CBP-mediated acetylation of histone H3 lysine 27 antagonizes Drosophila Polycomb silencing

By F. Tie, Rakhee Banerjee, C. A. Stratton, Jayashree Prasad-Sinha, Vincent Stepanik, A. Zlobin, M. Diaz, P. Scacheri, P. Harte. Development, 2009

605 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e217fb8fa511c54090524770a0057d49d5d8562e

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In Molecular Biology

Citations in the corpus

Distinct roles of GCN5/PCAF‐mediated H3K9ac and CBP/p300‐mediated H3K18/27ac in nuclear receptor transactivation (2011, methodology): “It has been shown previously that CBP/p300 are capable of acetylating H3K18 and H3K27 in vitro and that knockdown of CBP in Drosophila S2 cells results in a substantial reduction of H3K18ac and H3K27ac, but has little effect on the global levels of H3K9ac, H3K14ac and H3K23ac (Tie et al, 2009).”
The physics of epigenetics (2015, background): “…that drive the two main silencing processes in animals, namely, the recruitment and spreading of HP1 (heterochromatin protein 1) by the H3K9me3 mark (Hathaway et al., 2012; Azzaz et al., 2014) and the recruitment of the polycomb architectural complex (PcG) by the H3K27me3 mark (Tie et al., 2009).”
ngs.plot: Quick mining and visualization of next-generation sequencing data by integrating genomic databases (2014, background): “As previously reported [67], H3K27ac is mutually exclusive with H3K27me3.”
Modification of enhancer chromatin: what, how and why? (2013, background): “One of the main substrates acetylated by p300/CBP in vivo is H3K27 (Jin et al., 2011; Pasini et al., 2010; Tie et al., 2009) (Figure 4).”
Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, background): “Indeed, recent studies support use of this ‘‘either/or’’ tactic to counteract PRC2 in vivo (Pasini et al., 2010b; Tie et al., 2009).”
Genome Regulation by Polycomb and Trithorax: 70 Years and Counting. (2017, positive): “On the activating side, Trx associates with dCBP and is required for H3K27 acetylation to block PRC2-mediated methylation (Tie et al., 2009).”
Histone H3K27ac separates active from poised enhancers and predicts developmental state (2010, background): “This mark can be deposited by both p300 andCREB binding protein (CBP) (14) and is associated with active promoters in mammalian cells (15).”