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Blood, 1 April 2005, Vol. 105, No. 7, pp. 2741-2748. Prepublished online as a Blood First Edition Paper on December 9, 2004; DOI 10.1182/blood-2004-02-0703. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2004-02-0703v1 105/7/2741    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 Lenox, L. E. Articles by Paulson, R. F. Search for Related Content PubMed PubMed Citation Articles by Lenox, L. E. Articles by Paulson, R. F. Related Collections Hematopoiesis and Stem Cells Red Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS BMP4 and Madh5 regulate the erythroid response to acute anemia Laurie E. Lenox, John M. Perry, and Robert F. Paulson From the Department of Veterinary Science, Graduate Program in Biochemistry, Microbiology and Molecular Biology, and Huck Institute for Life Sciences Cell and Developmental Biology Option, Pennsylvania State University, University Park, PA. Acute anemia initiates a systemic response that results in the rapid mobilization and differentiation of erythroid progenitors in the adult spleen. The flexed-tail (f) mutant mice exhibit normal steady-state erythropoiesis but are unable to rapidly respond to acute erythropoietic stress. Here, we show that f/f mutant mice have a mutation in Madh5. Our analysis shows that BMP4/Madh5-dependent signaling, regulated by hypoxia, initiates the differentiation and expansion of erythroid progenitors in the spleen. These findings suggest a new model where stress erythroid progenitors, resident in the spleen, are poised to respond to changes in the microenvironment induced by acute anemia. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. Gutierrez, S. Tsukamoto, M. Suzuki, H. Yamamoto-Mukai, M. Yamamoto, S. Philipsen, and K. Ohneda Ablation of Gata1 in adult mice results in aplastic crisis, revealing its essential role in steady-state and stress erythropoiesis Blood, April 15, 2008; 111(8): 4375 - 4385. [Abstract] [Full Text] [PDF] M. M. Rhodes, P. Kopsombut, M. C. Bondurant, J. O. Price, and M. J. 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Yamamoto Real-time monitoring of stress erythropoiesis in vivo using Gata1 and beta-globin LCR luciferase transgenic mice Blood, July 15, 2006; 108(2): 726 - 733. [Abstract] [Full Text] [PDF] 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] T. Utsugisawa, J. L. Moody, M. Aspling, E. Nilsson, L. Carlsson, and S. Karlsson A Road Map Toward Defining the Role of Smad Signaling in Hematopoietic Stem Cells Stem Cells, April 1, 2006; 24(4): 1128 - 1136. [Abstract] [Full Text] [PDF] A. Subramanian, H. E. Teal, P. H. Correll, and R. F. Paulson Resistance to Friend Virus-Induced Erythroleukemia in W/Wv Mice Is Caused by a Spleen-Specific Defect Which Results in a Severe Reduction in Target Cells and a Lack of Sf-Stk Expression J. 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