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This Article Full Text Full Text (PDF) 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 Jegalian, A. G. Articles by Wu, H. Search for Related Content PubMed PubMed Citation Articles by Jegalian, A. G. Articles by Wu, H. Related Collections Hematopoiesis and Stem Cells Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 April 2002, Vol. 99, No. 7, pp. 2603-2605 BRIEF REPORT Erythropoietin receptor haploinsufficiency and in vivo interplay with granulocyte-macrophage colony-stimulating factor and interleukin 3 Armin G. Jegalian, Adriana Acurio, Glenn Dranoff, and Hong Wu From the Molecular Biology Institute, Department of Molecular and Medical Pharmacology, and Howard Hughes Medical Institute, University of California Los Angeles School of Medicine; and the Department of Adult Oncology, Dana-Farber Cancer Institute and Department of Medicine, Harvard Medical School, Boston, MA. Erythropoietin (EPO) and its receptor (EPOR) are critical for definitive erythropoiesis, as mice lacking either gene product die during embryogenesis with severe anemia. Here we demonstrate that mice expressing just one functional allele of the EpoR have lower hematocrits and die more frequently than do wild-type littermates on anemia induction. Furthermore, EpoR+/ erythroid colony-forming unit (CFU-E) progenitors are reduced both in frequency and in responsiveness to EPO stimulation. To evaluate the interaction between EPO and granulocyte-macrophage colony-stimulating factor (GM-CSF) or interleukin 3 (IL-3), GM-CSF/ or IL-3/ mice were interbred with EpoR+/ mice. Deletion of either GM-CSF or IL-3 also leads to reduction in CFU-E numbers and hematocrits but does not significantly alter steady-state erythroid burst-forming unit numbers. These results suggest EpoR haploinsufficiency and promotion of in vivo erythropoiesis by GM-CSF and IL-3. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Liu, R. Pop, C. Sadegh, C. Brugnara, V. H. Haase, and M. Socolovsky Suppression of Fas-FasL coexpression by erythropoietin mediates erythroblast expansion during the erythropoietic stress response in vivo Blood, July 1, 2006; 108(1): 123 - 133. [Abstract] [Full Text] [PDF] G. Terszowski, C. Waskow, P. Conradt, D. Lenze, J. Koenigsmann, D. Carstanjen, I. Horak, and H.-R. Rodewald Prospective isolation and global gene expression analysis of the erythrocyte colony-forming unit (CFU-E) Blood, March 1, 2005; 105(5): 1937 - 1945. [Abstract] [Full Text] [PDF] K. Li, C. Miller, S. Hegde, and D. Wojchowski Roles for an Epo Receptor Tyr-343 Stat5 Pathway in Proliferative Co-signaling with Kit J. Biol. Chem., October 17, 2003; 278(42): 40702 - 40709. [Abstract] [Full Text] [PDF] T. J. Blake, B. J. Jenkins, R. J. D'Andrea, and T. J. Gonda Functional cross-talk between cytokine receptors revealed by activating mutations in the extracellular domain of the {beta}-subunit of the GM-CSF receptor J. Leukoc. Biol., December 1, 2002; 72(6): 1246 - 1255. [Abstract] [Full Text] [PDF] J. Renkonen, O. Tynninen, P. Hayry, T. Paavonen, and R. Renkonen Glycosylation Might Provide Endothelial Zip Codes for Organ-Specific Leukocyte Traffic into Inflammatory Sites Am. J. Pathol., August 1, 2002; 161(2): 543 - 550. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020