ArticleJournal of virology2001
Induction of pRb degradation by the human papillomavirus type 16 E7 protein is essential to efficiently overcome p16INK4a-imposed G1 cell cycle Arrest.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Accuracy of HPV E6/E7 oncoprotein tests to detect high-grade cervical lesions: a systematic literature review and meta-analysis.British journal of cancer · 2024Pooled it
- Quantitative assessment of STAT3 and HPV16 E6 transcripts using Flow-FISH approach for early detection of progressive cervical lesions.World journal of experimental medicine · 2026Article
- Diversity of polyomaviruses and papillomaviruses in penguins from eastern and western Antarctica.Microbial genomics · 2025Article
- Splicing of HPV16 E6 promotes aggressive invasion in oropharyngeal cancer via endocytosis of E-cadherin.bioRxiv : the preprint server for biology · 2025Article
- CRISPR-Cas technologies: Emerging tools from research to clinical application.Journal of microbiology (Seoul, Korea) · 2025Review
- Advances in understanding the mechanisms of the human papillomavirus oncoproteins.Biochemical Society transactions · 2025Review
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- Immortalization of Mesenchymal Stem Cells for Application in Regenerative Medicine and Their Potential Risks of Tumorigenesis.International journal of molecular sciences · 2024Review
- Characterization of multiple human papillomavirus types in the human vagina following ovarian hormonal stimulation.Virology journal · 2024Article
- Merkel Cell Polyomavirus targets SET/PP2A complex to promote cellular proliferation and migration.Virology · 2024Article
- High-Risk HPV CISH Detection in Cervical Biopsies with Weak and/or Focal p16 Immunohistochemical Positivity.International journal of molecular sciences · 2024Article
- HPV-associated oropharyngeal cancer: in search of surrogate biomarkers for early lesions.Oncogene · 2024Review
- Clinical, morphologic and molecular heterogeneity of HPV-associated oropharyngeal cancer.Oncogene · 2023Review
- p16Infectious agents and cancer · 2023Article
- Relationship between Human Papillomavirus Status and the Cervicovaginal Microbiome in Cervical Cancer.Microorganisms · 2023Review
- Identification of novel HLA-A*11:01-restricted HPV16 E6/E7 epitopes and T-cell receptors for HPV-related cancer immunotherapy.Journal for immunotherapy of cancer · 2022Article
- Lyon IARC Polyomavirus Displays Transforming Activities in Primary Human Cells.Journal of virology · 2022Article
- Article
- Peptide-Based Nanovaccines in the Treatment of Cervical Cancer: A Review of Recent Advances.International journal of nanomedicine · 2022Review
- Prevalence of genital HPV infection in STI and healthy populations and risk factors for viral persistence.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has previously been shown that the E7 protein from the cutaneous human papillomavirus type 1 (HPV1), which is associated with benign skin lesions, binds the product of the tumor suppressor gene retinoblastoma (pRb) with an efficiency similar to that of the E7 protein from the oncogenic HPV type 16. Despite this ability, HPV1 E7 does not display any activity in transforming primary cells. In addition, the two viral proteins differ in their mechanisms of targeting pRb. HPV16 E7 promotes pRb destabilization, while cells expressing HPV1 E7 do not show any decrease in pRb levels. In this study, we show that HPV1 E7, in contrast to HPV16 E7, has only a weak activity to neutralize the effect of cyclin-dependent kinase inhibitor p16INK4a. By generation of HPV1/16 E7 chimeric proteins, we have identified a central motif in the two E7 proteins, which determines their different abilities to overcome the p16INK4a-mediated cell cycle arrest. This motif is located downstream of the pRb-binding domain and comprises only three amino acids in HPV16 E7. Swapping this central motif in the two viral proteins causes an exchange of their activities involved in circumventing the inhibitory function of p16INK4a. Most importantly, our data show that the efficiency of the E7 proteins in neutralizing the inhibitory effect of p16INK4a correlates with their ability to promote pRb degradation.
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