@article{saint-andre_models_2016,
	title = {Models of human core transcriptional regulatory circuitries},
	volume = {26},
	issn = {1549-5469},
	doi = {10.1101/gr.197590.115},
	abstract = {A small set of core transcription factors (TFs) dominates control of the gene expression program in embryonic stem cells and other well-studied cellular models. These core TFs collectively regulate their own gene expression, thus forming an interconnected auto-regulatory loop that can be considered the core transcriptional regulatory circuitry (CRC) for that cell type. There is limited knowledge of core TFs, and thus models of core regulatory circuitry, for most cell types. We recently discovered that genes encoding known core TFs forming CRCs are driven by super-enhancers, which provides an opportunity to systematically predict CRCs in poorly studied cell types through super-enhancer mapping. Here, we use super-enhancer maps to generate CRC models for 75 human cell and tissue types. These core circuitry models should prove valuable for further investigating cell-type-specific transcriptional regulation in healthy and diseased cells.},
	language = {eng},
	number = {3},
	journal = {Genome Research},
	author = {Saint-André, Violaine and Federation, Alexander J. and Lin, Charles Y. and Abraham, Brian J. and Reddy, Jessica and Lee, Tong Ihn and Bradner, James E. and Young, Richard A.},
	month = mar,
	year = {2016},
	pmid = {26843070},
	pmcid = {PMC4772020},
	keywords = {Humans, Transcription Factors, Gene Regulatory Networks, Gene Expression Regulation, Binding Sites, Protein Binding, Cell Line, Human Embryonic Stem Cells, Organ Specificity, Transcription, Genetic},
	pages = {385--396},
	file = {Full Text:/Users/deborah.gerard/Zotero/storage/9J4G4S38/Saint-André et al. - 2016 - Models of human core transcriptional regulatory ci.pdf:application/pdf},
}

@article{loven_selective_2013,
	title = {Selective inhibition of tumor oncogenes by disruption of super-enhancers},
	volume = {153},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2013.03.036},
	abstract = {Chromatin regulators have become attractive targets for cancer therapy, but it is unclear why inhibition of these ubiquitous regulators should have gene-specific effects in tumor cells. Here, we investigate how inhibition of the widely expressed transcriptional coactivator BRD4 leads to selective inhibition of the MYC oncogene in multiple myeloma (MM). BRD4 and Mediator were found to co-occupy thousands of enhancers associated with active genes. They also co-occupied a small set of exceptionally large super-enhancers associated with genes that feature prominently in MM biology, including the MYC oncogene. Treatment of MM tumor cells with the BET-bromodomain inhibitor JQ1 led to preferential loss of BRD4 at super-enhancers and consequent transcription elongation defects that preferentially impacted genes with super-enhancers, including MYC. Super-enhancers were found at key oncogenic drivers in many other tumor cells. These observations have implications for the discovery of cancer therapeutics directed at components of super-enhancers in diverse tumor types.},
	language = {eng},
	number = {2},
	journal = {Cell},
	author = {Lovén, Jakob and Hoke, Heather A. and Lin, Charles Y. and Lau, Ashley and Orlando, David A. and Vakoc, Christopher R. and Bradner, James E. and Lee, Tong Ihn and Young, Richard A.},
	month = apr,
	year = {2013},
	pmid = {23582323},
	pmcid = {PMC3760967},
	keywords = {Antineoplastic Agents, Azepines, Cell Cycle Proteins, Cell Line, Tumor, Chromatin, Enhancer Elements, Genetic, Gene Expression Regulation, Neoplastic, Genome-Wide Association Study, Humans, Mediator Complex, Multiple Myeloma, Neoplasms, Nuclear Proteins, Transcription Elongation, Genetic, Transcription Factors, Transcription, Genetic, Triazoles},
	pages = {320--334},
	file = {Full Text:/Users/deborah.gerard/Zotero/storage/YU2EHHIC/Lovén et al. - 2013 - Selective inhibition of tumor oncogenes by disrupt.pdf:application/pdf},
}

@article{heinz_simple_2010,
	title = {Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and {B} cell identities},
	volume = {38},
	issn = {1097-4164},
	doi = {10.1016/j.molcel.2010.05.004},
	abstract = {Genome-scale studies have revealed extensive, cell type-specific colocalization of transcription factors, but the mechanisms underlying this phenomenon remain poorly understood. Here, we demonstrate in macrophages and B cells that collaborative interactions of the common factor PU.1 with small sets of macrophage- or B cell lineage-determining transcription factors establish cell-specific binding sites that are associated with the majority of promoter-distal H3K4me1-marked genomic regions. PU.1 binding initiates nucleosome remodeling, followed by H3K4 monomethylation at large numbers of genomic regions associated with both broadly and specifically expressed genes. These locations serve as beacons for additional factors, exemplified by liver X receptors, which drive both cell-specific gene expression and signal-dependent responses. Together with analyses of transcription factor binding and H3K4me1 patterns in other cell types, these studies suggest that simple combinations of lineage-determining transcription factors can specify the genomic sites ultimately responsible for both cell identity and cell type-specific responses to diverse signaling inputs.},
	language = {eng},
	number = {4},
	journal = {Molecular Cell},
	author = {Heinz, Sven and Benner, Christopher and Spann, Nathanael and Bertolino, Eric and Lin, Yin C. and Laslo, Peter and Cheng, Jason X. and Murre, Cornelis and Singh, Harinder and Glass, Christopher K.},
	month = may,
	year = {2010},
	pmid = {20513432},
	pmcid = {PMC2898526},
	keywords = {Animals, B-Lymphocytes, Binding Sites, Cell Lineage, Macrophages, Male, Mice, Mice, Inbred C57BL, Oligonucleotide Array Sequence Analysis, Proto-Oncogene Proteins, Regulatory Elements, Transcriptional, Trans-Activators, Transcription Factors},
	pages = {576--589},
	file = {Full Text:/Users/deborah.gerard/Zotero/storage/GA45DV89/Heinz et al. - 2010 - Simple combinations of lineage-determining transcr.pdf:application/pdf},
}