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Prepublished online as a Blood First Edition Paper on April 3, 2003; DOI 10.1182/blood-2002-06-1848. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-06-1848v1 102/3/858    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 van Loo, P. F. Articles by Hendriks, R. W. Search for Related Content PubMed PubMed Citation Articles by van Loo, P. F. Articles by Hendriks, R. W. Related Collections Hematopoiesis and Stem Cells Immunobiology Red Cells Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 August 2003, Vol. 102, No. 3, pp. 858-866 HEMATOPOIESIS Impaired hematopoiesis in mice lacking the transcription factor Sp3 Pieter Fokko van Loo, Peter Bouwman, Kam-Wing Ling, Sabine Middendorp, Guntram Suske, Frank Grosveld, Elaine Dzierzak, Sjaak Philipsen, and Rudolf W. Hendriks From the Department of Cell Biology and the Department of Immunology, Erasmus MC, Rotterdam, The Netherlands; and the Institut für Molekularbiologie und Tumorforschung Philipps-Universität Marburg, Germany As the zinc-finger transcription factor specificity protein 3 (Sp3) has been implicated in the regulation of many hematopoietic-specific genes, we analyzed the role of Sp3 in hematopoiesis. At embryonic day 18.5 (E18.5), Sp3-/- mice exhibit a partial arrest of T-cell development in the thymus and B-cell numbers are reduced in liver and spleen. However, pre–B-cell proliferation and differentiation into immunoglobulin M–positive (IgM+) B cells in vitro are not affected. At E14.5 and E16.5, Sp3-/- mice exhibit a significant delay in the appearance of definitive erythrocytes in the blood, paralleled by a defect in the progression of differentiation of definitive erythroid cells in vitro. Perinatal death of the null mutants precludes the analysis of adult hematopoiesis in Sp3-/- mice. We therefore investigated the ability of E12.5 Sp3-/- liver cells to contribute to the hematopoietic compartment in an in vivo transplantation assay. Sp3-/- cells were able to repopulate the B- and T-lymphoid compartment, albeit with reduced efficiency. In contrast, Sp3-/- cells showed no significant engraftment in the erythroid and myeloid lineages. Thus, the absence of Sp3 results in cell-autonomous hematopoietic defects, affecting in particular the erythroid and myeloid cell lineages. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. F. van Loo, E. A. F. Mahtab, L. J. Wisse, J. Hou, F. Grosveld, G. Suske, S. Philipsen, and A. C. Gittenberger-de Groot Transcription Factor Sp3 Knockout Mice Display Serious Cardiac Malformations Mol. Cell. Biol., December 15, 2007; 27(24): 8571 - 8582. [Abstract] [Full Text] [PDF] A. P. W. Funnell, C. A. Maloney, L. J. Thompson, J. Keys, M. Tallack, A. C. Perkins, and M. Crossley Erythroid Kruppel-Like Factor Directly Activates the Basic Kruppel-Like Factor Gene in Erythroid Cells Mol. Cell. Biol., April 1, 2007; 27(7): 2777 - 2790. [Abstract] [Full Text] [PDF] N. J. Dempsey, L. S. Ojalvo, D. W. Wu, and J. A. Little Induction of an embryonic globin gene promoter by short-chain fatty acids Blood, December 1, 2003; 102(12): 4214 - 4222. [Abstract] [Full Text] [PDF]

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