Suz12 is essential for mouse development and for EZH2 histone methyltransferase activity

By Diego Pasini, A. Bracken, M. Jensen, E. L. Denchi, K. Helin. EMBO Journal, 2004

942 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f53031299f1ad84289dbeca9e771aec7b50d6655

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Citations in the corpus

A double take on bivalent promoters. (2013, background): “2010), which parallels the post-implantation lethality phenotypes observed in PRC2 knockout mouse models (Faust et al. 1995; O’Carroll et al. 2001; Pasini et al. 2004).”
Transcriptional regulation by Polycomb group proteins (2013, background): “; and from the Novo Nordisk Foundation, the Danish Cancer Society and the Danish Council for Strategic Research (12-110503) to K.”
The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells. (2007, methodology): “…(07-219; Upstate Biotechnology), antiH3K4Me3 (ab8580; Abcam), an equal mix of anti-CBX8 “LAST” and “GALD” (Bracken et al. 2006), an equal mix of anti-CBX7 “GAPEL” and “RELF” described above, and mouse monoclonals specific for EZH2 (AC22) (Pasini et al. 2004b) and BMI1 (AF27) described above.”
EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency. (2008, background): “Robust H3K27me1 in Suz12 / cells suggests a dispensable role of SUZ12 in mediating H3K27me1 (Pasini et al., 2004).”
Ki-67: more than a proliferation marker (2018, background): “The associated proteins include UHRF1, which binds H3K9me3 and DNA methyltransferase DNMT1 (Bostick et al. 2007); SUZ12, a component of H3K27 methyltransferase complex PRC2 (Pasini et al. 2004); and TIP5, the major component of the nucleolar remodeling complex (NoRC) which contributes to the silent ”
Pharmacologic disruption of Polycomb-repressive complex 2-mediated gene repression selectively induces apoptosis in cancer cells. (2007, background): “It is known that PRC2 complex is subjected to proteosome-mediated degradation (Pasini et al. 2004).”
Histone methylation by PRC2 is inhibited by active chromatin marks. (2011, background): “Structure of the Nurf55-Su(z)12 Subcomplex of PRC2 The H3-Nurf55 structure prompted us to investigate how Nurf55 might bind histone tails in the presence of Su(z)12, its interaction partner in PRC2 (Nekrasov et al., 2005; Pasini et al., 2004).”
Occupying chromatin: Polycomb mechanisms for getting to genomic targets, stopping transcriptional traffic, and staying put (2013, positive): “However, the EZH2 subunit is inactive on its own andmust be assembled with SUZ12 and EED to produce methyltransferase activity (Cao and Zhang, 2004; Ketel et al., 2005; Pasini et al., 2004).”
A model for transmission of the H3K27me3 epigenetic mark (2008, background): “Therefore, it is believed that maintenance of the H3K27me3 mark during cell division is essential for normal embryogenesi”
The diverse functions of histone lysine methylation (2005, background): “Furthermore, whereas all forms of H3-K27 methylation require EED 79 , SUZ12 seems to be dispensable for the monomethylation of H3-K27 in vivo , although it is indispensable for the enzymatic activity in vitro 80,81 .”
Polycomb group proteins: multi-faceted regulators of somatic stem cells and cancer. (2010, positive): “…Ezh2, Suz12, Eed, or Ring1b leads to a loss of H3K27me3 and H2AK119ub1 marks, a spontaneous increase in developmental gene expression, and consequently, differentiation defects of embryonic stem cells (Chamberlain et al., 2008; Pasini et al., 2007; Shen et al., 2008; van der Stoop et al., 2008).”
How is pluripotency determined and maintained? (2007, background): “5 Normal Normal Normal NT NT Pasini et al., 2004; Lee et al., 2006 PRC1 Rnf2 (Ring1b) Die at E7.”
Variant PRC1 Complex-Dependent H2A Ubiquitylation Drives PRC2 Recruitment and Polycomb Domain Formation (2014, background): “A series of auxiliary proteins, including SUZ12 and EED, associate with EZH1/2 and modulate targeting, chromatin binding, and catalytic activity (Cao and Zhang, 2004; Ketel et al., 2005; Margueron et al., 2009; Pasini et al., 2004).”
Ezh1 and Ezh2 maintain repressive chromatin through different mechanisms (2008, background): “Given that ES cells depleted of either Suz12 or Eed are also depleted of H3K27me2/3, but not of H3K27me1 (Pasini et al., 2004; Schoeftner et al., 2006), this suggests that PRC2Ezh complexes initiate methylation on monomethylated histones and add one or two additional methyl marks.”