Histone H3K27ac separates active from poised enhancers and predicts developmental state

By M. Creyghton, A. Cheng, G. Welstead, T. Kooistra, Bryce W. Carey, Eveline J. Steine, J. Hanna, Michael A. Lodato, G. Frampton, Phillip A. Sharp and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2010

4,057 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c14bcf138bb06caeb72c1698f7ff64680e030406

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Citations in the corpus

Latent enhancers activated by stimulation in differentiated cells. (2013, positive): “Enhancers are marked by monomethylated K4 on the histone H3 N-terminal tail (H3K4me1) (Heintzman et al., 2007, 2009) and have been classified into poised and active enhancers based on the absence or presence of histone acetylation, respectively (Creyghton et al., 2010; Rada-Iglesias et al., 2011).”
c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells (2012, positive): “The p300 binding sites are sorted into 100 bins based on the H3k27ac level, an estimate of enhancer activity (Creyghton et al., 2010; Rada-Iglesias et al., 2011)).”
Analysis of nascent RNA identifies a unified architecture of initiation regions at mammalian promoters and enhancers (2014, positive): “Previous work suggests that enhancer chromatin undergoes a progression from a closed state to an open state required for transcription factor binding 14, 41–43 .”
YY1 Is a Structural Regulator of Enhancer-Promoter Loops (2017, positive): “To identify proteins that bind active enhancers and promoters, we sought candidates from chromatin immunoprecipitation with mass spectrometry (ChIP-MS), using antibodies directed toward histones with modifications characteristic of enhancer and promoter chromatin (H3K27ac and H3K4me3, respectively) ”
Establishment of regions of genomic activity during the Drosophila maternal to zygotic transition (2014, background): “Flanking nucleosomes were enriched with H3K4me1, H3K27ac, and H3K18ac, marks previously shown to be enriched at active enhancers (Heintzman et al., 2007; Wang et al., 2008; Creyghton et al., 2010; Kharchenko et al., 2011; Rada-Iglesias et al., 2011) and depleted for H3K4me3 and H3K36me3.”
Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, background): “The widespread enrichment of K27Ac at active gene promoters and enhancers (Creyghton et al., 2010; Wang et al., 2008) suggests that this mechanism could be commonly utilized in metazoan genomes.”
High-throughput functional testing of ENCODE segmentation predictions (2014, positive): “In particular, highlevelsof the covalent histone modifications H3K27ac and H3K36me3 are thought to mark active enhancers and transcribed gene bodies or even heterochromatic regions (Barski et al. 2007; Creyghton et al. 2010; Chantalat et al. 2011).”
Transcription factor binding in human cells occurs in dense clusters formed around cohesin anchor sites. (2013, neutral): “…sensitive predictor of TF clusters than other well established correlates, including histone H3 K27 acetylation, FAIRE or DNase I hypersensitivity (Creyghton et al., 2010; Giresi et al., 2007; Thurman et al., 2012; Figures 4E and S4; Table S4), suggesting that cohesin may have a role in cluster…”
Tissue-Resident Macrophage Enhancer Landscapes Are Shaped by the Local Microenvironment (2014, background): “Poised Enhancers Reflect Both Developmental Origin and Tissue Specificity H3K4me1-marked enhancers are considered either active or poised, as demarcated by the presence or absence of the H3K27ac mark (Creyghton et al., 2010).”
The interplay of histone modifications – writers that read (2015, positive): “H3K27ac and H3K4me1 are associated with active enhancers [3], and high levels of H3K4me3 and H3 and H4 acetylation are found at the promoters of active genes [4–6].”