Enhancer function: new insights into the regulation of tissue-specific gene expression

By Chin-Tong Ong, V. Corces. Nature reviews genetics, 2011

955 citations recorded by the source corpus.

Enhancer function underlies regulatory processes by which cells establish patterns of gene expression. Recent results suggest that many enhancers are specified by particular chromatin marks in pluripotent cells, which may be modified later in development to alter patterns of gene expression and cell differentiation choices. These marks may contribute to the repertoire of epigenetic mechanisms responsible for cellular memory and determine the timing of transcription factor accessibility to the enhancer. Mechanistically, cohesin and non-coding RNAs are emerging as crucial players responsible for facilitating enhancer–promoter interactions at some genes. Surprisingly, these interactions may be required not only to facilitate initiation of transcription but also to activate the release of RNA polymerase II (RNAPII) from promoter-proximal pausing.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ace5fe628e29abf1b1ad49f86f85e9ef648a374f

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Citations in the corpus

Transcriptional Regulation and its Misregulation in Disease (2013, positive): “Transcription factors typically regulate gene expression by binding enhancer elements and recruiting co-activators and RNA polymerase II to target genes (Lelli et al., 2012; Ong and Corces, 2011; Spitz and Furlong, 2012).”
YY1 Is a Structural Regulator of Enhancer-Promoter Loops (2017, positive): “Graphical abstract INTRODUCTION Cell-type-specific gene expression programs in humans are generally controlled by gene regulatory elements called enhancers (Buecker and Wysocka, 2012; Bulger and Groudine, 2011; Levine et al., 2014; Ong and Corces, 2011; Ren and Yue, 2015).”
Transcription factor binding in human cells occurs in dense clusters formed around cohesin anchor sites. (2013, neutral): “This information is embedded into at least three different types of gene regulatory elements: promoters, enhancers, and insulators (Ong and Corces, 2011).”
Selective Inhibition of Tumor Oncogenes by Disruption of Super-Enhancers (2013, background): “The y axis shows the average background subtracted ChIP-seq signal in units of rpm/bp. 322 Cell 153, 320–334, April 11, 2013 ª2013 Elsevier Inc. et al., 2012; Ong and Corces, 2011; Spitz and Furlong, 2012).”
Super-enhancers in the control of cell identity and disease. (2013, neutral): “…which play key roles in the control of cell type-specific gene expression programs (Bulger and Groudine, 2011; Calo and Wysocka, 2013; Carey, 1998; Lelli et al., 2012; Levine and Tjian, 2003; Maston et al., 2006; Ong and Corces, 2011; Panne, 2008; Spitz and Furlong, 2012; Xie and Ren, 2013).”
NeST, a long noncoding RNA, controls microbial susceptibility and epigenetic activation of the Ifng locus (2013, positive): “Simultaneous binding of cohesin, T-bet, and CTCF results in a complex three-dimensional conformation that is predicted to bring the NeST and IFN-g coding regions into direct proximity (Hadjur et al., 2009; Ong and Corces, 2011; Sekimata et al., 2009).”
dbSUPER: a database of super-enhancers in mouse and human genome (2015, background): “It is known that enhancers tend to loop and associate with target genes in order to activate their transcription (40), while most of these interactions occur within a distance of ≈50 kb of the enhancer (41).”
Transcriptional Addiction in Cancer (2017, neutral): “The master TFs bind cooperatively to enhancer DNA elements and recruit coactivators and the transcription apparatus (Banerji et al., 1981; Benoist and Chambon, 1981; Bulger and Groudine, 2011; Gruss et al., 1981; Jolma et al., 2015; Lelli et al., 2012; Levine et al., 2014; Malik and Roeder, 2010; On”
Transcriptional Amplification in Tumor Cells with Elevated c-Myc (2012, positive): “Furthermore, enhancers loop into proximity of core promoters at active genes (Bulger and Groudine, 2011; Göndör and Ohlsson, 2009; Kagey et al., 2010; Ong and Corces, 2011) and this proximity may facilitate binding of c-Myc to nearby enhancer elements once binding to sites in core promoters is satur”