Cell Signaling Technology

Product Pathways - Lymphocyte Signaling

ETO Antibody #4498

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk Endogenous 60 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

ETO Antibody detects endogenous levels of ETO protein.

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.

Western Blotting

Western Blotting

Western blotting analysis of extracts of MOLT4 and K562 cells using ETO Antibody.

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).

  1. Davis, J.N. et al. (2003) Gene 303, 1-10.
  2. Downing, J.R. et al. (1993) Blood 81, 2860-5.
  3. Klampfer, L. et al. (1996) Proc Natl Acad Sci USA 93, 14059-64.
  4. Peterson, L.F. et al. (2007) Blood 109, 4392-8.
  5. Elagib, K.E. and Goldfarb, A.N. (2007) Cancer Lett 251, 179-86.
  6. Salat, D. et al. (2008) Mol Cell Biol 28, 3502-12.
  7. Nervi, C. et al. Epigenetics 3, 1-4.

Application References

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Companion Products

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

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