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ETO Antibody #4498

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  • WB

    Product Specifications

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 60
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    ETO Antibody detects endogenous levels of ETO protein.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acid sequence surrounding Ser270 of human ETO. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    ETO belongs to a family of evolutionarily conserved nuclear factors. Although it has no DNA binding domains it is reported to act as a transcriptional corepressor (1). It is best characterized as the fusion partner of AML1 in acute myeloid leukemia with the t(8;21) translocation which gives rise to the AML-ETO fusion protein (2). AML1 is a transcription factor that is involved in the differentiation of all hematopoietic lineages. The fusion protein lacks the activation domain of AML1 and behaves as a dominant negative AML1, repressing AML1 target genes. AML-ETO also causes activation of other genes through a mechanism that involves Bcl-2 and enhanced expression of p21 waf1/cip1 (3,4). The AML-ETO fusion protein is thought to cause the expansion of a hematopoietic stem cell population that has limited lineage commitment and genomic instability (5). Recent evidence derived from chromatin immunoprecipitation (ChIP) experiments has demonstrated that ETO may play a role in the regulation of Notch target genes, and AML-ETO has been shown to disrupt repression of Notch target genes (6). Therefore, both AML and Notch target genes are deregulated by AML-ETO. Epigenetic silencing of the microRNA-223 gene has also been attributed to activities of AML-ETO, contributing to the differentiation block in t(8;21) leukemia (7).

    Alternate Names

    acute myelogenous leukemia 1 translocation 1, cyclin-D related; AML1-MTG8; AML1T1; CBFA2T1; CDR; core-binding factor, runt domain, alpha subunit 2; cyclin D-related; Cyclin-D-related protein; Eight twenty one protein; ETO; MGC2796; MTG8; MTG8b; myeloid translocation gene on 8q22; Protein CBFA2T1; Protein ETO; Protein MTG8; runt related transcription factor 1; runt-related transcription factor 1; RUNX1 partner transcriptional co-repressor 1; RUNX1 translocation partner 1; RUNX1T1; translocated to, 1; translocated to, 1 (cyclin D related); translocated to, 1 (cyclin D-related); Zinc finger MYND domain-containing protein 2; ZMYND2

    For Research Use Only. Not for Use in Diagnostic Procedures.
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