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EED encodes a member of the Polycomb-group (PcG) family. Additionally we are shipping Embryonic Ectoderm Development Antibodies (96) and Embryonic Ectoderm Development Proteins (17) and many more products for this protein.
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we present a patient with a clinical diagnosis of Weaver syndrome and novel de novo sequence variant in EED. Our observation together with previous reports [2, 3, 5] suggests that EED gene testing is warranted in patients with the overgrowth syndrome features and suspicion of Weaver syndrome with normal results for EZH2 (show EZH2 ELISA Kits) gene sequencing.
Data suggest the polycomb repressive complex 2 subunits EZH2 (show EZH2 ELISA Kits), SUZ12, and EED protein axis as promising therapeutic target for treating sarcoma.
we analyzed eight probands with clinically suspected Weaver syndrome by whole-exome sequencing and identified three mutations: a 25.4-kb deletion partially involving EZH2 and CUL1 ,a missense mutation , and a missense mutation in SUZ12 inherited from her father .In vitro functional analyses demonstrated that the identified EED and SUZ12 missense mutations cause decreased decreased trimethylation of lysine 27 of H3
These findings support that Weaver syndrome is a disorder with locus heterogeneity and can be due to pathogenic variants in either EZH2 (show EZH2 ELISA Kits) or EED. This case highlights the utility of exome sequencing as a clinical diagnostic tool for novel gene discovery as well as the importance of re-examination of exome data as new information about gene-disease associations becomes available.
we have found two unrelated families of different ethnicities, with a similar rare phenotype, both associated with de novo mutations in this member of the PRC2 complex, we are confident that EED is indeed a novel overgrowth gene.
Mutations of SUZ12 and EED are reported to have tumor suppressive functions. (Review)
These results suggest that the SNPs of the EED gene might not be associated with susceptibility to CRC (show CALR ELISA Kits).
An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 (show PRC1 ELISA Kits) and 2, is reported.
Data show that overall enhancer of zeste 2 (EZH2), embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12) expression in the colorectal cancer (CRC) tissues was significantly increased than in the non-cancerous tissue.
EED, a component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (show HIST3H3 ELISA Kits) (H3K27), was involved in epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)) of cancer cells induced by Transforming Growth Factor-beta (TGF-beta).
Eed deficiency in chondrocytes causes severe kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic differentiation and cell death with reduced Hif1a (show HIF1A ELISA Kits) expression
The progenitors in Eed mutant mice that were induced to differentiate did not develop into properly formed nephrons. Lhx1 (show LHX1 ELISA Kits), normally expressed in the renal vesicle, was overexpressed in kidneys of Eed mutant mice. Thus, PRC2 has a crucial role in suppressing the expression of genes that maintain the progenitor state, allowing nephron differentiation to proceed.
discovery of differentiation stage-specific and dose-dependent roles of EED in normal hematopoiesis and leukemogenesis
our work provides in vivo evidence that the structural integrity of EED to H3K27me3 propagation is critical, especially for embryonic development and hematopoietic homeostasis, and that its perturbation increases the predisposition to hematologic malignancies
Deletion of Eed but not Ezh2 (show EZH2 ELISA Kits) from embryonic urothelial progenitors caused premature differentiation of Krt5 (show KRT5 ELISA Kits)+ basal cells and ectopic expression of squamous cell markers.
in the skin epithelium, EED, Suz12, and Ezh1 (show EZH1 ELISA Kits)/2 function largely as subunits of the PRC2 complex and have roles in skin development
EED is required for proper erythropoiesis and for formation of hematopoietic progenitor and stem cells, but is dispensable for endothelial lineage commitment and early vascular patterning
Genetic inactivation of Ezh2 (show EZH2 ELISA Kits) or Eed cooperates with NRASQ61K in leukemogenesis.
EED affects the lymphoid versus myeloid decision processes within the lymphomyeloid lineage
Inactivation of Eed impedes MLL-AF9-mediated leukemogenesis through Cdkn2a-dependent and Cdkn2a-independent mechanisms in a murine model.
This gene encodes a member of the Polycomb-group (PcG) family. PcG family members form multimeric protein complexes, which are involved in maintaining the transcriptional repressive state of genes over successive cell generations. This protein interacts with enhancer of zeste 2, the cytoplasmic tail of integrin beta7, immunodeficiency virus type 1 (HIV-1) MA protein, and histone deacetylase proteins. This protein mediates repression of gene activity through histone deacetylation, and may act as a specific regulator of integrin function. Two transcript variants encoding distinct isoforms have been identified for this gene.
polycomb protein eed
, embryonic ectoderm development
, WD protein associating with integrin cytoplasmic tails 1
, polycomb protein EED
, embryonic ectoderm development protein variant 1
, polycomb protein eed-B
, embryonic ectoderm development protein
, lethal, Chr 7, Rinchik 5
, polycomb protein eed-A