ArticleJournal of virology1997
Different mechanisms contribute to the E2-mediated transcriptional repression of human papillomavirus type 18 viral oncogenes.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 124 citations in OpenAlex.
- Article
- A Novel Method for Predicting Oncogenic Types of Human Papillomavirus.Diagnostics (Basel, Switzerland) · 2025Article
- Human Papilloma Virus-Infected Cells.Sub-cellular biochemistry · 2023Article
- Regulation of Human Papillomavirus 18 Genome Replication, Establishment, and Persistence by Sequences in the Viral Upstream Regulatory Region.Journal of virology · 2021Article
- Multiple Roles of Brd4 in the Infectious Cycle of Human Papillomaviruses.Frontiers in molecular biosciences · 2021Review
- Human Papillomavirus 16 (HPV16) E2 Repression of TWIST1 Transcription Is a Potential Mediator of HPV16 Cancer Outcomes.mSphere · 2020Article
- Human Papillomavirus Replication Regulation by Acetylation of a Conserved Lysine in the E2 Protein.Journal of virology · 2018Article
- Integration of Human Papillomavirus Genomes in Head and Neck Cancer: Is It Time to Consider a Paradigm Shift?Viruses · 2017Review
- Splicing and Polyadenylation of Human Papillomavirus Type 16 mRNAs.International journal of molecular sciences · 2017Review
- Viral Interplay with the Host Sumoylation System.Advances in experimental medicine and biology · 2017Review
- Post-Transcriptional Regulation of KLF4 by High-Risk Human Papillomaviruses Is Necessary for the Differentiation-Dependent Viral Life Cycle.PLoS pathogens · 2016Article
- Review
- The Role of F-Box Proteins during Viral Infection.International journal of molecular sciences · 2013Article
- Interferon-β induced microRNA-129-5p down-regulates HPV-18 E6 and E7 viral gene expression by targeting SP1 in cervical cancer cells.PloS one · 2013Article
- Differentiation-dependent changes in levels of C/EBPβ repressors and activators regulate human papillomavirus type 31 late gene expression.Journal of virology · 2012Article
- Virology and molecular pathogenesis of HPV (human papillomavirus)-associated oropharyngeal squamous cell carcinoma.The Biochemical journal · 2012Review
- Identification and analysis of papillomavirus E2 protein binding sites in the human genome.Journal of virology · 2012Article
- The HPV E2-Host Protein-Protein Interactions: A Complex Hijacking of the Cellular Network.The open virology journal · 2012Article
- Small molecule inhibitors of human papillomavirus protein - protein interactions.The open virology journal · 2011Article
- Replication and transcription of human papillomavirus type 58 genome in Saccharomyces cerevisiae.Virology journal · 2010Article
Corrections and comments
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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
Transcription of the human papillomavirus type 18 (HPV18) E6 and E7 oncogenes is repressed by the viral E2 protein. In C33 cells, we have previously shown that of the four E2 binding sites (E2 BS) present in the HPV18 long control region (LCR), only the binding site adjacent to the TATA box (E2 BS 1) was involved in E2-mediated repression. In the present study, we sought to determine whether this phenomenon was conserved in other cell lines. We first showed that all three E2 BS proximal to the P105 promoter were required for full repression of its activity in HeLa and HaCaT cells. Repression by E2 at E2 BS 2 occurred through the displacement of Sp1. Second, a truncated E2 product, lacking the N-terminal transactivation domain, repressed transcription more efficiently than the full-length protein. Repression was abolished when the N-terminal domain of E2 was replaced by the activation domain of VP16. The VP16-E2 chimeric protein could activate transcription from an LCR mutated in its TATA box. DNA-protein binding studies showed that E2 associates with its four binding sites in the LCR with similar affinities. However, challenge of such complexes with excess binding sites demonstrated that interaction with E2 BS 4 was the most stable while interaction with E2 BS 1 was the least stable. Furthermore, complexes with the full-length E2 were less stable than those formed with the N-terminally truncated protein.
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