ArticleJournal of virology2005
Epstein-Barr virus nuclear protein 3A domains essential for growth of lymphoblasts: transcriptional regulation through RBP-Jkappa/CBF1 is critical.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed.
- Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Review
- Article
- Epstein-Barr virus peptides derived from latent cycle proteins alter NKG2A + NK cell effector function.Scientific reports · 2020Article
- The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency.Pathogens (Basel, Switzerland) · 2018Review
- The Epstein-Barr Virus Regulome in Lymphoblastoid Cells.Cell host & microbe · 2017Article
- Epigenetic Impact on EBV Associated B-Cell Lymphomagenesis.Biomolecules · 2016Review
- Methylation status and AP1 elements are involved in EBV-mediated miR-155 expression in EBV positive lymphoma cells.Virology · 2016Article
- RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Nucleic acids research · 2016Article
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
- Epstein-Barr Virus Nuclear Antigen 3 (EBNA3) Proteins Regulate EBNA2 Binding to Distinct RBPJ Genomic Sites.Journal of virology · 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
- Epstein-Barr virus oncoprotein super-enhancers control B cell growth.Cell host & microbe · 2015Article
- Epstein-Barr virus nuclear antigen 3A partially coincides with EBNA3C genome-wide and is tethered to DNA through BATF complexes.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- 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
- Soluble rhesus lymphocryptovirus gp350 protects against infection and reduces viral loads in animals that become infected with virus after challenge.PLoS pathogens · 2011Article
- Article
- Epstein-Barr virus nuclear antigens 3C and 3A maintain lymphoblastoid cell growth by repressing p16INK4A and p14ARF expression.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Experimental reverse genetic replacement of Epstein-Barr virus nuclear antigen 3A (EBNA3A) with a conditional mutant EBNA3A revealed that EBNA3A is critical for continued lymphoblastoid cell (LCL) growth. Wild-type (wt) EBNA3A expressed in the LCLs specifically sustained growth under nonpermissive conditions, whereas EBNA3B or EBNA3C expression had no effect (S. Mauro, E. Johannsen, D. Illanes, A. Cooper, and E. Kieff, J. Virol. 77:10437-10447, 2003). This genetic system and related biochemical assays have now been used to discover that EBNA3A lacking amino acid residues 170 to 240 (delta170-240), TLGC202 to AAGA202, or delta300-386, which are deficient in repression of EBNA2 activation of an RBP-Jkappa/CBF1-dependent EBV Cp enhancer, are null mutations for LCL growth, whereas EBNA3A delta2-124, delta410-439, delta440-470, delta470-500, delta500-523, delta523-612, and delta620-820, which are wt in repression are wt for LCL growth. Thus, EBNA3A regulation of transcription through RBP-Jkappa/CBF1 is critical for LCL growth. EBNA3A mutants deleted of amino acid residues 240 to 300, 386 to 410, or 827 to 944 were intermediate, null, or intermediate, respectively, for LCL growth despite being wt for RBP-Jkappa association and repression. Amino acid residues 240 to 300, 386 to 410, and, particularly, C-terminal residues 827 to 944 are therefore likely to contribute to LCL growth through RBP-Jkappa-independent mechanisms.
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