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Article

Inactivation of intergenic enhancers by EBNA3A initiates and maintains polycomb signatures across a chromatin domain encoding CXCL10 and CXCL9.

PLoS pathogens - 1 Sept 2013

Harth-Hertle Marie L, Scholz Barbara A, Erhard Florian, Glaser Laura V, Dölken Lars, Zimmer Ralf, Kempkes Bettina

Abstract excerpt

Epstein-Barr virus (EBV) causes a persistent infection in human B cells by establishing specific transcription programs to control B cell activation and differentiation. Transcriptional reprogramming of EBV infected B cells is predominantly driven by the action of EBV nuclear antigens, among them the transcriptional repressor EBNA3A. By comparing gene expression profiles of wt and EBNA3A negative EBV infected B...

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Topics

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Share to Cellular Reprogramming
Share to Chemokine CXCL10

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromatin Assembly and Disassembly

Share to DNA, Intergenic

Share to Epstein-Barr Virus Infections

Share to Epstein-Barr Virus Nuclear Antigens

Share to Immunoglobulin J Recombination Signal Sequence-Binding Protein

Share to Polycomb-Group Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 24068939
DOI: 10.1371/journal.ppat.1003638
PMCID: PMC3777872

Genes

CXCL10
CXCL9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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