ArticleJournal of virology2012
Downregulation of integrin receptor-signaling genes by Epstein-Barr virus EBNA 3C via promoter-proximal and -distal binding elements.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Epstein-Barr virus and host cell 3D genome organization.Journal of medical virology · 2023Review
- Review
- Regulation of B cell receptor signalling by Epstein-Barr virus nuclear antigens.The Biochemical journal · 2022Article
- microRNA-21: a key modulator in oncogenic viral infections.RNA biology · 2021Review
- Epstein-Barr virus nuclear antigen 3C (EBNA3C) interacts with the metabolism sensing C-terminal binding protein (CtBP) repressor to upregulate host genes.PLoS pathogens · 2021Article
- Requirement for PRC1 subunit BMI1 in host gene activation by Epstein-Barr virus protein EBNA3C.Nucleic acids research · 2019Article
- Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression ofJournal of virology · 2018Article
- An EBNA3C-deleted Epstein-Barr virus (EBV) mutant causes B-cell lymphomas with delayed onset in a cord blood-humanized mouse model.PLoS pathogens · 2018Article
- Epstein-Barr Virus (EBV) Latent Protein EBNA3A Directly Targets and Silences theJournal of virology · 2018Article
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- SNRK (Sucrose Nonfermenting 1-Related Kinase) Promotes Angiogenesis In Vivo.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Article
- Core binding factor (CBF) is required for Epstein-Barr virus EBNA3 proteins to regulate target gene expression.Nucleic acids research · 2017Article
- Article
- RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Nucleic acids research · 2016Article
- EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B Cells.PLoS pathogens · 2016Article
- Epstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic Sites.Journal of virology · 2015Article
- Epstein-Barr virus latency: current and future perspectives.Current opinion in virology · 2015Review
- Epstein-Barr Virus Proteins EBNA3A and EBNA3C Together Induce Expression of the Oncogenic MicroRNA Cluster miR-221/miR-222 and Ablate Expression of Its Target p57KIP2.PLoS pathogens · 2015Article
- The EBNA3 family of Epstein-Barr virus nuclear proteins associates with the USP46/USP12 deubiquitination complexes to regulate lymphoblastoid cell line growth.PLoS pathogens · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) establishes a persistent latent infection in B lymphocytes and is associated with the development of numerous human tumors. Epstein-Barr nuclear antigen 3C (EBNA 3C) is essential for B-cell immortalization, has potent cell cycle deregulation capabilities, and functions as a regulator of both viral- and cellular-gene expression. We performed transcription profiling on EBNA 3C-expressing B cells and identified several chemokines and members of integrin receptor-signaling pathways, including CCL3, CCL4, CXCL10, CXCL11, ITGA4, ITGB1, ADAM28, and ADAMDEC1, as cellular target genes that could be repressed by the action of EBNA 3C alone. Chemotaxis assays demonstrated that downregulation of CXCL10 and -11 by EBNA 3C is sufficient to reduce the migration of cells expressing the CXCL10 and -11 receptor CXCR3. Gene repression by EBNA 3C was accompanied by decreased histone H3 lysine 9/14 acetylation and increased histone H3 lysine 27 trimethylation. In an EBV-positive cell line expressing all latent genes, we identified binding sites for EBNA 3C at ITGB1 and ITGA4 and in a distal regulatory region between ADAMDEC1 and ADAM28, providing the first demonstration of EBNA 3C association with cellular-gene control regions. Our data implicate indirect mechanisms in CXCL10 and CXCL11 repression by EBNA 3C. In summary, we have unveiled key cellular pathways repressed by EBNA 3C that are likely to contribute to the ability of EBV-immortalized cells to modulate immune responses, adhesion, and B-lymphocyte migration to facilitate persistence in the host.
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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.