og:image: http://journals.plos.org/plospathogens/article/figure/image?id=10.1371/journal.ppat.1006664.g007&size=inline
citation_author_institution: Department of Gene Vectors, Helmholtz Center Munich, Munich, Germany
citation_title: EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells
twitter:card: summary
keywords: B cells,Chromatin,Cell binding,Gene expression,Transcription factors,Gene regulation,Estrogens,Genomic signal processing
citation_reference: citation_title=The Varied Roles of Notch in Cancer;citation_author=JC Aster;citation_author=WS Pear;citation_author=SC Blacklow;citation_journal_title=Annual review of pathology;citation_publication_date=2016;
citation_publisher: Public Library of Science
citation_journal_title: PLOS Pathogens
description: Author summary Epstein-Barr virus (EBV) infection is closely linked to cancer development. At particular risk are immunocompromised individuals like post-transplant patients which can develop B cell lymphomas. In healthy individuals EBV preferentially infects B cells and establishes a latent infection without causing apparent clinical symptoms in most cases. Upon infection, Epstein-Barr virus nuclear antigen 2 (EBNA2) initiates a B cell specific gene expression program that causes activation and proliferation of the infected cells. EBNA2 is a transcription factor well known to use a cellular protein, CBF1/CSL, as a DNA adaptor. CBF1/CSL is a sequence specific DNA binding protein robustly expressed in all tissues. Here we show that EBNA2 can form complexes with early B cell factor 1 (EBF1), a B cell specific DNA binding transcription factor, and EBF1 stabilizes EBNA2 chromatin binding. This EBNA2/EBF1 complex might serve as a novel target to develop future small molecule strategies that act as antivirals in latent B cell infection.
citation_date: 02.10.2017
title: EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells
og:description: Author summary Epstein-Barr virus (EBV) infection is closely linked to cancer development. At particular risk are immunocompromised individuals like post-transplant patients which can develop B cell lymphomas. In healthy individuals EBV preferentially infects B cells and establishes a latent infection without causing apparent clinical symptoms in most cases. Upon infection, Epstein-Barr virus nuclear antigen 2 (EBNA2) initiates a B cell specific gene expression program that causes activation and proliferation of the infected cells. EBNA2 is a transcription factor well known to use a cellular protein, CBF1/CSL, as a DNA adaptor. CBF1/CSL is a sequence specific DNA binding protein robustly expressed in all tissues. Here we show that EBNA2 can form complexes with early B cell factor 1 (EBF1), a B cell specific DNA binding transcription factor, and EBF1 stabilizes EBNA2 chromatin binding. This EBNA2/EBF1 complex might serve as a novel target to develop future small molecule strategies that act as antivirals in latent B cell infection.
twitter:image: http://journals.plos.org/plospathogens/article/figure/image?id=10.1371/journal.ppat.1006664.g007&size=inline
citation_issn: 1553-7374
twitter:site: @plospathogens
dc:title: EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells
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citation_pdf_url: http://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006664&type=printable
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twitter:title: EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells
og:type: article
citation_journal_abbrev: PLOS Pathogens
og:title: EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells
citation_author: Laura V. Glaser
citation_issue: 10
citation_firstpage: e1006664
citation_doi: 10.1371/journal.ppat.1006664
twitter:description: Author summary Epstein-Barr virus (EBV) infection is closely linked to cancer development. At particular risk are immunocompromised individuals like post-transplant patients which can develop B cell lymphomas. In healthy individuals EBV preferentially infects B cells and establishes a latent infection without causing apparent clinical symptoms in most cases. Upon infection, Epstein-Barr virus nuclear antigen 2 (EBNA2) initiates a B cell specific gene expression program that causes activation and proliferation of the infected cells. EBNA2 is a transcription factor well known to use a cellular protein, CBF1/CSL, as a DNA adaptor. CBF1/CSL is a sequence specific DNA binding protein robustly expressed in all tissues. Here we show that EBNA2 can form complexes with early B cell factor 1 (EBF1), a B cell specific DNA binding transcription factor, and EBF1 stabilizes EBNA2 chromatin binding. This EBNA2/EBF1 complex might serve as a novel target to develop future small molecule strategies that act as antivirals in latent B cell infection.
dc.identifier: 10.1371/journal.ppat.1006664
citation_volume: 13
og:url: http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006664
Content-Language: en