SEARCH:   Advanced

Blood, 1 December 2007, Vol. 110, No. 12, pp. 3871-3880. Prepublished online as a Blood First Edition Paper on August 22, 2007; DOI 10.1182/blood-2007-03-082065. This Article Full Text Full Text (PDF) Supplemental Methods, Tables, and Figures All Versions of this Article: blood-2007-03-082065v1 110/12/3871    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 Frontelo, P. Articles by Bieker, J. J. Search for Related Content PubMed PubMed Citation Articles by Frontelo, P. Articles by Bieker, J. J. Related Collections Gene Expression Hematopoiesis Hemostasis, Thrombosis, and Vascular Biology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Novel role for EKLF in megakaryocyte lineage commitment Pilar Frontelo1, Deepa Manwani1, Mariann Galdass1, Holger Karsunky2, Felix Lohmann1, Patrick G. Gallagher3, and James J. Bieker1 1 Mount Sinai School of Medicine, New York, NY; 2 Stanford University School of Medicine, CA; and 3 Department of Pediatrics, Yale University School of Medicine, New Haven, CT Megakaryocytes and erythroid cells are thought to derive from a common progenitor during hematopoietic differentiation. Although a number of transcriptional regulators are important for this process, they do not explain the bipotential result. We now show by gain- and loss-of-function studies that erythroid Krüppel-like factor (EKLF), a transcription factor whose role in erythroid gene regulation is well established, plays an unexpected directive role in the megakaryocyte lineage. EKLF inhibits the formation of megakaryocytes while at the same time stimulating erythroid differentiation. Quantitative examination of expression during hematopoiesis shows that, unlike genes whose presence is required for establishment of both lineages, EKLF is uniquely down-regulated in megakaryocytes after formation of the megakaryocyte-erythroid progenitor. Expression profiling and molecular analyses support these observations and suggest that megakaryocytic inhibition is achieved, at least in part, by EKLF repression of Fli-1 message levels. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Krüppeling megakaryopoiesis Gerd A. Blobel Blood 2007 110: 3823-3824. [Full Text] [PDF] This article has been cited by other articles: F. Lohmann and J. J. Bieker Activation of Eklf expression during hematopoiesis by Gata2 and Smad5 prior to erythroid commitment Development, June 15, 2008; 135(12): 2071 - 2082. [Abstract] [Full Text] [PDF] P. G. Fuhrken, C. Chen, P. A. Apostolidis, M. Wang, W. M. Miller, and E. T. Papoutsakis Gene Ontology-driven transcriptional analysis of CD34+ cell-initiated megakaryocytic cultures identifies new transcriptional regulators of megakaryopoiesis Physiol Genomics, April 21, 2008; 33(2): 159 - 169. [Abstract] [Full Text] [PDF] M. Siatecka, L. Xue, and J. J. Bieker Sumoylation of EKLF Promotes Transcriptional Repression and Is Involved in Inhibition of Megakaryopoiesis Mol. Cell. Biol., December 15, 2007; 27(24): 8547 - 8560. [Abstract] [Full Text] [PDF]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020