS1 kinase and activates YAP1 by degrading PTPN14.bioRxiv : the preprint server for biology · 2024Article
- Article
- HPV-18 E7 Interacts with Elk-1 Leading to Elevation of the Transcriptional Activity of Elk-1 in Cervical Cancer.Biomolecules & therapeutics · 2022Article
- Review
- Merkel cell polyomavirus large T antigen binding to pRb promotes skin hyperplasia and tumor development.PLoS pathogens · 2022Article
- YAP1 activation by human papillomavirus E7 promotes basal cell identity in squamous epithelia.eLife · 2022Article
- A model of impaired Langerhans cell maturation associated with HPV induced epithelial hyperplasia.iScience · 2021Article
- Article
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Modeling and Molecular Dynamics of the 3D Structure of the HPV16 E7 Protein and Its Variants.International journal of molecular sciences · 2021Article
- Restoring the DREAM Complex Inhibits the Proliferation of High-Risk HPV Positive Human Cells.Cancers · 2021Article
- A Conserved Amino Acid in the C Terminus of Human Papillomavirus E7 Mediates Binding to PTPN14 and Repression of Epithelial Differentiation.Journal of virology · 2020Article
- Structural basis for recognition of the tumor suppressor protein PTPN14 by the oncoprotein E7 of human papillomavirus.PLoS biology · 2019Article
- Review
- Regulation of Cellular Metabolism by High-Risk Human Papillomaviruses.International journal of molecular sciences · 2018Review
- Oxidative stress in female cancers.Oncotarget · 2018Review
- Modulation of antigen presenting cell functions during chronic HPV infection.Papillomavirus research (Amsterdam, Netherlands) · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
High-risk human papillomaviruses encode two oncogenes, E6 and E7, expressed in nearly all cervical cancers. Although E7 protein is best known for its ability to inactivate the retinoblastoma tumor suppressor protein, pRb, many other activities for E7 have been proposed in in vitro studies. Herein, we describe studies that allowed us to define unambiguously the pRb-dependent and -independent activities of E7 for the first time in vivo. In these studies, we crossed mice transgenic for human papillomavirus 16 E7 to knock-in mice genetically engineered to express a mutant form of pRb (pRb(DeltaLXCXE)) that is selectively defective for binding E7. pRb inactivation was necessary for E7 to induce DNA synthesis and to overcome differentiation-dependent cell cycle withdrawal and DNA damage-induced cell cycle arrest. While most of E7's effects on epidermal differentiation were found to require pRb inactivation, a modest delay in terminal differentiation with resulting hyperplasia was observed in E7 mice on the Rb(DeltaLXCXE) mutant background. E7-induced p21 upregulation was also pRb dependent, and genetic Rb inactivation was sufficient to reproduce this effect. While E7-mediated p21 induction was partially p53 dependent, neither p53 nor p21 induction by E7 required p19(ARF). These data show that E7 upregulates the expression of p53 and p21 via pRb-dependent mechanisms distinct from the proposed p19-Mdm2 pathway. These results extend our appreciation of the importance of pRb as a relevant target for high-risk E7 oncoproteins.
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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.