ArticleJournal of virology1994
The human papillomavirus type 16 E2 transcription factor binds with low cooperativity to two flanking sites and represses the E6 promoter through displacement of Sp1 and TFIID.
Article in Journal of virology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 188 citations in OpenAlex.
- Review
- Sequence-Dependent Interaction of the Human Papillomavirus E2 Protein with the DNA Elements on Its DNA Replication Origin.International journal of molecular sciences · 2023Article
- Human Papillomavirus 16 (HPV16) E2 Repression of TWIST1 Transcription Is a Potential Mediator of HPV16 Cancer Outcomes.mSphere · 2020Article
- Review
- Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle.Seminars in immunopathology · 2020Review
- Regulation of HPV transcription.Clinics (Sao Paulo, Brazil) · 2018Review
- Viral DNA integration and methylation of human papillomavirus type 16 in high-grade oral epithelial dysplasia and head and neck squamous cell carcinoma.Oncotarget · 2018Article
- HPV DNA methylation at the early promoter and E1/E2 integrity: A comparison between HPV16, HPV18 and HPV45 in cervical cancer.Papillomavirus research (Amsterdam, Netherlands) · 2018Article
- High-Risk Alphapapillomavirus Oncogenes Impair the Homologous Recombination Pathway.Journal of virology · 2017Article
- Article
- Increased methylation of human papillomavirus type 16 DNA is associated with the severity of cervical lesions in infected females from northeast China.Oncology letters · 2017Article
- Viral E6 is overexpressed via high viral load in invasive cervical cancer with episomal HPV16.BMC cancer · 2017Article
- CCCTC-binding factor recruitment to the early region of the human papillomavirus 18 genome regulates viral oncogene expression.Journal of virology · 2015Article
- Article
- Review
- Human Papillomavirus (HPV)-associated Oral Cancers and Treatment Strategies.Journal of dental research · 2014Review
- Article
- Viral load, integration and methylation of E2BS3 and 4 in human papilloma virus (HPV) 16-positive vaginal and vulvar carcinomas.PloS one · 2014Article
- Sequence variation in the E2-binding domain of HPV16 and biological function evaluation in Tunisian cervical cancers.BioMed research international · 2014Article
- Methylation of human papillomavirus Type 16 CpG sites at E2-binding site 1 (E2BS1), E2BS2, and the Sp1-binding site in cervical cancer samples as determined by high-resolution melting analysis-PCR.Journal of clinical microbiology · 2013Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The E6 promoters of all genital human papillomaviruses have a characteristic alignment of transcription factor binding sites. Activation of the basic transcription complex at the TATA box depends upon a sequence-aberrant Sp1 site. Repression of E6 promoters is achieved by two binding sites for the viral E2 protein positioned between the Sp1 site and the TATA box. We have purified the human papillomavirus type 16 E2 protein after expression in Escherichia coli and studied its binding and repression properties with oligonucleotides representing the homologous promoter sequences. A Kd value of 3 x 10(-10) M indicated binding properties expected for a native protein. We found low cooperativity in the binding of two E2 dimers to flanking sites, both when these sites were separated by 3 nucleotides, as in the natural promoter, and when they were further apart. E2 protein, bound close to the distal Sp1 site, displaced the Sp1 factor even when the aberrant sequence was replaced by a typical Sp1 core recognition site. The high affinity of E2 protein for its binding site even led to Sp1 displacement at concentrations of E2 protein nearly 2 orders of magnitude lower than those of Sp1. Functional analyses of mutated E6 promoter sequences showed repression by this distal E2 binding site in the complete absence of binding to the proximal E2 binding site. From our findings and observations published by others, we conclude that each of the E2 binding sites in the E6 promoter of genital human papillomaviruses plays a separate role by displacing the transcription factors Sp1 and TFIID.
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