Lymphocyte Signaling

プロトコール

抗体比較

ポジティブコントロール

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.

本製品は試験研究用です。

ETO Antibody

©1999-2012 Cell Signaling Technology, Inc.

問合せ

ETO AntibodyのCSTジャパン