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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].. De plus, nous expédions EZH1 Anticorps (119) et EZH1 Protéines (7) et beaucoup plus de produits pour cette protéine.
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identification of EZH1 as a repressor of haematopoietic multipotency in the early mammalian embryo
pVHL (Montrer VHL Kits ELISA) 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 (Montrer EZH2 Kits ELISA) fail to differentiate into ectoderm lineages.
Expression of the EZH2 (Montrer EZH2 Kits ELISA) homolog EZH1 is reduced in EZH2 (Montrer EZH2 Kits ELISA)-deficient CML (Montrer BCR Kits ELISA) LICs, creating a scenario resembling complete loss of PRC2. EZH2 (Montrer EZH2 Kits ELISA) dependence of CML (Montrer BCR Kits ELISA) LICs raises prospects for improved therapy of TKI-resistant CML (Montrer BCR Kits ELISA) and/or eradication of disease by addition of EZH2 (Montrer EZH2 Kits ELISA) inhibitors
a hot-spot mutation in EZH1 is the second most frequent genetic alteration in autonomous thyroid adenomas; the association between EZH1 and TSHR (Montrer TSHR Kits ELISA) 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 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 (Montrer EZH2 Kits ELISA) and EZH1 are important in the counter-balancing mechanisms controlling proliferation/resting of lymphoid cells. The disruption of the balanced EZH2/EZH1 (Montrer EZH2 Kits ELISA) ratio may play important roles in the pathogenesis of lymphomas
The related enzymatic subunits EZH1 and EZH2 (Montrer EZH2 Kits ELISA) undergo an expression switch during blood cell development.
EZH1 maintains repressive chromatin through different mechanisms.
Suggest that EZH1 and -2 are novel targets of miR (Montrer MLXIP Kits ELISA)-214-3p, and miR (Montrer MLXIP Kits ELISA)-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 (Montrer EED Kits ELISA), 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 (Montrer EZH2 Kits ELISA)-PRC2.
These results clearly demonstrated an essential role of Ezh1 in the pathogenesis of hematopoietic malignancies induced by Ezh2 (Montrer EZH2 Kits ELISA) insufficiency, and highlighted the differential functions of Ezh1 and Ezh2 (Montrer EZH2 Kits ELISA) 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 (Montrer TLR4 Kits ELISA)-like receptor (TLR)-triggered inflammatory cytokine production by suppressing the Toll-interacting protein (Tollip (Montrer TOLLIP Kits ELISA)), contributing to full activation of the innate immunity.
presence of Ezh1 helps to maintain PRC2 occupancy on its target genes in myoblasts where Jarid2 (Montrer JARID2 Kits ELISA) is not expressed.
Deletion of Ezh1 and Ezh2 (Montrer EZH2 Kits ELISA) from skin results in a marked change in fate determination in epidermal progenitor cells, leading to an increase in the number of lineage-committed Merkel cells, specialized subtype of skin cells involved in mechanotransduction.
Study shows that the PRC2 core components are enriched in retinal progenitors and downregulated in differentiated cells. Knockdown of the PRC2 core component Ezh2 (Montrer EZH2 Kits ELISA) 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