ArticleCell host & microbe2015
Epstein-Barr virus oncoprotein super-enhancers control B cell growth.
Article in Cell host & microbe, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05245344 (Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study), which is not on this map. Cited by 130 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.
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.
Effects of Ozanimod on Immune-mediated Mechanisms of Neurodegeneration in Multiple Sclerosis - a Preclinical Study
Who cites it
130 citing papers in PubMed, 183 citations in OpenAlex.
- Epigenetic regulation of humoral immunity: molecular mechanisms, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- EBNA1 inhibitors reveal CDC7 and POU2F1 as direct functional targets in EBV epithelial cancers.mBio · 2026Article
- Archaic Introgression Shapes Genetic Variation at Loci Associated With DNA Virus Load in Modern Humans.Genome biology and evolution · 2026Article
- Redistribution of super-enhancers promotes malignancy in human hepatocellular carcinoma.Journal of advanced research · 2026Article
- Genome-wide mapping of EBV-induced genomic variations identifies the role of MUC19 in EBV latency.mBio · 2025Article
- Epstein-Barr virus-transformed B-cells from a hypoxia model of the germinal center requires external unsaturated fatty acids.PLoS pathogens · 2025Article
- Aflatoxin B1 induces subtle but coordinated histone modifications in Epstein-Barr virus infected and non-infected Burkitt lymphoma cells.Environment international · 2025Article
- PARP1 Inhibition Halts EBV+ Lymphoma Progression by Disrupting the EBNA2/MYC Axis.Journal of medical virology · 2025Article
- EBV Latency Programs: Molecular and Epigenetic Regulation and Its Role in Disease Pathogenesis.Journal of medical virology · 2025Review
- EBNA leader protein orchestrates chromatin architecture remodeling during Epstein-Barr virus-induced B cell transformation.Nucleic acids research · 2025Article
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Selective Enhancer Dependencies in MYC-Intact and MYC-Rearranged Germinal Center B-cell Diffuse Large B-cell Lymphoma.Blood cancer discovery · 2025Article
- Multiple sclerosis and infection: history, EBV, and the search for mechanism.Microbiology and molecular biology reviews : MMBR · 2025Review
- Super enhancers as key drivers of gene regulatory networks in normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2025Review
- SE-lncRNAs in Cancer: Classification, Subcellular Localisation, Function and Corresponding TFs.Journal of cellular and molecular medicine · 2024Review
- Decoding Critical Targets and Signaling Pathways in EBV-Mediated Diseases Using Large Language Models.Viruses · 2024Article
- HIV-associated cancers and lymphoproliferative disorders caused by Kaposi sarcoma herpesvirus and Epstein-Barr virus.Clinical microbiology reviews · 2024Review
- High aggressiveness of papillary thyroid cancer: from clinical evidence to regulatory cellular networks.Cell death discovery · 2024Review
- Epstein-Barr virus protein EBNA-LP engages YY1 through leucine-rich motifs to promote naïve B cell transformation.PLoS pathogens · 2024Article
- Effects of super-enhancers in cancer metastasis: mechanisms and therapeutic targets.Molecular cancer · 2024Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Super-enhancers are clusters of gene-regulatory sites bound by multiple transcription factors that govern cell transcription, development, phenotype, and oncogenesis. By examining Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs), we identified four EBV oncoproteins and five EBV-activated NF-κB subunits co-occupying ∼1,800 enhancer sites. Of these, 187 had markedly higher and broader histone H3K27ac signals, characteristic of super-enhancers, and were designated "EBV super-enhancers." EBV super-enhancer-associated genes included the MYC and BCL2 oncogenes, which enable LCL proliferation and survival. EBV super-enhancers were enriched for B cell transcription factor motifs and had high co-occupancy of STAT5 and NFAT transcription factors (TFs). EBV super-enhancer-associated genes were more highly expressed than other LCL genes. Disrupting EBV super-enhancers by the bromodomain inhibitor JQ1 or conditionally inactivating an EBV oncoprotein or NF-κB decreased MYC or BCL2 expression and arrested LCL growth. These findings provide insight into mechanisms of EBV-induced lymphoproliferation and identify potential therapeutic interventions.
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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.