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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1198-1207. Prepublished online as a Blood First Edition Paper on April 20, 2006; DOI 10.1182/blood-2006-02-004184. This Article Full Text (PDF) All Versions of this Article: blood-2006-02-004184v1 108/4/1198    most recent Alert me when this article is cited Alert me if a correction is posted 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 Dumitriu, B. Articles by Lefebvre, V. Search for Related Content PubMed PubMed Citation Articles by Dumitriu, B. Articles by Lefebvre, V. Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 16, 2006 Accepted March 25, 2006 Sox6 cell-autonomously stimulates erythroid cell survival, proliferation, and terminal maturation and is thereby an important enhancer of definitive erythropoiesis during mouse development Bogdan Dumitriu, Michael R Patrick, Jane P Petschek, Srujana Cherukuri, Ursula Klingmuller, Paul L Fox, and Veronique Lefebvre* Department of Biomedical Engineering and Orthopaedic Research Center, Cleveland Clinic Department of Cell Biology, Lerner Research Institute, Cleveland Clinic German Cancer Research Center * Corresponding author; email: lefebvv{at}ccf.org. Erythropoiesis, the essential process of hematopoietic stem cell development into erythrocytes, is controlled by lineage-specific transcription factors that determine cell fate and differentiation and by the hormone erythropoietin that stimulates cell survival and proliferation. Here, we identify the Sry-related HMG box transcription factor Sox6 as an important enhancer of definitive erythropoiesis. Sox6 is highly expressed in proerythroblasts and erythroblasts in the fetal liver, neonatal spleen, and bone marrow. Mouse fetuses and pups lacking Sox6 develop erythroid cells slowly and feature misshapen, short-lived erythrocytes. They compensate for anemia by elevating the serum level of erythropoietin and progressively enlarging their erythropoietic tissues. Erythroid-specific inactivation of Sox6 causes the same phenotype, demonstrating cell-autonomous roles for Sox6 in erythroid cells. Sox6 potentiates the ability of erythropoietin signaling to promote proerythroblast survival and has an effect additive to that of erythropoietin in stimulating proerythroblast and erythroblast proliferation. Sox6 also critically facilitates erythroblast and reticulocyte maturation, including hemoglobinization, cell condensation and enucleation, and ensures erythrocyte cytoskeleton long-term stability. It does not control adult globin and erythrocyte cytoskeleton genes, but acts by stabilizing F-actin levels. Sox6 thus enhances erythroid cell development at multiple levels and thereby ensures adequate production and quality of red blood cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Knocking the Sox off EPO signaling Kevin D. Bunting Blood 2006 108: 1119-1120. [Full Text] [PDF] This article has been cited by other articles: V. G. Sankaran, S. H. Orkin,, and C. R. Walkley Rb intrinsically promotes erythropoiesis by coupling cell cycle exit with mitochondrial biogenesis Genes & Dev., February 15, 2008; 22(4): 463 - 475. [Abstract] [Full Text] [PDF]

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