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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].. Zusätzlich bieten wir Ihnen EZH1 Kits (10) und EZH1 Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal EZH1 Primary Antibody für ELISA, WB - ABIN249717
Abel, Brody, Valdes, Erdos, McKinley, Castilla, Merajver, Couch, Friedman, Ostermeyer, Lynch, King, Welcsh, Osborne-Lawrence, Spillman, Bowcock, Collins, Weber: Characterization of EZH1, a human homolog of Drosophila Enhancer of zeste near BRCA1. in Genomics 1997
Human Polyclonal EZH1 Primary Antibody für WB - ABIN4309822
Grimaldi, Christian, Steel, Henriet, Poutanen, Brosens: Down-regulation of the histone methyltransferase EZH2 contributes to the epigenetic programming of decidualizing human endometrial stromal cells. in Molecular endocrinology (Baltimore, Md.) 2011
identification of EZH1 as a repressor of haematopoietic multipotency in the early mammalian embryo
pVHL (zeige VHL Antikörper) loss causes the transcriptional activation of hypoxia-inducible factor (HIF) target genes, including many genes that encode histone lysine demethylases.
Data show that embryonic stem cells with deletion of EZH1 or EZH2 (zeige EZH2 Antikörper) fail to differentiate into ectoderm lineages.
Expression of the EZH2 (zeige EZH2 Antikörper) homolog EZH1 is reduced in EZH2 (zeige EZH2 Antikörper)-deficient CML (zeige BCR Antikörper) LICs, creating a scenario resembling complete loss of PRC2. EZH2 (zeige EZH2 Antikörper) dependence of CML (zeige BCR Antikörper) LICs raises prospects for improved therapy of TKI-resistant CML (zeige BCR Antikörper) and/or eradication of disease by addition of EZH2 (zeige EZH2 Antikörper) inhibitors
a hot-spot mutation in EZH1 is the second most frequent genetic alteration in autonomous thyroid adenomas; the association between EZH1 and TSHR (zeige TSHR Antikörper) mutations suggests a 2-hit model for the pathogenesis of these tumors, whereby constitutive activation of the cAMP pathway and EZH1 mutations cooperate to induce the hyperproliferation of thyroid cells
EZH1, SUZ12 and UXT (zeige UXT Antikörper) work synergistically to regulate pathway activation in the nucleus.
The authors report a novel PRC2-Ezh1 function that utilizes Ezh1beta as an adaptive stress sensor in the cytoplasm, thus allowing postmitotic cells to maintain tissue integrity in response to environmental changes.
These evidences suggest that EZH2 (zeige EZH2 Antikörper) and EZH1 are important in the counter-balancing mechanisms controlling proliferation/resting of lymphoid cells. The disruption of the balanced EZH2/EZH1 (zeige EZH2 Antikörper) ratio may play important roles in the pathogenesis of lymphomas
The related enzymatic subunits EZH1 and EZH2 (zeige EZH2 Antikörper) undergo an expression switch during blood cell development.
EZH1 maintains repressive chromatin through different mechanisms.
The combined loss of Ezh1 and Ezh2 (zeige EZH2 Antikörper) in chondrocytes severely impairs skeletal growth in mice.
Suggest that EZH1 and -2 are novel targets of miR (zeige MLXIP Antikörper)-214-3p, and miR (zeige MLXIP Antikörper)-214-3p might be one potential miRNA for the prevention of cardiac fibrosis.
Ezh1 is required for neonatal heart regeneration and development.
in the skin epithelium, EED (zeige EED Antikörper), Suz12, and Ezh1/2 function largely as subunits of the PRC2 complex and have roles in skin development
the expression level of Ezh1 determines the restoration of H3K27 methylation in the absence of the canonical EZH2 (zeige EZH2 Antikörper)-PRC2.
These results clearly demonstrated an essential role of Ezh1 in the pathogenesis of hematopoietic malignancies induced by Ezh2 (zeige EZH2 Antikörper) insufficiency, and highlighted the differential functions of Ezh1 and Ezh2 (zeige EZH2 Antikörper) in hematopoiesis.
Loss of EZH1 is associated with increased liver injury and a blunted regenerative response.
Data show that histone lysine methyltransferase Ezh1 promotes toll (zeige TLR4 Antikörper)-like receptor (TLR)-triggered inflammatory cytokine production by suppressing the Toll-interacting protein (Tollip (zeige TOLLIP Antikörper)), contributing to full activation of the innate immunity.
presence of Ezh1 helps to maintain PRC2 occupancy on its target genes in myoblasts where Jarid2 (zeige JARID2 Antikörper) is not expressed.
Study shows that the PRC2 core components are enriched in retinal progenitors and downregulated in differentiated cells. Knockdown of the PRC2 core component Ezh2 (zeige EZH2 Antikörper) leads to reduced retinal progenitor proliferation.
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
enhancer of zeste homolog 1 (Drosophila)
, enhancer of zeste homolog 1-like
, histone-lysine N-methyltransferase EZH1-like
, histone-lysine N-methyltransferase EZH1
, enhancer of zeste 1
, enhancer of zeste homolog 1
, Enhancer of zeste homolog 2-A
, Polycomb protein EZH2-A
, histone-lysine N-methyltransferase EZH2