ArticleJournal of virology2003
Functional interaction of nuclear factor y and sp1 is required for activation of the epstein-barr virus C promoter.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- 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
- Cell-type and transcription factor specific enrichment of transcriptional cofactor motifs in ENCODE ChIP-seq data.BMC genomics · 2013Article
- Analysis of Epstein-Barr virus-regulated host gene expression changes through primary B-cell outgrowth reveals delayed kinetics of latent membrane protein 1-mediated NF-κB activation.Journal of virology · 2012Article
- The nucleotide polymorphisms within the Epstein-Barr virus C and Q promoters from nasopharyngeal carcinoma affect transcriptional activity in vitro.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2012Article
- Identification and functional characterization of the left origin of lytic replication of murine gammaherpesvirus 68.Virology · 2009Article
- Cell cycle association of the retinoblastoma protein Rb and the histone demethylase LSD1 with the Epstein-Barr virus latency promoter Cp.Journal of virology · 2008Article
- Specificity proteins Sp1 and Sp3 interact with the rat GTP cyclohydrolase I proximal promoter to regulate transcription.Journal of neurochemistry · 2008Article
- Chromatin profiling of Epstein-Barr virus latency control region.Journal of virology · 2007Article
- Transcriptional activation by EBV nuclear antigen 1 is essential for the expression of EBV's transforming genes.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Regulation of Epstein-Barr virus latency type by the chromatin boundary factor CTCF.Journal of virology · 2006Article
- Inhibition of Epstein-Barr virus-induced growth proliferation by a nuclear antigen EBNA2-TAT peptide.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- The EBV nuclear antigen 1 (EBNA1) enhances B cell immortalization several thousandfold.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two Epstein-Barr virus (EBV) latent cycle promoters, Wp and Cp, are activated sequentially during virus-induced transformation of primary B lymphocytes. Immediately postinfection, viral transcription initiates from Wp, leading to expression of EBV nuclear antigen 2 (EBNA2) and EBNA5. Within 36 h, there is a switch in promoter usage from Wp to the upstream Cp, which leads to expression of EBNA1 to EBNA6. EBNA2 appears to be required for the Wp-to-Cp switch, but the switching mechanism is not fully understood at the molecular level. In a previous investigation we showed that there is an EBNA2-independent activity of reporter constructs containing deletion fragments of Cp in B-lymphoid cell lines, and we demonstrated that Cp activity is highly dependent on several cellular transcription factors, including nuclear factor Y (NF-Y) and Sp1. In the present work, we analyzed the effect of NF-Y on Cp activity in greater detail. We demonstrate that (i) a dominant negative analogue of NF-Y abolishes Cp activity, (ii) NF-Y and Sp1 costimulate Cp, and (iii) the oriPI-EBNA1-induced transactivation of Cp requires concomitant expression of NF-Y and Sp1, although additional factors seem necessary for optimal activation. Furthermore, using the lymphoblastoid cell line EREB2-5, in which EBNA2 function is regulated by estrogen, we demonstrate that inactivation of EBNA2 results in decreased expression of NF-Y and down-regulation of Cp. On reconstitution of the EBNA2 function, the cells enter the cell cycle, NF-Y levels increase, and a concomitant Wp-to-Cp switch occurs. Taken together, our results suggest that NF-Y is essential for Cp activation and that up-regulation of NF-Y may contribute to a successful Wp-to-Cp switch during B-cell transformation.
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