ArticleNucleic acids research2000
Activation of the BRLF1 promoter and lytic cycle of Epstein-Barr virus by histone acetylation.
Article in Nucleic acids research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 93 citations in OpenAlex.
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- Single-Cell Profiling of HDAC Inhibitor-Induced EBV Lytic Heterogeneity Defines Abortive and Refractory States in B Lymphoblasts.bioRxiv : the preprint server for biology · 2025Article
- RNA helicases, DDX5 and DDX17, facilitate lytic reactivation of gammaherpesviruses.PLoS pathogens · 2025Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Epstein-Barr virus and spontaneous lymphoblastoid cell lines: establishment, molecular characteristics, immune modulation, and therapeutic insight.Clinical and experimental immunology · 2025Review
- Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.PLoS pathogens · 2024Article
- Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.bioRxiv : the preprint server for biology · 2024Article
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- Epigenetic lifestyle of Epstein-Barr virus.Seminars in immunopathology · 2020Review
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Therapies based on targeting Epstein-Barr virus lytic replication for EBV-associated malignancies.Cancer science · 2018Review
- Review
- Role of Litopenaeus vannamei Yin Yang 1 in the Regulation of the White Spot Syndrome Virus Immediate Early GeneJournal of virology · 2017Article
- TRIM5α Promotes Ubiquitination of Rta from Epstein-Barr Virus to Attenuate Lytic Progression.Frontiers in microbiology · 2016Article
- Identification of transcription factor AML-1 binding site upstream of human cytomegalovirus UL111A gene.PloS one · 2015Article
- Activation and repression of Epstein-Barr Virus and Kaposi's sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acids.Journal of virology · 2014Article
- Article
- Epstein-Barr viral productive amplification reprograms nuclear architecture, DNA replication, and histone deposition.Cell host & microbe · 2013Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone acetylation alters the chromatin structure and activates the genes that are repressed by histone deacetylation. This investigation demonstrates that treating P3HR1 cells with trichostatin A (TSA) activates the Epstein-Barr virus (EBV) lytic cycle, allowing the virus to synthesize three viral lytic proteins-Rta, Zta and EA-D. Experimental results indicate that TSA and 12-O:-tetradecanoylphorbol-13-acetate synergistically activate the transcription of BRLF1, an immediate-early gene of EBV. Chromatin immunoprecipitation assay reveals that histone H4 at the BRLF1 promoter is acetylated after P3HR1 cells are treated with TSA, suggesting that histone acetylation activates BRLF1 transcription. Furthermore, results in this study demonstrate that mutation of a YY1-binding site in the BRLF1 promoter activates BRLF1 transcription 1.6- and 2.3-fold in P3HR1 cells and C33A cells, respectively. Real time PCR analysis reveals that the mutation also increases the histone acetylation level of the nucleosomes at the BRLF1 promoter 1. 64- and 3.08-fold in P3HR1 and C33A cells, respectively. Results presented herein suggest that histone deacetylation plays an important role in maintaining the viral latency and histone acetylation at the BRLF1 promoter allows the virus to express Rta and to activate the viral lytic cycle.
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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.