Role of Histone H3 Lysine 27 Methylation in Polycomb-Group Silencing

By R. Cao, Liangjun Wang, Hengbin Wang, L. Xia, H. Erdjument‐Bromage, Paul Tempst, Richard S. Jones, Yi Zhang. Science, 2002

3,986 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a9e77a6ead31533ebe25e1b34b664db18c0f5210

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In Molecular Biology

1. Yi Zhang
2. Richard A. Young
3. D. Reinberg
4. K. Helin
5. C. D. Allis
6. J. Simon
7. Martin Sauvageau
8. G. Sauvageau

Citations in the corpus

• Ezh2 controls B cell development through histone H3 methylation and Igh rearrangement (2003, background): “The E(Z) methylates in vitro lysine 9 (H3-K9) and lysine 27 (H3-K27) of histone H”
• Repression of E-cadherin by the polycomb group protein EZH2 in cancer (2008, background): “Oncogene (2008) 27, 7274–7284 & 2008 Macmillan Publishers Limited All rights reserved 0950-9232/08 $32.00 www.nature.com/onc lysine 27 (Cao et al., 2002; Kirmizis et al., 2004).”
• The Polycomb Group Protein Suz12 Is Required for Embryonic Stem Cell Differentiation (2007, background): “However, in contrast to the model that has PRC1 recruitment dependent on its ability to specifically bind H3K27me3 (7, 8, 19), we found that PRC1 recruitment is independent of H3K27me3 on three of the five Cbx8 targets (Pax7, Fgf3, and Fgf4) and on the Bmi1 target (Pax7).”
• Histone methylation by PRC2 is inhibited by active chromatin marks. (2011, background): “Among the PcG protein complexes, Polycomb repressive complex 2 (PRC2) is a histone methyl-transferase (HMTase) that methylates Lys27 of H3 (H3K27) (Cao et al., 2002; Czermin et al., 2002; Kuzmichev et al., 2004; Mü ller et al., 2002).”
• Polycomb group proteins Ring1A/B link ubiquitylation of histone H2A to heritable gene silencing and X inactivation. (2004, background): “Muller et al., 2002; Cao et al., 2002; Kuzmichev et al., 2002; Fischle et al., 2003; Min et al., 2003).”
• Variant PRC1 Complex-Dependent H2A Ubiquitylation Drives PRC2 Recruitment and Polycomb Domain Formation (2014, background): “The co-occupancy of polycomb group proteins at target sites has largely been viewed in the context of a hierarchical recruitment model (Cao et al., 2002; Wang et al., 2004b).”
• Targeted recruitment of Set1 histone methylase by elongating Pol II provides a localized mark and memory of recent transcriptional activity. (2003, background): “et al., 2002) or to repressor binding sites (Cao et al., 2002; Czermin et al., 2002; Kuzmichev et al., 2002; Muller et al., 2002; Ogawa et al., 2002).”
• Control of developmental regulators by Polycomb in human embryonic stem cells. (2006, background): “…methylation is thought to provide a binding surface for PRC1, which facilitates oligomerization, condensation of chromatin structure, and inhibition of chromatin remodeling activity in order to maintain silencing (Shao et al., 1999; Francis et al., 2001; Cao et al., 2002; Czermin et al., 2002).”
• The General Transcription Machinery and General Cofactors (2006, background): “, 2001) and human PRC2 (Cao et al., 2002; Kuzmichev et al., 2002), PRC3 (Kuzmichev et al.”
• Pharmacologic disruption of Polycomb-repressive complex 2-mediated gene repression selectively induces apoptosis in cancer cells. (2007, background): “PRCs contain intrinsic histone methyltransferase (HMTase) activity and maintain gene repression through methylation of core histones (Beisel et al. 2002; Cao et al. 2002; Milne et al. 2002; Muller et al. 2002; Nakamura et al. 2002).”