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Merck
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Key Documents

09-774

Sigma-Aldrich

Anti-EED Antibody

from rabbit

Sinónimos:

embryonic ectoderm development

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human, mouse

species reactivity (predicted by homology)

dog, chicken, bovine, opossum, rat

technique(s)

western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

dog ... Eed(476779)
human ... EED(8726)
mouse ... Eed(13626)
rat ... Eed(293104)

General description

Polycomb group proteins are important for maintaining transcriptional silencing. One conserved PcG complex, PRC2, is composed of several proteins including the histone methyltransferase EZH2, the WD-repeat protein EED (Embryonic ectoderm development), and the Zn-finger protein Suz12. Transcriptional repression mediated by EED involves histone deacetylation, while the EZH2 methylates histone H3 on lysine 27. EED protein is present in four isoforms. These EED isoforms selectively associate with distinct EZH2-containing complexes, resulting in differential targeting of their associated methyltransferase activity. These complexes play a role in Hox gene silencing, X-inactivation, germline development, stem cell pluripotency and cancer metastasis.

Specificity

This antibody recognizes EED, Mr ~ 62-70 kDa.

Immunogen

A synthetic peptide corresponding to a.a. 429-441 of human EED, conjugated to KLH.
Epitope: a.a. 429-441

Application

Use Anti-EED Antibody (Rabbit Polyclonal Antibody) validated in WB to detect EED also known as embryonic ectoderm development.

Quality

Western Blot Analysis: 1 μg/mL of this lot detected EED on 10 μg of Jurkat cell lysate.

Target description

~53 kDa observed. Uniprot describes three isoforms at 51 kDa (isoform 1), 53 kDa (isoform 2), and 46 kDa (isoform 3).

Linkage

Replaces: 09-727

Physical form

Format: Purified

Analysis Note

Control
Jurkat Cell Lysate

3T3/A31 cell lysate

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Falak Sher et al.
Cellular reprogramming, 13(1), 1-6 (2010-10-29)
Recently, we have demonstrated the expression of the polycomb group protein Ezh2 in embryonic and adult neural stem cells. Although Ezh2 remained highly expressed when neural stem cells differentiate into oligodendrocyte precursor cells, it is downregulated during the differentiation into
Taichi Takashina et al.
Cancer science, 107(7), 955-962 (2016-04-27)
Recent discoveries have revealed that human cancer involves aberrant epigenetic alterations. We and others have previously shown that the histone methyltransferase EZH2, the catalytic subunit of polycomb repressive complex 2 (PRC2), is frequently overexpressed in non-small-cell lung cancer (NSCLC) and
Bin Shi et al.
Cancer medicine, 8(14), 6383-6392 (2019-08-29)
The aims of this study were to investigate the link between enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies and in human lung cancer tissue microarrays. Enhancer of zeste homolog 2 and HDAC1 mRNA expression
Sylvia Mahara et al.
Proceedings of the National Academy of Sciences of the United States of America, 113(26), E3735-E3744 (2016-06-16)
Despite the established oncogenic function of Polycomb repressive complex 2 (PRC2) in human cancers, its role as a tumor suppressor is also evident; however, the mechanism underlying the regulation of the paradoxical functions of PRC2 in tumorigenesis is poorly understood.
Stefanie Göllner et al.
Nature medicine, 23(1), 69-78 (2016-12-13)
In acute myeloid leukemia (AML), therapy resistance frequently occurs, leading to high mortality among patients. However, the mechanisms that render leukemic cells drug resistant remain largely undefined. Here, we identified loss of the histone methyltransferase EZH2 and subsequent reduction of

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