@article {352471,
	title = {Epstein-Barr virus oncoprotein super-enhancers control B cell growth},
	journal = {Cell Host Microbe},
	volume = {17},
	number = {2},
	year = {2015},
	month = {2015 Feb 11},
	pages = {205-16},
	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.},
	keywords = {B-Lymphocytes, Cell proliferation, Gene Expression Profiling, Gene Expression Regulation, Herpesvirus 4, Human, Host-Pathogen Interactions, Molecular Sequence Data, Oncogene Proteins, Sequence Analysis, DNA, Transcription, Genetic, Viral Proteins},
	issn = {1934-6069},
	doi = {10.1016/j.chom.2014.12.013},
	author = {Zhou, Hufeng and Schmidt, Stefanie C S and Jiang, Sizun and Willox, Bradford and Bernhardt, Katharina and Liang, Jun and Johannsen, Eric C and Kharchenko, Peter and Gewurz, Benjamin E and Kieff, Elliott and Zhao, Bo}
}
