Journal
CANCER CELL
Volume 9, Issue 4, Pages 249-260Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2006.03.012
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Funding
- NCI NIH HHS [CA 23108, R01 CA108056] Funding Source: Medline
- NIAMS NIH HHS [T32 AR07576] Funding Source: Medline
- NIGMS NIH HHS [T32 GM08704] Funding Source: Medline
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AML1/ETO is the chimeric protein resulting from the t(8;21) in acute myeloid leukemia. The Nervy homology 2 (NHR2) domain in ETO mediates oligornerization and AML1/ETO's interactions with ETO, MTGR1, and MTG16, and with the corepressor molecules mSin3A and HDAC1 and HDAC3. We solved the NHR2 domain structure and found it to be an alpha-helical tetramer. We show that oligomerization contributes to AML1/ETO's inhibition of granulocyte differentiation, is essential for its ability to enhance the clonogenic potential of primary mouse bone marrow cells, and affects AML1/ETO's activity on several endogenous genes. Oligomerization is also required for AML1/ETO's interactions with ETO, MTGR1, and MTG16, but not with other corepressor molecules.
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