ArticleJournal of virology1998
Identification of a negative cis element within the ZII domain of the Epstein-Barr virus lytic switch BZLF1 gene promoter.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 49 citations in OpenAlex.
- A distinct isoform of lymphoid enhancer binding factor 1 (LEF1) epigenetically restricts EBV reactivation to maintain viral latency.PLoS pathogens · 2023Article
- Review
- Reactivation of Epstein-Barr Virus by HIF-1α Requires p53.Journal of virology · 2020Article
- Identification of ARKL1 as a Negative Regulator of Epstein-Barr Virus Reactivation.Journal of virology · 2019Article
- Article
- Inhibition of Epstein-Barr virus reactivation by the flavonoid apigenin.Journal of biomedical science · 2017Article
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- Role of ATM in the formation of the replication compartment during lytic replication of Epstein-Barr virus in nasopharyngeal epithelial cells.Journal of virology · 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
- Inhibition of Epstein-Barr virus lytic cycle by an ethyl acetate subfraction separated from Polygonum cuspidatum root and its major component, emodin.Molecules (Basel, Switzerland) · 2014Article
- Epstein-Barr virus induces global changes in cellular mRNA isoform usage that are important for the maintenance of latency.Journal of virology · 2013Article
- Epigenetic modification of the Epstein-Barr virus BZLF1 promoter regulates viral reactivation from latency.Frontiers in genetics · 2013Article
- An Epstein-Barr Virus (EBV) mutant with enhanced BZLF1 expression causes lymphomas with abortive lytic EBV infection in a humanized mouse model.Journal of virology · 2012Article
- Shutoff of BZLF1 gene expression is necessary for immortalization of primary B cells by Epstein-Barr virus.Journal of virology · 2012Article
- Epigenetic histone modification of Epstein-Barr virus BZLF1 promoter during latency and reactivation in Raji cells.Journal of virology · 2012Article
- Involvement of Jun dimerization protein 2 (JDP2) in the maintenance of Epstein-Barr virus latency.The Journal of biological chemistry · 2011Article
- The ZIIR element of the Epstein-Barr virus BZLF1 promoter plays a central role in establishment and maintenance of viral latency.Journal of virology · 2011Article
- The Epstein-Barr virus BRRF1 protein, Na, induces lytic infection in a TRAF2- and p53-dependent manner.Journal of virology · 2011Article
- Cellular microRNAs 200b and 429 regulate the Epstein-Barr virus switch between latency and lytic replication.Journal of virology · 2010Article
- Either ZEB1 or ZEB2/SIP1 can play a central role in regulating the Epstein-Barr virus latent-lytic switch in a cell-type-specific manner.Journal of virology · 2010Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Epstein-Barr virus (EBV) lytic switch gene, BZLF1, is tightly regulated in latently infected B cells. The BZLF1 gene promoter (Zp) contains several cis elements that have been previously shown to respond to inducers of the viral lytic cycle. These include four copies of an element referred to as the ZI domains and an element that contains a consensus CRE/AP-1 motif (ZII domain). In addition, Zp is autoregulated through two sites that bind the BZLF1 gene product Zta. The ZI domains have been shown to bind the ubiquitous cellular transcription factors Sp1 and Sp3 and/or the myocyte enhancer factor 2D (Liu et al., EMBO J. 16:143-153, 1997; Liu et al., Virology 228:9-16, 1997). Here we present a functional analysis of the ZII domain and show: (i) ATF-1 and ATF-2 appear to be the predominant cellular factors that bind to the CRE/AP-1 motif present in the ZII domain; and (ii) the region immediately upstream of the CRE/AP-1 motif contains a potent negative cis element, mutation of which results in a >10-fold increase in Zp activity. The negative cis element (ZIIR) in the ZII domain decreases both basal and induced Zp activity and thus is likely to play an important role in regulating reactivation of EBV. In addition, analysis of heterologous promoter constructs indicates that the function of ZIIR is context sensitive. Attempts to demonstrate a cellular factor binding to ZIIR have been unsuccessful, leaving unresolved the mechanism by which repression is mediated.
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