ArticleProceedings of the National Academy of Sciences of the United States of America2009
Epstein-Barr virus nuclear protein EBNA3C residues critical for maintaining lymphoblastoid cell growth.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 42 citations in OpenAlex.
- Exploring EBNA3C Genetic Variability and Recombination in Epstein-Barr Virus-Associated Cancers.International journal of molecular sciences · 2026Article
- Review
- 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
- Proteasomal inhibition triggers viral oncoprotein degradation via autophagy-lysosomal pathway.PLoS pathogens · 2020Article
- Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression ofJournal of virology · 2018Article
- 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
- RUNX super-enhancer control through the Notch pathway by Epstein-Barr virus transcription factors regulates B cell growth.Nucleic acids research · 2016Article
- Article
- EBNA3C Directs Recruitment of RBPJ (CBF1) to Chromatin during the Process of Gene Repression in EBV Infected B Cells.PLoS pathogens · 2016Article
- The Modulation of Apoptotic Pathways by Gammaherpesviruses.Frontiers in microbiology · 2016Review
- 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
- Dissecting the contribution of EBNA3C domains important for EBV-induced B-cell growth and proliferation.Oncotarget · 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
- EBNA3C regulates p53 through induction of Aurora kinase B.Oncotarget · 2015Article
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- 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
- Genomic diversity of Epstein-Barr virus genomes isolated from primary nasopharyngeal carcinoma biopsy samples.Journal of virology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) is essential for efficient conversion of primary human B lymphocytes to lymphoblastoid cell lines (LCLs) and for continued LCL growth. We used a transcomplementation assay in the context of LCLs transformed by an EBV with a conditional EBNA3C to identify the EBNA3C amino acids (aa) necessary for maintaining LCL growth. Surprisingly, we found that most EBNA3C aa were essential for continued LCL growth. Only EBNA3C mutants deleted for residues within aa 507-515, 516-620, 637-675, or 676-727 maintained full LCL growth, and EBNA3C mutants deleted for residues within aa 728-732 or 910-992 maintained slow LCL growth. In contrast, EBNA3C lacking aa 180-231, which mediate RBP-Jkappa association and are necessary for EBNA3C abrogation of EBNA2-induced transcription through RBP-Jkappa, could not support LCL growth. Furthermore, 2 EBNA3C alanine substitution mutants within aa 180-231, which were wild-type (wt) in abrogating EBNA2-mediated transcription through RBP-Jkappa, maintained LCL growth, and 2 alanine substitution mutants within aa 180-231, which were null in abrogating EBNA2-mediated transcription through RBP-Jkappa, did not maintain LCL growth. This indicates that EBNA3C regulation of transcription through RBP-Jkappa is critical to maintaining LCL growth. Several other EBNA3C functions also are critical for LCL growth, because EBNA3C mutants deleted for residues within aa 130-159, 251-506, or 733-909 were wt in abrogating transcription through RBP-Jkappa and expression level, but did not maintain LCL growth.
Indexed as
Identifiers
What OpenQuestion holds
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.