Mechanisms of Polycomb gene silencing: knowns and unknowns
By J. Simon, Robert E. Kingston. Nature reviews. Molecular cell biology, 2009
1,421 citations recorded by the source corpus.
Subfields: Applied Mathematics, Education
View Paper: https://www.semanticscholar.org/paper/5f5f2c1e6805d816de13fe9b5bbd2d96f78322d8
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Citations in the corpus
- The Polycomb Complex PRC2 and its Mark in Life (2011, background): “Two other PcG complexes were characterized in Drosophila , PHO-repressive complex (PhoRC) and Polycomb repressive deubiquitinase (PR-DUB), and their components have orthologues in mammals; however, the conservation of their functions has not yet been addresse”
- Transcriptional enhancers: from properties to genome-wide predictions (2014, neutral): “80 ).”
- The histone H3.3K27M mutation in pediatric glioma reprograms H3K27 methylation and gene expression. (2013, background): “…cells (Bernstein et al. 2006; Barski et al. 2007) as well as inactivated X chromosomes in female mammals (Plath et al. 2003) and plays an important role in regulating expression of developmentally regulated genes (Zhang and Reinberg 2001; Simon and Kingston 2009; Margueron and Reinberg 2011).”
- Charting histone modifications and the functional organization of mammalian genomes (2011, background): “These patterns result from complex mechanisms involving trans -acting factors that are subject to intense investigation but remain poorly understoo”
- ncRNA- and Pc2 Methylation-Dependent Gene Relocation between Nuclear Structures Mediates Gene Activation Programs (2011, neutral): “(F) Effect of knockdown of Pc2, Bmi1 and PHC1 on relocation of MCM3 locus between PcG bodies and interchromatin granules.”
- Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer. (2010, neutral): “Similar findings have been reported for cancers of the breast, brain, colon, ovary, pancreas, and prostate (Al-Hajj et al., 2003; Li et al., 2007; O’Brien et al., 2007; Singh et al., 2003; Zhang et al., 2008b).”
- Biogenesis and Function of Nuclear Bodies (2011, background): “PcG proteins form at least two classes of complexes designated Polycomb repressive complexes 1 and 2 (PRC1 and PRC2) that are thought to collaborate to repress gene transcription [95].”
- PCGF Homologs, CBX Proteins, and RYBP Define Functionally Distinct PRC1 Family Complexes (2012, background): “344 Molecular Cell 45, 344–356, February 10, 2012 a2012 Elsevier In which catalyze two repressive histone PTMs: monoubiquitination of histone H2A at lysine-119 (H2AK119ub1) and methylation of histone H3 at lysine-27 (H3K27me), respectively (Margueron and Reinberg, 2011; Simon and Kingston, 2009).”
- Phosphorylation of EZH2 activates STAT3 signaling via STAT3 methylation and promotes tumorigenicity of glioblastoma stem-like cells (2013, background): “One possibility is that a cofactor of PRC2 component preferentially expressed in stem cell population (Simon and Kingston, 2009) might facilitate the AKT-EZH2”
- Senescence impairs successful reprogramming to pluripotent stem cells. (2009, background): “The core of mammalian PRC1 is constituted by: a polycomb component containing a chromo domain (PC)(CBX2, 4, 6, 7 or 8), a polyhomeotic component (PH) (PH 1, 2, or 3) a posterior sex combs element (PSC) (such as BMI or MEL18) and a RING protein (RING1A or B) (Simon and Kingston, 2009)(Figure 1.”
- Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, background): “This impairs K27me3 accumulation, but observed consequences could also reflect PRC2 methylation of nonhistone targets and/or noncatalytic functions of PRC2 (Margueron and Reinberg, 2011; Simon and Kingston, 2009).”