Recombinant Human EED protein(Met1-Arg441), His&GST-tagged

• Cat.No.: EED-6921H
• Product Overview: Recombinant Human EED (O75530-1) (Met 1-Arg 441) was expressed in Insect Cells, fused with the N-terminal polyhistidine-tagged GST tag at the N-terminus.

Specification

• Species: Human
• Source: Insect Cells
• Tag: GST&His
• Protein Length: 1-441 a.a.
• Form: Lyophilized from sterile 20mM Tris, 500mM NaCl, pH 8.0, 2mM GSH, 10% gly Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization.
• Molecular Mass: The recombinant human EED/GST chimera consists of 678 amino acids and has a calculated molecular mass of 78 kDa. It migrates as an approximately 75-85 kDa band in SDS-PAGE under reducing conditions.
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Purity: > 93 % as determined by SDS-PAGE
• Storage: Samples are stable for up to twelve months from date of receipt at -20°C to -80°C. Store it under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: It is recommended that sterile water be added to the vial to prepare a stock solution of 0.2 ug/ul. Centrifuge the vial at 4°C before opening to recover the entire contents.
• Publications:
  Polycomb repressive complex 2 binds and stabilizes NANOG to suppress differentiationrelated genes to promote self-renewal (2023)

Gene Information

• Gene Name: EED embryonic ectoderm development [ Homo sapiens ]
• Official Symbol: EED
• Synonyms: EED; embryonic ectoderm development; polycomb protein EED; HEED; WAIT 1; WD protein associating with integrin cytoplasmic tails 1; WAIT1
• Gene ID: 8726
• mRNA Refseq: NM_003797
• Protein Refseq: NP_003788
• MIM: 605984
• UniProt ID: O75530

Case Study

Case 1: Zhang F, et al. Aging (Albany NY). 2021

Study reveals EED-driven epigenetic regulation via miR-338-5p/METTL3/CDCP1 axis promotes gastric cancer progression, highlighting EED as a novel therapeutic target for GC treatment. EED suppresses miR-338-5p via histone methylation, enhancing METTL3-mediated m6A modification of CDCP1 to drive tumor metastasis, offering insights into epigenetic therapies and miRNA-targeted strategies for cancer recurrence prevention.

Fig1. Evaluation of EED knockdown efficiency in MGC-803, and HGC-27 cells.

Fig2. RT-qPCR to examine EED and miR-338-5p expression after overexpressing EED and DZNep treatment, with β-actin and U6 as internal control, respectively.

Case 2: Dong H, et al. Cancer Res. 2019

BR-001, an allosteric PRC2 inhibitor targeting EED’s H3K27me3-binding pocket, suppresses tumor growth in colon cancer models by modulating the immune microenvironment. It enhances CD8+ T-cell infiltration via CXCL10 upregulation, demonstrating synergy potential with immune-oncology therapies. This EED-targeted epigenetic therapy highlights novel strategies for PRC2-driven cancers and tumor microenvironment reprogramming.

Fig1. Biochemical activity of BR-001 inhibition of EED–H3K27me3 interaction

Fig2. DSF analysis for EED in the absence of compound (DMSO control), in the presence of BR-001 with 50 or 100 μmol/L.

Application

1. Therapeutic Potential of Recombinant EED Protein in Epigenetic Regulation Recombinant embryonic ectoderm development (EED) protein, a core component of the polycomb repressive complex 2 (PRC2), offers novel avenues for targeting epigenetic dysregulation in cancers. By mimicking or modulating PRC2 activity, recombinant EED could restore balanced histone methylation (H3K27me3), counteracting aberrant gene silencing that drives tumor progression. Its application in drug discovery platforms enables high-throughput screening for EED-targeted inhibitors, such as allosteric compounds like BR-001, accelerating the development of precision therapies for PRC2-driven malignancies. 2. Mechanistic Insights and Preclinical Applications In vitro and in vivo studies demonstrate recombinant EED’s utility in dissecting PRC2-mediated epigenetic mechanisms. For example, it aids in mapping EED-inhibitor interactions, optimizing compounds that disrupt H3K27me3-binding pockets to block PRC2 activity. Additionally, recombinant EED facilitates research into tumor microenvironment modulation, revealing links between PRC2 inhibition, CXCL10 upregulation, and enhanced CD8+ T-cell infiltration—key factors for improving immune-oncology combination therapies. 3. Challenges and Innovations in Delivery Despite its promise, recombinant EED faces hurdles like protein stability and targeted delivery to tumor sites. Advances in fusion proteins, nanoparticle carriers, or gene-editing systems (e.g., CRISPR) may enhance its bioavailability and specificity. Integrating recombinant EED with biomarkers for H3K27me3 levels could also personalize epigenetic therapies, maximizing efficacy in cancers reliant on PRC2 hyperactivity, such as colon or gastric malignancies.

Fig1. The mechanism graph of the regulatory network and function of EED-mediated miR-338-5p methylation. (Fangbin Zhang, 2021)

Fig2. Known Non-Canonical Roles of EZH2. (Justin Korfhage, 2019)