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EED encodes a member of the Polycomb-group (PcG) family. Additionally we are shipping Embryonic Ectoderm Development Antibodies (83) and Embryonic Ectoderm Development Kits (25) and many more products for this protein.
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Human EED Protein expressed in Baculovirus infected Insect Cells - ABIN2004205
Montgomery, Yee, Montgomery, Magnuson: Molecular and functional mapping of EED motifs required for PRC2-dependent histone methylation. in Journal of molecular biology 2007
Human EED Protein expressed in Wheat germ - ABIN1352339
Guil, Soler, Portela, Carrère, Fonalleras, Gómez, Villanueva, Esteller: Intronic RNAs mediate EZH2 regulation of epigenetic targets. in Nature structural & molecular biology 2012
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 Proteins) 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 Proteins).
An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 (show PRC1 Proteins) and 2, is reported.
Data show that overall enhancer of zeste 2 (EZH2 (show EZH2 Proteins)), embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12 (show SUZ12 Proteins)) expression in the colorectal cancer (CRC (show CALR Proteins)) tissues was significantly increased than in the non-cancerous tissue.
EED, a component of Polycomb (show CBX2 Proteins) repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (show HIST3H3 Proteins) (H3K27), was involved in epithelial-mesenchymal transition (EMT (show ITK Proteins)) of cancer cells induced by Transforming Growth Factor-beta (TGF-beta).
Polycomb (show CBX2 Proteins) repressive complex 2 is recurrently inactivated through EED or SUZ12 (show SUZ12 Proteins) loss in malignant peripheral nerve sheath tumors.
EZH2 (show EZH2 Proteins)-EED is necessary and sufficient for binding to the lncRNA HOTAIR.
Although inactivating mutations in PRC2-encoding genes EZH2 (show EZH2 Proteins), EED, and SUZ12 (show SUZ12 Proteins) are present in T-cell acute lymphoblastic leukemia and in myeloid malignancies, gain-of-function mutations in EZH2 (show EZH2 Proteins) are frequently observed in B-cell lymphoma.
EED mutants impair polycomb (show CBX2 Proteins) repressive complex 2 and is associated with myelodysplastic syndrome and related neoplasms
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 Proteins) 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 Proteins)-Dio3 (show DIO3 Proteins) region of mouse chromosome 12, miR (show MLXIP Proteins)-323-3p, targets Eed (embryonic ectoderm development) mRNA.
Ectopic gain of EED along with depletion of KDM6B in preimplantation mouse embryos abrogates CDX2 (show CDX2 Proteins) and GATA3 (show GATA3 Proteins) gene expression in the nascent trophoectoderm lineage.
It was shown that Ring1B (show RNF2 Proteins) interacted with multiple complexes in embryonic stem cells. Although H2A.Z (show H2AFZ Proteins) co-localized with Eed, Ring1B (show RNF2 Proteins) and CpG islands in chromatin, H2A.Z (show H2AFZ Proteins) still blanketed polycomb (show CBX2 Proteins) target loci in the absence of Suz12 (show SUZ12 Proteins), Eed, or Ring1B (show RNF2 Proteins).
Data indicate that binding of EZH2 (show EZH2 Proteins), SUZ12 (show SUZ12 Proteins) and EED, the 3 subunits of Plybomb repressive complex 2 (PRC2), is required for PRC2 full activity, and late during viral infection, a significant increase in PRC2 protein association with chromatin.
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