ArticleJournal of virology2000
The Epstein-Barr virus promoter initiating B-cell transformation is activated by RFX proteins and the B-cell-specific activator protein BSAP/Pax5.
Article in Journal of virology, 2000. 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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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.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Review
- Article
- Review
- B Cell-Specific Transcription Activator PAX5 Recruits p300 To Support EBNA1-Driven Transcription.Journal of virology · 2020Article
- Article
- The Epstein-Barr virus BamHI C promoter is not essential for B cell immortalization in vitro, but it greatly enhances B cell growth transformation.Journal of virology · 2015Article
- Viral reprogramming of the Daxx histone H3.3 chaperone during early Epstein-Barr virus infection.Journal of virology · 2014Article
- Epigenetic regulation of EBV persistence and oncogenesis.Seminars in cancer biology · 2014Review
- Dynamic Epstein-Barr virus gene expression on the path to B-cell transformation.Advances in virus research · 2014Review
- Keeping it quiet: chromatin control of gammaherpesvirus latency.Nature reviews. Microbiology · 2013Review
- EBV genome carrying B lymphocytes that express the nuclear protein EBNA-2 but not LMP-1: Type IIb latency.Oncoimmunology · 2013Article
- An atlas of the Epstein-Barr virus transcriptome and epigenome reveals host-virus regulatory interactions.Cell host & microbe · 2012Article
- Contributions of CTCF and DNA methyltransferases DNMT1 and DNMT3B to Epstein-Barr virus restricted latency.Journal of virology · 2012Article
- Epstein-Barr virus BamHI W repeat number limits EBNA2/EBNA-LP coexpression in newly infected B cells and the efficiency of B-cell transformation: a rationale for the multiple W repeats in wild-type virus strains.Journal of virology · 2011Article
- trans-Repression of protein expression dependent on the Epstein-Barr virus promoter Wp during latency.Journal of virology · 2011Article
- RNA polymerase II stalling promotes nucleosome occlusion and pTEFb recruitment to drive immortalization by Epstein-Barr virus.PLoS pathogens · 2011Article
- Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- CTCF prevents the epigenetic drift of EBV latency promoter Qp.PLoS pathogens · 2010Article
- Epstein-Barr virus exploits BSAP/Pax5 to achieve the B-cell specificity of its growth-transforming program.Journal of virology · 2007Article
- B cell activator PAX5 promotes lymphomagenesis through stimulation of B cell receptor signaling.The Journal of clinical investigation · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV)-induced B-cell growth transformation, a central feature of the virus' strategy for colonizing the human B-cell system, requires full virus latent gene expression and is initiated by transcription from the viral promoter Wp. Interestingly, when EBV accesses other cell types, this growth-transforming program is not activated. The present work focuses on a region of Wp which in reporter assays confers B-cell-specific activity. Bandshift studies indicate that this region contains three factor binding sites, termed sites B, C, and D, in addition to a previously characterized CREB site. Here we show that site C binds members of the ubiquitously expressed RFX family of proteins, notably RFX1, RFX3, and the associated factor MIBP1, whereas sites B and D both bind the B-cell-specific activator protein BSAP/Pax5. In reporter assays with mutant Wp constructs, the loss of factor binding to any one of these sites severely impaired promoter activity in B cells, while the wild-type promoter could be activated in non-B cells by ectopic BSAP expression. We suggest that Wp regulation by BSAP helps to ensure the B-cell specificity of EBV's growth-transforming function.
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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.