ReviewFuture microbiology2013
Regulation of the life cycle of HPVs by differentiation and the DNA damage response.
Review in Future microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- Oral Innate Immunity and the Role of Oral Epithelial Cells.Advances in experimental medicine and biology · 2026Review
- Harnessing the Power of Microbiota: How Do KeyBiology · 2025Review
- Genome integration of human DNA oncoviruses.Journal of virology · 2025Review
- Review
- Inhibition of human cytomegalovirus entry into mucosal epithelial cells.Antiviral research · 2024Article
- A novel HPV16 splicing enhancer critical for viral oncogene expression and cell immortalization.Nucleic acids research · 2024Article
- Focal Adhesion Kinase Binds to the HPV E2 Protein to Regulate Initial Replication after Infection.Pathogens (Basel, Switzerland) · 2023Article
- Polymorphisms in the Nonhomologous End-joining DNA Repair Pathway are Associated with HPV Integration in Cervical Dysplasia.Cancer prevention research (Philadelphia, Pa.) · 2023Article
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- Like Brothers in Arms: How Hormonal Stimuli and Changes in the Metabolism Signaling Cooperate, Leading HPV Infection to Drive the Onset of Cervical Cancer.International journal of molecular sciences · 2022Review
- hnRNP G/RBMX enhances HPV16 E2 mRNA splicing through a novel splicing enhancer and inhibits production of spliced E7 oncogene mRNAs.Nucleic acids research · 2022Article
- Article
- Review
- Regulation of the Human Papillomavirus Lifecyle through Post-Translational Modifications of the Viral E2 Protein.Pathogens (Basel, Switzerland) · 2021Review
- HRRD: a manually-curated database about the regulatory relationship between HPV and host RNA.Scientific reports · 2020Article
- Using a Human Papillomavirus Model to Study DNA Replication and Repair of Wild Type and Damaged DNA Templates in Mammalian Cells.International journal of molecular sciences · 2020Review
- Heterogeneous Nuclear Ribonucleoprotein A1 (hnRNP A1) and hnRNP A2 Inhibit Splicing to Human Papillomavirus 16 Splice Site SA409 through a UAG-Containing Sequence in the E7 Coding Region.Journal of virology · 2020Article
- Pyk2 Regulates Human Papillomavirus Replication by Tyrosine Phosphorylation of the E2 Protein.Journal of virology · 2020Article
- Regulation of the Human Papillomavirus Life Cycle by DNA Damage Repair Pathways and Epigenetic Factors.Viruses · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
HPVs are the causative agents of cervical and other anogenital cancers. HPVs infect stratified epithelia and link their productive life cycles to cellular differentiation. Low levels of viral genomes are stably maintained in undifferentiated cells and productive replication or amplification is restricted to differentiated suprabasal cells. Amplification is dependent on the activation of the ATM DNA damage factors that are recruited to viral replication centers and inhibition of this pathway blocks productive replication. The STAT-5 protein appears to play a critical role in mediating activation of the ATM pathway in HPV-positive cells. While HPVs need to activate the DNA damage pathway for replication, cervical cancers contain many genomic alterations suggesting that this pathway is circumvented during progression to malignancy.
Indexed as
Identifiers
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.