ArticleThe EMBO journal1992
Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells.
Article in The EMBO journal, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 194 citations in OpenAlex.
- Human papillomavirus-encoded microRNAs: key regulators in cervical cancer development.RNA biology · 2026Review
- Insights into expression and localization of HPV16 LCR-associated transcription factors and association with LCR activity in HNSCC.Molecular therapy. Oncology · 2025Article
- TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma.Frontiers in immunology · 2024Review
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- Nuclear proinflammatory cytokine S100A9 enhances expression of human papillomavirus oncogenes via transcription factor TEAD1.Journal of virology · 2023Article
- Oncogenic Viruses-Encoded microRNAs and Their Role in the Progression of Cancer: Emerging Targets for Antiviral and Anticancer Therapies.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Characterization of Human Papillomavirus 16 from Kinshasa (Democratic Republic of the Congo)-Implications for Pathogenicity and Vaccine Effectiveness.Microorganisms · 2022Article
- Viral Encoded miRNAs in Tumorigenesis: Theranostic Opportunities in Precision Oncology.Microorganisms · 2022Review
- Article
- Phytochemicals as Potential Chemopreventive and Chemotherapeutic Agents for Emerging Human Papillomavirus-Driven Head and Neck Cancer: Current Evidence and Future Prospects.Frontiers in pharmacology · 2021Review
- The Transcriptional Cofactor VGLL1 Drives Transcription of Human Papillomavirus Early Genes via TEAD1.Journal of virology · 2020Article
- Review
- Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns.Frontiers in cellular and infection microbiology · 2020Review
- Association of Human Papillomavirus Type 16 Long Control Region Variations with Cervical Cancer in a Han Chinese Population.International journal of medical sciences · 2020Article
- Regulation of the Hippo Pathway Transcription Factor TEAD.Trends in biochemical sciences · 2017Review
- The TEAD Family and Its Oncogenic Role in Promoting Tumorigenesis.International journal of molecular sciences · 2016Review
- Emerging roles of TEAD transcription factors and its coactivators in cancers.Cancer biology & therapy · 2013Review
- The transcription factors TBX2 and TBX3 interact with human papillomavirus 16 (HPV16) L2 and repress the long control region of HPVs.Journal of virology · 2013Article
- Association of human papillomavirus type 16 long control region mutation and cervical cancer.Virology journal · 2013Article
- Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The human papillomavirus (HPV)-16 oncogenes, E6 and E7, are transcribed preferentially in keratinocytes and cervical carcinoma cells due to a 5' enhancer. An abundant peptide binding to a 37 nt enhancer element was purified from human keratinocytes by sequence-specific DNA chromatography. This protein was identified as transcriptional enhancer factor (TEF)-1 by complex mobility, binding to wild-type and mutant SV40 and HPV-16 enhansons and antigenic reactivity with two anti-TEF-1 antibodies. TEF-1 is cell-specific, but its transactivation also depends on a limiting, cell-specific TEF-1 'co-activator'. We show that both TEF-1 and the TEF-1 co-activator are active in human keratinocytes and essential for HPV-16 transcription. TEF-1 binding in vivo was necessary for HPV-16 P97 promoter activity. Excess TEF-1 and chimeric GAL4-TEF-1 specifically inhibited the P97 promoter by 'squelching', indicating that HPV-16 transcription also requires a limiting TEF-1 co-activator. TEF-1 and the TEF-1 co-activator functions mirrored HPV-16 transcription by their presence in keratinocytes and cervical carcinoma cells and their absence from lymphoid B-cells, but also functioned in liver cells where the HPV-16 promoter is inactive. TEF-1 and its associated co-activator are thus part of a complex mechanism which determines the restricted cell range of the HPV-16 E6 and E7 oncogene promoter.
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