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Render Timestamp: 2024-07-26T10:02:06.634Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

ETO Antibody #4498

Filter:
  • WB

    Supporting Data

    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).

      For Research Use Only. Not For Use In Diagnostic Procedures.
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