ArticleJournal of virology1997
The Epstein-Barr virus-induced Ca2+/calmodulin-dependent kinase type IV/Gr promotes a Ca(2+)-dependent switch from latency to viral replication.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Endoplasmic reticulum & mitochondrial calcium homeostasis: The interplay with viruses.Mitochondrion · 2021Article
- B cells infected with Type 2 Epstein-Barr virus (EBV) have increased NFATc1/NFATc2 activity and enhanced lytic gene expression in comparison to Type 1 EBV infection.PLoS pathogens · 2020Article
- Calcium mobilization is responsible for Thapsigargin induced Epstein Barr virus lytic reactivation inHeliyon · 2018Article
- Epstein-Barr virus-encoded LMP2A stimulates migration of nasopharyngeal carcinoma cells via the EGFR/CaBiology open · 2017Article
- 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
- Stimulus duration and response time independently influence the kinetics of lytic cycle reactivation of Epstein-Barr virus.Journal of virology · 2009Article
- Identification and characterization of a new E3 ubiquitin ligase in white spot syndrome virus involved in virus latency.Virology journal · 2008Article
- Virus and cell RNAs expressed during Epstein-Barr virus replication.Journal of virology · 2006Article
- Contribution of C/EBP proteins to Epstein-Barr virus lytic gene expression and replication in epithelial cells.Journal of virology · 2006Article
- Identification of protein tyrosine kinases required for B-cell- receptor-mediated activation of an Epstein-Barr Virus immediate-early gene promoter.Journal of virology · 2004Article
- Virally targeted therapies for EBV-associated malignancies.Oncogene · 2003Review
- Signal Transduction and Transcription Factor Modification during Reactivation of Epstein-Barr Virus from Latency.Journal of virology · 2002Article
- MEF2-mediated recruitment of class II HDAC at the EBV immediate early gene BZLF1 links latency and chromatin remodeling.EMBO reports · 2002Article
- Identification of a novel element involved in regulation of the lytic switch BZLF1 gene promoter of Epstein-Barr virus.Journal of virology · 2001Article
- Kaposi's sarcoma-associated herpesvirus encodes a bZIP protein with homology to BZLF1 of Epstein-Barr virus.Journal of virology · 1999Article
- Identification of a negative cis element within the ZII domain of the Epstein-Barr virus lytic switch BZLF1 gene promoter.Journal of virology · 1998Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The switch from latency to viral replication in Epstein-Barr virus (EBV)-transformed human B cells is mediated by Zta, the protein product of immediate-early EBV gene BZLF1. BZLF1 transcription is normally suppressed in EBV-transformed B cells but can be induced in some cell lines upon ligation of surface immunoglobulin by mechanisms that include the activation of Ca(2+)-dependent signaling pathways. The multifunctional Ca2+/calmodulin-dependent kinase type IV/Gr (CaMKIV/Gr) is normally absent in primary human B cells, but its expression is induced by the EBV oncoprotein LMP1 in the course of B-cell growth transformation by EBV. In this study, we demonstrate that activated CaMKIV/Gr induces transcription from the BZLF1 promoter and upregulates the expression of Zta in permissive cells. Transcriptional activation of the BZLF1 promoter by CaMKIV/Gr is dependent on the CREB/AP1 binding element ZII and is greatly augmented by the Ca2+/calmodulin-dependent phosphatase calcineurin. These results outline a virus-regulated mechanism involving CaMKIV/Gr which promotes transition from latency to productive viral replication in response to Ca(2+)-mobilizing extracellular signals.
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