ArticleJournal of virology1999
The Epstein-Barr virus BZLF1 protein interacts physically and functionally with the histone acetylase CREB-binding protein.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 107 citations in OpenAlex.
- Phospholipid scramblase 1: a frontline defense against viral infections.Frontiers in cellular and infection microbiology · 2025Review
- Anti-EBV: Artificial intelligence driven predictive modeling for repurposing drugs as potential antivirals against Epstein-Barr virus.Computational and structural biotechnology journal · 2025Article
- The Interferon-Inducible Human PLSCR1 Protein Is a Restriction Factor of Human Cytomegalovirus.Microbiology spectrum · 2022Article
- Structural basis of DNA methylation-dependent site selectivity of the Epstein-Barr virus lytic switch protein ZEBRA/Zta/BZLF1.Nucleic acids research · 2022Article
- Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.International journal of molecular sciences · 2021Review
- Review
- Ubiquitin Modification of the Epstein-Barr Virus Immediate Early Transactivator Zta.Journal of virology · 2020Article
- The bZIP Proteins of Oncogenic Viruses.Viruses · 2020Review
- Epigenetic lifestyle of Epstein-Barr virus.Seminars in immunopathology · 2020Review
- Interaction of phospholipid scramblase 1 with the Epstein-Barr virus protein BZLF1 represses BZLF1-mediated lytic gene transcription.The Journal of biological chemistry · 2019Article
- BZLF1 interacts with chromatin remodelers promoting escape from latent infections with EBV.Life science alliance · 2019Article
- Repression of CIITA by the Epstein-Barr virus transcription factor Zta is independent of its dimerization and DNA binding.The Journal of general virology · 2016Article
- Fresh Insights into Disease Etiology and the Role of Microbial Pathogens.Current rheumatology reports · 2016Review
- Inhibition of mTORC1 inhibits lytic replication of Epstein-Barr virus in a cell-type specific manner.Virology journal · 2014Article
- Epstein-Barr virus infection induces aberrant TLR activation pathway and fibroblast-myofibroblast conversion in scleroderma.The Journal of investigative dermatology · 2014Article
- Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.Advances in virus research · 2014Review
- Essential role of Rta in lytic DNA replication of Epstein-Barr virus.Journal of virology · 2013Article
- Viral genome methylation differentially affects the ability of BZLF1 versus BRLF1 to activate Epstein-Barr virus lytic gene expression and viral replication.Journal of virology · 2013Article
- BZLF1 governs CpG-methylated chromatin of Epstein-Barr Virus reversing epigenetic repression.PLoS pathogens · 2012Article
- The B-cell specific transcription factor, Oct-2, promotes Epstein-Barr virus latency by inhibiting the viral immediate-early protein, BZLF1.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The Epstein-Barr virus (EBV) immediate-early protein BZLF1 (Z) is a key regulator of the EBV latent-to-lytic switch. Z is a transcriptional activator which induces EBV early gene expression. We demonstrate here that Z interacts with CREB-binding protein (CBP), a histone acetylase and transcriptional coactivator. This interaction requires the amino-terminal region of CBP as well as the transactivation and leucine zipper domains of Z. We show that CBP enhances Z-mediated transactivation of EBV early promoters, in reporter gene assays and in the context of the endogenous genome. We also demonstrate that Z decreases CREB transactivation function and that this inhibitory effect is reversed by overexpression of CBP. We show that Z also interacts directly with CREB. However, mutational analysis indicates that Z inhibition of CREB activity requires the direct interaction between Z and CBP but not the direct interaction between Z and CREB. We propose that Z interacts with CBP to enhance viral early gene transcription. In addition, the Z-CBP interaction may control host cellular transcription factor activity through competition for limiting amounts of cellular CBP.
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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.