ArticleMolecular and cellular biology2000
Alleviation of human papillomavirus E2-mediated transcriptional repression via formation of a TATA binding protein (or TFIID)-TFIIB-RNA polymerase II-TFIIF preinitiation complex.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Sequence-Dependent Interaction of the Human Papillomavirus E2 Protein with the DNA Elements on Its DNA Replication Origin.International journal of molecular sciences · 2023Article
- HPV16 and HPV18 Genome Structure, Expression, and Post-Transcriptional Regulation.International journal of molecular sciences · 2022Review
- Molecular pathways in the development of HPV-induced cervical cancer.EXCLI journal · 2021Review
- Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle.Seminars in immunopathology · 2020Review
- Cervical cancer stem cells and other leading factors associated with cervical cancer development.Oncology letters · 2019Review
- Acetylation of E2 by P300 Mediates Topoisomerase Entry at the Papillomavirus Replicon.Journal of virology · 2019Article
- Disruption of CTCF-YY1-dependent looping of the human papillomavirus genome activates differentiation-induced viral oncogene transcription.PLoS biology · 2018Article
- Human Papillomavirus Replication Regulation by Acetylation of a Conserved Lysine in the E2 Protein.Journal of virology · 2018Article
- Involvement of Brd4 in different steps of the papillomavirus life cycle.Virus research · 2017Review
- BRD4 Phosphorylation Regulates HPV E2-Mediated Viral Transcription, Origin Replication, and Cellular MMP-9 Expression.Cell reports · 2016Article
- Regulation of mammalian transcription and splicing by Nuclear RNAi.Nucleic acids research · 2016Review
- The papillomavirus E2 proteins.Virology · 2013Review
- Binding site specificity and factor redundancy in activator protein-1-driven human papillomavirus chromatin-dependent transcription.The Journal of biological chemistry · 2011Article
- HPV16 E2 could act as down-regulator in cellular genes implicated in apoptosis, proliferation and cell differentiation.Virology journal · 2011Article
- Interaction of the papillomavirus E8--E2C protein with the cellular CHD6 protein contributes to transcriptional repression.Journal of virology · 2010Article
- Article
- Chromatin adaptor Brd4 modulates E2 transcription activity and protein stability.The Journal of biological chemistry · 2009Article
- One-step affinity tag purification of full-length recombinant human AP-1 complexes from bacterial inclusion bodies using a polycistronic expression system.Protein expression and purification · 2008Article
- Interaction of papillomavirus E2 protein with the Brm chromatin remodeling complex leads to enhanced transcriptional activation.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Transcription in human papillomaviruses (HPVs) is mainly regulated by cellular transcription factors and virus-encoded E2 proteins that act as sequence-specific DNA-binding proteins. Although the functions of E2 as a transcriptional activator and a repressor have been well documented, the role of cellular factors involved in E2-mediated regulation of the HPV promoters and the mechanism by which E2 modulates viral gene expression remain unclear. Using reconstituted cell-free transcription systems, we found that cellular enhancer-binding factors and general cofactors, such as TAF(II)s, TFIIA, Mediator, and PC4, are not required for E2-mediated repression. Unlike other transcriptional repressors that function through recruitment of histone deacetylase or corepressor complexes, HPV E2 is able to directly target components of the general transcription machinery to exert its repressor activity on the natural HPV E6 promoter. Interestingly, preincubation of TATA binding protein (TBP) or TFIID with HPV template is not sufficient to overcome E2-mediated repression, which can be alleviated only via formation of a minimal TBP (or TFIID)-TFIIB-RNA polymerase II-TFIIF preinitiation complex. Our data therefore indicate that E2 does not simply work by displacing TBP or TFIID from binding to the adjacent TATA box. Instead, E2 appears to function as an active repressor that directly inhibits HPV transcription at steps after TATA recognition by TBP or TFIID.
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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.