ArticleJournal of virology2003
Direct activation of cyclin-dependent kinase 2 by human papillomavirus E7.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
- Plant Bioactive Constituents and Their Potential Benefits in HPV-Positive Oropharyngeal Squamous Cell Carcinoma-A Narrative Review.Current issues in molecular biology · 2026Review
- Cell cycle gene expression and microbial profiles associated with HPV related cervical neoplasia and cervical microbiome shifts.Scientific reports · 2026Article
- Cyclin Dependent Kinases in Antiviral Drug Discovery.Current medicinal chemistry · 2025Review
- Molecular aspects of cervical cancer: a pathogenesis update.Frontiers in oncology · 2024Review
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- Review
- The Not-So-Good, the Bad and the Ugly: HPV E5, E6 and E7 Oncoproteins in the Orchestration of Carcinogenesis.Viruses · 2021Review
- The Role of Ataxia Telangiectasia Mutant and Rad3-Related DNA Damage Response in Pathogenesis of Human Papillomavirus.Pathogens (Basel, Switzerland) · 2020Review
- Cyclin-dependent kinases and CDK inhibitors in virus-associated cancers.Infectious agents and cancer · 2020Review
- Impact of Replication Stress in Human Papillomavirus Pathogenesis.Journal of virology · 2019Review
- iTRAQ-Based Global Phosphoproteomics Reveals Novel Molecular Differences BetweenFrontiers in cellular and infection microbiology · 2019Article
- Recent Insights into the Control of Human Papillomavirus (HPV) Genome Stability, Loss, and Degradation.Journal of clinical medicine · 2015Article
- Manipulation of cellular DNA damage repair machinery facilitates propagation of human papillomaviruses.Seminars in cancer biology · 2014Review
- Role of Cdk1 in DNA damage-induced G1 checkpoint abrogation by the human papillomavirus E7 oncogene.Cell cycle (Georgetown, Tex.) · 2014Article
- Article
- The papillomavirus E7 proteins.Virology · 2013Review
- Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.Virology · 2012Review
- RNA interference for the treatment of papillomavirus disease.The open virology journal · 2012Article
- E6 and E7 from human papillomavirus type 16 cooperate to target the PDZ protein Na/H exchange regulatory factor 1.Journal of virology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Addition of human papillomavirus (HPV) E7 CDK2/cyclin A or CDK2/cyclin E, purified from either insect cells or bacteria, dramatically upregulates histone H1 kinase activity. Activation is substrate specific, with a smaller effect noted for retinoblastoma protein (Rb). The CDK2 stimulatory activity is equivalent in high-risk (HPV type 16 [HPV16] and HPV31) and low-risk (HPV6b) E7. Mutational analyses of HPV16 E7 indicate that the major activity resides in amino acids 9 to 38, spanning CR1 and CR2, and does not require casein kinase II or Rb-binding domain functions. Synthetic peptides spanning HPV16 amino acid residues 9 to 38 also activate CDK2. Peptides containing this sequence that carry biotin on the carboxy terminus, as well as a photoactivated cross-linking group (benzophenone), also activate the complex and covalently associate with the CDK2/cyclin A complex in a specific manner requiring UV. Cross-linking studies that use protein monomers detect association of the E7 peptides with cyclin A but not CDK2. Together, our results indicate a novel mechanism whereby E7 promotes HPV replication by directly altering CDK2 activity and substrate specificity.
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What OpenQuestion holds
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.