ReviewVirology2009
Papillomavirus E6 proteins.
Review in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 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
162 citing papers in PubMed, 325 citations in OpenAlex.
- Sequence-Anchored Shared Tumor-Specific Epitopes for Pre-Manufactured HLA-Matched mRNA Cancer Vaccine Libraries: A Pan-Cancer Framework.Biomolecules · 2026Article
- 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
- Therapeutic scheduling of WEE1 inhibition preserves T cell function and promotes immune control of HPVbioRxiv : the preprint server for biology · 2026Article
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- Genotypic distribution and molecular epidemiology of HPV in women in the UAE using PNA-based RT PCR.PloS one · 2026Article
- Molecular heterogeneity of HPV-associated cancers and strategies to overcome treatment resistance.Cancer heterogeneity and plasticity · 2026Article
- Review
- Virtual Screening, Molecular Docking and Molecular Dynamics Simulation of Bioactive Compounds from Various Indonesian Medicinal Plants as Potential Inhibitors of Human Papillomavirus Type 16 E6 Protein in Cervical Cancer Development.Tropical life sciences research · 2025Article
- Discovering Active Chemotherapeutic Agents for Sexually Transmitted Diseases to Inhibit Pathogenic HPV-16-E6 Protein.Current drug discovery technologies · 2025Article
- The Natural History of Cervical Cancer and the Case for MicroRNAs: Is Human Papillomavirus Infection the Whole Story?International journal of molecular sciences · 2024Review
- The role of HR-HPV integration in the progression of premalignant lesions into different cancer types.Heliyon · 2024Review
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- A novel HPV16 splicing enhancer critical for viral oncogene expression and cell immortalization.Nucleic acids research · 2024Article
- Discovery of reactive peptide inhibitors of human papillomavirus oncoprotein E6.Chemical science · 2023Article
- Can prophylactic HPV vaccination reduce the recurrence of cervical lesions after surgery? Review and prospect.Infectious agents and cancer · 2023Review
- HPV16E1 downregulation altered the cell characteristics involved in cervical cancer development.Scientific reports · 2023Article
- p53-dependent R-loop formation and HPV pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- LKB1/STK11 Tumor Suppressor Reduces Angiogenesis by Directly Interacting with VEGFR2 in Tumorigenesis.Biomolecules & therapeutics · 2023Article
- The Immune Response Generated against HPV Infection in Men and Its Implications in the Diagnosis of Cancer.Microorganisms · 2023Review
102 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The papillomaviruses are small DNA viruses that encode approximately eight genes, and require the host cell DNA replication machinery for their viral DNA replication. Thus papillomaviruses have evolved strategies to induce host cell DNA synthesis balanced with strategies to protect the cell from unscheduled replication. While the papillomavirus E1 and E2 genes are directly involved in viral replication by binding to and unwinding the origin of replication, the E6 and E7 proteins have auxillary functions that promote proliferation. As a consequence of disrupting the normal checkpoints that regulate cell cycle entry and progression, the E6 and E7 proteins play a key role in the oncogenic properties of human papillomaviruses with a high risk of causing anogenital cancers (HR HPVs). As a consequence, E6 and E7 of HR HPVs are invariably expressed in cervical cancers. This article will focus on the E6 protein and its numerous activities including inactivating p53, blocking apoptosis, activating telomerase, disrupting cell adhesion, polarity and epithelial differentiation, altering transcription and reducing immune recognition.
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.