SEARCH:   Advanced

Blood, 22 January 2009, Vol. 113, No. 4, pp. 883-886. Prepublished online as a Blood First Edition Paper on November 25, 2008; DOI 10.1182/blood-2008-04-153742. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-04-153742v1 113/4/883    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yan, M. Articles by Zhang, D.-E. Search for Related Content PubMed PubMed Citation Articles by Yan, M. Articles by Zhang, D.-E. Related Collections Myeloid Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  MYELOID NEOPLASIA Brief Report RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis Ming Yan1, Eun-Young Ahn1, Scott W. Hiebert2, and Dong-Er Zhang13 1 Moores Cancer Center, University of California San Diego, La Jolla; 2 Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN; and 3 Department of Pathology and Division of Biological Sciences, University of California San Diego, La Jolla The 8;21 translocation, which involves the gene encoding the RUNX family DNA-binding transcription factor AML1 (RUNX1) on chromosome 21 and the ETO (MTG8) gene on chromosome 8, generates AML1-ETO fusion proteins. Previous analyses have demonstrated that full-length AML1-ETO blocks AML1 function and requires additional mutagenic events to promote leukemia. More recently, we have identified an alternatively spliced form of AML1-ETO, AML1-ETO9a, from t(8;21) acute myeloid leukemia (AML) patient samples. AML1-ETO9a lacks the C-terminal NHR3 and NHR4 domains of AML1-ETO and is highly leukemogenic in the mouse model. Here, we report that the AML1 DNA-binding domain and the ETO NHR2-dimerization domain, but not the ETO NHR1 domain, are critical for the induction of AML by AML1-ETO9a. A region between NHR1 and NHR2 affects latency of leukemogenesis. These results provide valuable insight into further analysis of the molecular mechanism of t(8;21) in leukemogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Park, W. Chen, T. Cierpicki, M. Tonelli, X. Cai, N. A. Speck, and J. H. Bushweller Structure of the AML1-ETO eTAFH domain-HEB peptide complex and its contribution to AML1-ETO activity Blood, April 9, 2009; 113(15): 3558 - 3567. [Abstract] [Full Text] [PDF] L. Roudaia, M. D. Cheney, E. Manuylova, W. Chen, M. Morrow, S. Park, C.-T. Lee, P. Kaur, O. Williams, J. H. Bushweller, et al. CBF{beta} is critical for AML1-ETO and TEL-AML1 activity Blood, March 26, 2009; 113(13): 3070 - 3079. [Abstract] [Full Text] [PDF]

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020