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EED encodes a member of the Polycomb-group (PcG) family. Additionally we are shipping Embryonic Ectoderm Development Antibodies (86) and Embryonic Ectoderm Development Proteins (15) and many more products for this protein.
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These findings support that Weaver (show KCNJ6 ELISA Kits) 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 (show SUZ12 ELISA Kits) 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 (show EZH2 ELISA Kits)), embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12 (show SUZ12 ELISA Kits)) expression in the colorectal cancer (CRC (show CALR ELISA Kits)) tissues was significantly increased than in the non-cancerous tissue.
EED, a component of Polycomb (show CBX2 ELISA Kits) 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).
Polycomb (show CBX2 ELISA Kits) repressive complex 2 is recurrently inactivated through EED or SUZ12 (show SUZ12 ELISA Kits) loss in malignant peripheral nerve sheath tumors.
EZH2 (show EZH2 ELISA Kits)-EED is necessary and sufficient for binding to the lncRNA HOTAIR.
Although inactivating mutations in PRC2-encoding genes EZH2 (show EZH2 ELISA Kits), EED, and SUZ12 (show SUZ12 ELISA Kits) are present in T-cell acute lymphoblastic leukemia and in myeloid malignancies, gain-of-function mutations in EZH2 (show EZH2 ELISA Kits) are frequently observed in B-cell lymphoma.
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 (show SUZ12 ELISA Kits), 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.
Data suggest that Eed (embryonic ectoderm development) is necessary to silence the pluripotency network during differentiation.
a microRNA encoded by the imprinted Dlk1 (show DLK1 ELISA Kits)-Dio3 (show DIO3 ELISA Kits) region of mouse chromosome 12, miR (show MLXIP ELISA Kits)-323-3p, targets Eed (embryonic ectoderm development) mRNA.
Ectopic gain of EED along with depletion of KDM6B (show Kdm6b ELISA Kits) in preimplantation mouse embryos abrogates CDX2 (show CDX2 ELISA Kits) and GATA3 (show GATA3 ELISA Kits) gene expression in the nascent trophoectoderm lineage.
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