ArticleThe Journal of biological chemistry2011
Binding site specificity and factor redundancy in activator protein-1-driven human papillomavirus chromatin-dependent transcription.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 41 citations in OpenAlex.
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Neuronal type-specific modulation of cognition and AP-1 signaling by early-life rearing conditions.Nature communications · 2025Article
- BRD4 as a potential target for human papillomaviruses associated cancer.Journal of medical virology · 2023Review
- The antiviral effects of a MEK1/2 inhibitor promote tumor regression in a preclinical model of human papillomavirus infection-induced tumorigenesis.Antiviral research · 2023Article
- A Genome-Wide RNAi Screen Reveals Common Host-Virus Gene Signatures: Implication for Dengue Antiviral Drug Discovery.GEN biotechnology · 2023Article
- AP-1 Subunit JUNB Promotes Invasive Phenotypes in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Role of the Transcription Factor FOSL1 in Organ Development and Tumorigenesis.International journal of molecular sciences · 2022Review
- Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers.Nucleic acids research · 2021Article
- Human Papillomavirus Infection in Head and Neck Squamous Cell Carcinomas: Transcriptional Triggers and Changed Disease Patterns.Frontiers in cellular and infection microbiology · 2020Review
- AAV-Mediated Expression of AP-1-Neutralizing RNA Decoy Oligonucleotides Attenuates Transplant Vasculopathy in Mouse Aortic Allografts.Molecular therapy. Methods & clinical development · 2019Article
- The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells.Antioxidants (Basel, Switzerland) · 2019Article
- Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells.Cancer cell international · 2019Article
- Antineoplastic effects of histone deacetylase inhibitors in neuroendocrine cancer cells are mediated through transcriptional regulation of Notch1 by activator protein 1.Cancer medicine · 2017Article
- Computational modeling of in vivo and in vitro protein-DNA interactions by multiple instance learning.Bioinformatics (Oxford, England) · 2017Article
- Involvement of Brd4 in different steps of the papillomavirus life cycle.Virus research · 2017Review
- Extrachromosomal HPV-16 LCR transcriptional activation by HDACi opposed by cellular differentiation and DNA integration.Oncotarget · 2016Article
- Article
- 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
- Papillomavirus-Associated Tumor Formation Critically Depends on c-Fos Expression Induced by Viral Protein E2 and Bromodomain Protein Brd4.PLoS pathogens · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Activator protein-1 (AP-1) regulates diverse gene responses triggered by environmental cues and virus-induced cellular stress. Although many signaling events leading to AP-1 activation have been described, the fundamental features underlying binding site selection and factor recruitment of dimeric AP-1 complexes to their target genes remain mostly uncharacterized. Using recombinant full-length human AP-1 dimers formed between c-Jun and Fos family members (c-Fos, FosB, Fra-1, Fra-2) for DNA binding and transcriptional analysis, we found that each of these AP-1 complex exhibits differential activity for distinct non-consensus AP-1 sites present in human papillomavirus (HPV), and each AP-1 complex is capable of activating transcription from in vitro-reconstituted HPV chromatin in a p300- and acetyl-CoA-dependent manner. Transcription from HPV chromatin requires AP-1-dependent and contact-driven recruitment of p300. Acetylation of dimeric AP-1 complexes by p300 enhances AP-1 binding to DNA. Using a human C-33A cervical cancer-derived cell line harboring the episomal HPV type 11 genome, we illustrate binding site selectivity recognized by c-Jun, JunB, JunD, and various Fos family members in a combinatorial and unique pattern, highlighting the diversity and importance of non-canonical binding site recognition by various AP-1 family proteins.
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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.