ArticlePLoS pathogens2017
EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Systematic investigation reveals extensive Epstein-Barr virus transcriptional regulation of the human genome.Cell genomics · 2026Article
- GBSC: graph-based sequence clustering method for similar short tandem repeats in protein sequences.Bioinformatics (Oxford, England) · 2026Article
- The role of Epstein-Barr virus in NK/T cell lymphoproliferative disorders: molecular mechanisms and potential therapeutic strategies.Frontiers in immunology · 2026Review
- Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.PLoS pathogens · 2024Article
- Differential carbonic anhydrase activities control EBV-induced B-cell transformation and lytic cycle reactivation.PLoS pathogens · 2024Article
- Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.bioRxiv : the preprint server for biology · 2024Article
- LMP1 and EBNA2 constitute a minimal set of EBV genes for transformation of human B cells.Frontiers in immunology · 2023Article
- EBNA2 mediates lipid metabolism and tumorigenesis through activation of ATF4 pathway.American journal of cancer research · 2023Article
- Regulation of B cell receptor signalling by Epstein-Barr virus nuclear antigens.The Biochemical journal · 2022Article
- Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis.Current microbiology · 2022Review
- Tnpo3 enables EBF1 function in conditions of antagonistic Notch signaling.Genes & development · 2022Article
- EBNA2-EBF1 complexes promote MYC expression and metabolic processes driving S-phase progression of Epstein-Barr virus-infected B cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Reduced IRF4 expression promotes lytic phenotype in Type 2 EBV-infected B cells.PLoS pathogens · 2022Article
- PLK1-dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV-infected mice.EMBO reports · 2021Article
- Assessing genome-wide dynamic changes in enhancer activity during early mESC differentiation by FAIRE-STARR-seq.Nucleic acids research · 2021Article
- Phase separation of Epstein-Barr virus EBNA2 protein reorganizes chromatin topology for epigenetic regulation.Communications biology · 2021Article
- Human Virus Transcriptional Regulators.Cell · 2020Review
- B Cell-Specific Transcription Activator PAX5 Recruits p300 To Support EBNA1-Driven Transcription.Journal of virology · 2020Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) infection converts resting human B cells into permanently proliferating lymphoblastoid cell lines (LCLs). The Epstein-Barr virus nuclear antigen 2 (EBNA2) plays a key role in this process. It preferentially binds to B cell enhancers and establishes a specific viral and cellular gene expression program in LCLs. The cellular DNA binding factor CBF1/CSL serves as a sequence specific chromatin anchor for EBNA2. The ubiquitous expression of this highly conserved protein raises the question whether additional cellular factors might determine EBNA2 chromatin binding selectively in B cells. Here we used CBF1 deficient B cells to identify cellular genes up or downregulated by EBNA2 as well as CBF1 independent EBNA2 chromatin binding sites. Apparently, CBF1 independent EBNA2 target genes and chromatin binding sites can be identified but are less frequent than CBF1 dependent EBNA2 functions. CBF1 independent EBNA2 binding sites are highly enriched for EBF1 binding motifs. We show that EBNA2 binds to EBF1 via its N-terminal domain. CBF1 proficient and deficient B cells require EBF1 to bind to CBF1 independent binding sites. Our results identify EBF1 as a co-factor of EBNA2 which conveys B cell specificity to EBNA2.
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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 Socratic graph.