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Blood, 1 January 2008, Vol. 111, No. 1, pp. 160-164. Prepublished online as a Blood First Edition Paper on September 13, 2007; DOI 10.1182/blood-2007-07-099754. This Article Full Text Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2007-07-099754v1 111/1/160    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 Koch, U. Articles by Radtke, F. Search for Related Content PubMed PubMed Citation Articles by Koch, U. Articles by Radtke, F. Related Collections Hematopoiesis and Stem Cells Cell Adhesion and Motility Signal Transduction Gene Expression Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS Brief Report Simultaneous loss of β- and -catenin does not perturb hematopoiesis or lymphopoiesis Ute Koch1, Anne Wilson2, Monica Cobas2, Rolf Kemler3, H. Robson MacDonald2, and Freddy Radtke1 1 Swiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Fédérale de Lausanne (EPFL), Epalinges, Switzerland; 2 Ludwig Institute for Cancer Research, Lausanne Branch, University of Lausanne, Epalinges, Switzerland; and 3 Department of Molecular Embryology, Max-Planck Institute of Immunology, Freiburg, Germany Hematopietic stem cells (HSCs) maintain life-long hematopoiesis in the bone marrow via their ability to self-renew and to differentiate into all blood lineages. Although a central role for the canonical wnt signaling pathway has been suggested in HSC self-renewal as well as in the development of B and T cells, conditional deletion of β-catenin (which is considered to be essential for Wnt signaling) has no effect on hematopoiesis or lymphopoiesis. Here, we address whether this discrepancy can be explained by a redundant and compensatory function of -catenin, a close homolog of β-catenin. Unexpectedly, we find that combined deficiency of β- and -catenin in hematopoietic progenitors does not impair their ability to self-renew and to reconstitute all myeloid, erythroid, and lymphoid lineages, even in competitive mixed chimeras and serial transplantations. These results exclude an essential role for canonical Wnt signaling (as mediated by β- and/or -catenin) during hematopoiesis and lymphopoiesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Xu, A. Sharma, D. L. Wiest, and J. M. Sen Pre-TCR-Induced {beta}-Catenin Facilitates Traversal through {beta}-Selection J. Immunol., January 15, 2009; 182(2): 751 - 758. [Abstract] [Full Text] [PDF] T. C. Luis, F. Weerkamp, B. A. E. Naber, M. R. M. Baert, E. F. E. de Haas, T. Nikolic, S. Heuvelmans, R. R. De Krijger, J. J. M. van Dongen, and F. J. T. Staal Wnt3a deficiency irreversibly impairs hematopoietic stem cell self-renewal and leads to defects in progenitor cell differentiation Blood, January 15, 2009; 113(3): 546 - 554. [Abstract] [Full Text] [PDF]

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