Embryonic Ectoderm Development (EED) ELISA Kits

Human Embryonic Ectoderm Development (EED) interaction partners

1. 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 gene sequencing.

2. Data suggest the polycomb repressive complex 2 subunits EZH2, SUZ12, and EED protein axis as promising therapeutic target for treating sarcoma.

3. 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

4. These findings support that Weaver syndrome is a disorder with locus heterogeneity and can be due to pathogenic variants in either EZH2 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.

5. 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.

6. Mutations of SUZ12 and EED are reported to have tumor suppressive functions. (Review)

7. These results suggest that the SNPs of the EED gene might not be associated with susceptibility to CRC.

8. An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2, is reported.

9. 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.

10. EED, a component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in epithelial-mesenchymal transition (EMT) of cancer cells induced by Transforming Growth Factor-beta (TGF-beta).

11. Polycomb repressive complex 2 is recurrently inactivated through EED or SUZ12 loss in malignant peripheral nerve sheath tumors.

12. EZH2-EED is necessary and sufficient for binding to the lncRNA HOTAIR.

13. Although inactivating mutations in PRC2-encoding genes EZH2, EED, and SUZ12 are present in T-cell acute lymphoblastic leukemia and in myeloid malignancies, gain-of-function mutations in EZH2 are frequently observed in B-cell lymphoma.

14. EED mutants impair polycomb repressive complex 2 and is associated with myelodysplastic syndrome and related neoplasms

15. Promoter polymorphism of the EED gene is associated with the susceptibility to ulcerative colitis.

16. Genetic defects in PRC2 components other than EZH2 are not common in myeloid malignancies.

17. The authors found that Sox2 and Eed positively regulate each other's expression and contribute to the maintenance of self-renewal in embryonic stem cells by controlling histone methylation and acetylation.

18. molecular basis of EED-methyllysine recognition, and the biochemical characterization of how the activity of a histone methyltransferase is oppositely regulated by two histone marks.

19. histone modification including PRC2-mediated repressive histone marker H3K27me3 and active histone marker acH4 may involve in CD11b transcription during HL-60 leukemia cells reprogramming to terminal differentiation[polycomb repressive complex 2 ]

20. EED is a nuclear factor and repressor of transcription and is recruited to the plasma membrane by HIV-1 nef

Mouse (Murine) Embryonic Ectoderm Development (EED) interaction partners

1. Eed, an essential component of the Polycomb group complex 2 (PRC2), is required for establishing H3K27me3 imprinting

2. The mouse nerves with EED-deficient Schwann cells display slow axonal regeneration with significantly low expression of axon guidance genes.

3. Using a genetic approach that deleted Eed specifically in the growing oocyte, results showed that oocytes lacked H3K27me3 and produced offspring with significant overgrowth that involved increased adiposity (percentage fat) and increased bone mineral density. These data demonstrate that EED is required in the oocyte for programming developmental outcomes that affect life-long outcomes in offspring.

4. Eed, an essential subunit of PRC2, is crucial to maintain the identity of CD4(+) T cells under TGFbeta-induced regulatory T cell (Treg)-polarizing conditions.

5. Eed deficiency in chondrocytes causes severe kyphosis and a growth defect with decreased chondrocyte proliferation, accelerated hypertrophic differentiation and cell death with reduced Hif1a expression

6. The progenitors in Eed mutant mice that were induced to differentiate did not develop into properly formed nephrons. Lhx1, 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.

7. discovery of differentiation stage-specific and dose-dependent roles of EED in normal hematopoiesis and leukemogenesis

8. 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

9. Deletion of Eed but not Ezh2 from embryonic urothelial progenitors caused premature differentiation of Krt5+ basal cells and ectopic expression of squamous cell markers.

10. in the skin epithelium, EED, Suz12, and Ezh1/2 function largely as subunits of the PRC2 complex and have roles in skin development

11. 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

12. Genetic inactivation of Ezh2 or Eed cooperates with NRASQ61K in leukemogenesis.

13. EED affects the lymphoid versus myeloid decision processes within the lymphomyeloid lineage

14. Inactivation of Eed impedes MLL-AF9-mediated leukemogenesis through Cdkn2a-dependent and Cdkn2a-independent mechanisms in a murine model.

15. Data suggest that Eed (embryonic ectoderm development) is necessary to silence the pluripotency network during differentiation.

16. An integral role for EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2, is reported.

17. a microRNA encoded by the imprinted Dlk1-Dio3 region of mouse chromosome 12, miR-323-3p, targets Eed (embryonic ectoderm development) mRNA.

18. Ectopic gain of EED along with depletion of KDM6B in preimplantation mouse embryos abrogates CDX2 and GATA3 gene expression in the nascent trophoectoderm lineage.

19. It was shown that Ring1B interacted with multiple complexes in embryonic stem cells. Although H2A.Z co-localized with Eed, Ring1B and CpG islands in chromatin, H2A.Z still blanketed polycomb target loci in the absence of Suz12, Eed, or Ring1B.

20. Data indicate that binding of EZH2, SUZ12 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.