Article
The acute myeloid leukemia fusion protein AML1-ETO targets E proteins via a paired amphipathic helix-like TBP-associated factor homology domain.
Proceedings of the National Academy of Sciences of the United States of America - 5 Jul 2006
Plevin Michael J, Zhang Jinsong, Guo Chun, Roeder Robert G, Ikura Mitsuhiko
Abstract excerpt
Up to 15% of acute myeloid leukemias (AMLs) are characterized by the abnormal expression of the eight-twenty-one (ETO) transcriptional corepressor within an AML1-ETO fusion protein. The t(8;21) chromosomal translocation serves not only to disrupt WT AML1 function but also to introduce ETO activity during hematopoiesis. AML1-ETO was recently shown to inhibit E protein transactivation by physically displacing WT...
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