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E Protein Silencing by the Leukemogenic AML1-ETO Fusion Protein.
- Source :
-
Science . 8/27/2004, Vol. 305 Issue 5688, p1286-1289. 4p. - Publication Year :
- 2004
-
Abstract
- The AML1-ETO fusion protein, generated by the t(8;21) chromosomal translocation, is causally involved in nearly 15% of acute myeloid leukemia (AMI) cases. This study shows that AML1-ETO, as well as ETO, inhibits transcriptional activation by E proteins through stable interactions that preclude recruitment of p300/CREB-binding protein (CBP) coactivators. These interactions are mediated by a conserved ETO TAF4 homology domain and a 17-amino acid p300/CBP and ETO target motif within AD1 activation domains of E proteins. In t(8;21) leukemic cells, very stable interactions between AML1-ETO and E proteins underlie a t(8;21) translocation-specific silencing of E protein function through an aberrant cofactor exchange mechanism. These studies identify E proteins as AML1-ETO targets whose dysregulation may be important for t(8;21) leukemogenesis, as well as an E protein silencing mechanism that is distinct from that associated with differentiation-inhibitory proteins. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00368075
- Volume :
- 305
- Issue :
- 5688
- Database :
- Academic Search Index
- Journal :
- Science
- Publication Type :
- Academic Journal
- Accession number :
- 14449278
- Full Text :
- https://doi.org/10.1126/science.1097937