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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Enhancer of zeste homolog 1

EZH1, ENX-2, Enhancer of zeste homolog 1
EZH1 is a component of a noncanonical Polycomb repressive complex-2 (PRC2) that mediates methylation of histone H3 (see MIM 602812) lys27 (H3K27) and functions in the maintenance of embryonic stem cell pluripotency and plasticity (Shen et al., 2008 [PubMed 19026780]).[supplied by OMIM, Mar 2009] (from NCBI)
Top mentioned proteins: Polycomb, EZH2, Histone, EED, MARK
Papers on EZH1
Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
van Wijnen et al., Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
PRC2 mediated H3K27 methylations in cellular identity and cancer.
Bracken et al., Dublin, Ireland. In Curr Opin Cell Biol, Dec 2015
It is composed of a trimeric core of SUZ12, EED and EZH1/2 and is responsible for catalysing both di-methylation and tri-methylation of Histone H3 at lysine 27 (H3K27me2/3).
Regulation of Retinal Development via the Epigenetic Modification of Histone H3.
Murakami et al., Tokyo, Japan. In Adv Exp Med Biol, Dec 2015
Ezh1 and Ezh2 are methyltransferases that act on H3K27, while Jmjd3 and Utx are demethylases.
Inactivation of Eed impedes MLL-AF9-mediated leukemogenesis through Cdkn2a-dependent and Cdkn2a-independent mechanisms in a murine model.
Neff et al., Aurora, United States. In Exp Hematol, Nov 2015
In leukemia mediated by the leukemogenic fusion MLL-AF9, complete ablation of canonical PRC2 function by genetic inactivation of the core component embryonic ectoderm development (Eed) or by combined pharmacologic inhibition of the PRC2 methyltransferases EZH2 and EZH1 has a strong anti-leukemic effect, and this effect has been linked to de-repression of the PRC2 target locus Cdkn2a.
Loss of EZH2 results in precocious mammary gland development and activation of STAT5-dependent genes.
Hennighausen et al., Bethesda, United States. In Nucleic Acids Res, Nov 2015
This coincided with enhanced occupancy of these loci by STAT5, EZH1 and RNA Pol II.
Ezh2 loss in hematopoietic stem cells predisposes mice to develop heterogeneous malignancies in an Ezh1-dependent manner.
Iwama et al., Chiba, Japan. In Blood, Oct 2015
Chromatin immunoprecipitation-sequence analysis of trimethylation of histone H3 at lysine 27 (H3K27me3) revealed a compensatory function of Ezh1, another enzymatic component of PRC2, in this process.
Targeting EZH2 and PRC2 dependence as novel anticancer therapy.
Wang et al., Chapel Hill, United States. In Exp Hematol, Aug 2015
Here, we summarize the recently developed strategies for inhibition of PRC2, which include a series of highly specific, highly potent, small-molecule inhibitors of EZH2 and EZH1, an EZH2-related methyltransferase.
Epigenetic Role of Histone 3 Lysine Methyltransferase and Demethylase in Regulating Apoptosis Predicting the Recurrence of Atypical Meningioma.
Kim et al., Ch'angwŏn, South Korea. In J Korean Med Sci, Aug 2015
Immunohistochemical staining was performed on archived paraffin-embedded tissues for pro-apoptotic factors (CASP3, IGFBP, TRAIL-R1, BAX, and XAF1), anti-apoptotic factors (survivin, ERK, RAF1, MDM2, and BCL2), and the histone modifying enzymes (MLL2, RIZ, EZH1, NSD2, KDM5c, JMJD2a, UTX, and JMJD5).
Role of PRC2-associated factors in stem cells and disease.
Di Croce et al., Barcelona, Spain. In Febs J, May 2015
The core canonical complex PRC2, which contains the EZH1/2, SUZ12 and EED proteins, may be extended and functionally manipulated through interactions with several other proteins.
Dynamic expression of chromatin modifiers during developmental transitions in mouse preimplantation embryos.
Peters et al., Basel, Switzerland. In Sci Rep, 2014
We also detected lineage-specific expression of several modifiers, including Ezh1, Prdm14, Scmh1 and Tet1 underscoring possible roles in cell fate decisions.
Cells adapt to the epigenomic disruption caused by histone deacetylase inhibitors through a coordinated, chromatin-mediated transcriptional response.
Turner et al., Birmingham, United Kingdom. In Epigenetics Chromatin, 2014
Inhibition of the H3K27 methylating enzymes, EZH1/2, altered the transcriptional response to HDACi, confirming the functional significance of H3K27 methylation for specific genes.
Polycomb repressive complex 2 regulates normal hematopoietic stem cell function in a developmental-stage-specific manner.
Orkin et al., Boston, United States. In Cell Stem Cell, 2014
Here, we prevent assembly of both Ezh1- and Ezh2-containing PRC2 complexes by conditional deletion of Eed, a core subunit, and assess hematopoiesis.
Ezh1 is required for hematopoietic stem cell maintenance and prevents senescence-like cell cycle arrest.
Gonzalez et al., Madrid, Spain. In Cell Stem Cell, 2012
The PcG members Ezh2 and Ezh1 are important determinants of embryonic stem cell identity, and the transcript levels of these histone methyltransferases are inversely correlated during development.
Polycomb protein Ezh1 promotes RNA polymerase II elongation.
Sartorelli et al., Bethesda, United States. In Mol Cell, 2012
Ezh1 has a role in promoting mRNA transcription.
EZH1 and EZH2 cogovern histone H3K27 trimethylation and are essential for hair follicle homeostasis and wound repair.
Fuchs et al., New York City, United States. In Genes Dev, 2011
while Ezh1/2-null hair follicles (HFs) arrest morphogenesis and degenerate due to defective proliferation and increased apoptosis, epidermis hyperproliferates and survives engraftment
An EZ mark to miss.
Crabtree et al., Stanford, United States. In Cell Stem Cell, 2009
Recently in Molecular Cell, Shen and colleagues (2008) revealed that EZH2 is dispensable for ESC derivation and self-renewal, and that EZH1 may unexpectedly compensate for its loss.
EZH1 mediates methylation on histone H3 lysine 27 and complements EZH2 in maintaining stem cell identity and executing pluripotency.
Orkin et al., Boston, United States. In Mol Cell, 2008
Ezh1 mediates methylation on histone H3 lysine 27 and complements Ezh2 in maintaining stem cell identity and executing pluripotency.
Ezh1 and Ezh2 maintain repressive chromatin through different mechanisms.
Reinberg et al., New York City, United States. In Mol Cell, 2008
EZH1 maintains repressive chromatin through different mechanisms.
Chromatin structure regulation in transforming growth factor-beta-directed epithelial-mesenchymal transition.
Zavadil et al., New York City, United States. In Cells Tissues Organs, 2006
Based on multiple models of disease-related EMT, we propose that Polycomb group epigenetic silencers and histone-lysine methyl-transferases EZH1 and EZH2 are candidate targets of H/E(spl)-mediated transcriptional repression, in a process accompanied by replacement of modified core histone H3 with de novo synthesized histone variant H3.3B.
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