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Blood, 1 February 2004, Vol. 103, No. 3, pp. 886-889. Prepublished online as a Blood First Edition Paper on October 2, 2003; DOI 10.1182/blood-2003-06-2149. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-06-2149v1 103/3/886    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 Lacaud, G. Articles by Keller, G. Search for Related Content PubMed PubMed Citation Articles by Lacaud, G. Articles by Keller, G. Related Collections Oncogenes and Tumor Suppressors Brief Reports Hematopoiesis Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief report Haploinsufficiency of Runx1 results in the acceleration of mesodermal development and hemangioblast specification upon in vitro differentiation of ES cells Georges Lacaud, Valerie Kouskoff, Anne Trumble, Staci Schwantz, and Gordon Keller From the Carl C. Icahn Center for Gene Therapy and Molecular Medicine, Mount Sinai School of Medicine, New York, NY; Cancer Research UK, Paterson Institute for Cancer Research, Christie Hospital, Manchester, United Kingdom; and the Laboratory of Molecular Neuro-Oncology, Rockefeller University, New York, NY. The AML1 gene (recently renamed Runx1), which encodes the DNA-binding subunit of a transcription factor of the core binding factor (CBF) family, is required for the establishment of definitive hematopoiesis. We have previously demonstrated that Runx1 is expressed in yolk sac mesodermal cells prior to the establishment of the blood islands and in the embryoid body (EB)–derived blast-colony–forming cells (BL-CFCs), the in vitro equivalent of the hemangioblast. Analysis of Runx1-deficient embryonic stem (ES) cells demonstrated that this gene is essential for the generation of normal numbers of blast colonies, the progeny of the BL-CFCs. In the present study, we analyzed the potential of Runx1+/– ES cells to determine if heterozygosity at the Runx1 locus impacts early developmental events leading to the commitment of the BL-CFCs. Our results indicate that Runx1 heterozygosity leads to an acceleration of mesodermal commitment and specification to the BL-CFCs and to the hematopoietic lineages in EBs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Wang, P. W. Faloon, Z. Tan, Y. Lv, P. Zhang, Y. Ge, H. 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[Abstract] [Full Text] [PDF] W. Sun and J. R. Downing Haploinsufficiency of AML1 results in a decrease in the number of LTR-HSCs while simultaneously inducing an increase in more mature progenitors Blood, December 1, 2004; 104(12): 3565 - 3572. [Abstract] [Full Text] [PDF] B. K. Hadland, S. S. Huppert, J. Kanungo, Y. Xue, R. Jiang, T. Gridley, R. A. Conlon, A. M. Cheng, R. Kopan, and G. D. Longmore A requirement for Notch1 distinguishes 2 phases of definitive hematopoiesis during development Blood, November 15, 2004; 104(10): 3097 - 3105. [Abstract] [Full Text] [PDF]

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