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Blood, 1 June 2006, Vol. 107, No. 11, pp. 4338-4345. Prepublished online as a Blood First Edition Paper on February 7, 2006; DOI 10.1182/blood-2005-12-5021. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-12-5021v1 107/11/4338    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 Desponts, C. Articles by Kerr, W. G. Search for Related Content PubMed PubMed Citation Articles by Desponts, C. Articles by Kerr, W. G. Related Collections Hematopoiesis and Stem Cells Cell Adhesion and Motility Signal Transduction Stem Cells in Hematology Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMATOPOIESIS SHIP deficiency enhances HSC proliferation and survival but compromises homing and repopulation Caroline Desponts, Amy L. Hazen, Kim H. T. Paraiso, and William G. Kerr From the Immunology Program, H. Lee Moffitt Comprehensive Cancer Center and Research Institute; and the Departments of Interdisciplinary Oncology and Biochemistry and Molecular Biology, College of Medicine, University of South Florida, Tampa, FL. The SH2 domain–containing inositol 5'-phosphatase-1 (SHIP) has the potential to modulate multiple signaling pathways downstream of receptors that impact hematopoietic stem cell (HSC) biology. Therefore, we postulated that SHIP might play an important role in HSC homeostasis and function. Consistent with this hypothesis, HSC proliferation and numbers are increased in SHIP–/– mice. Despite expansion of the compartment, SHIP–/– HSCs exhibit reduced capacity for long-term repopulation. Interestingly, we observe that SHIP–/– stem/progenitor cells home inefficiently to bone marrow (BM), and consistent with this finding, have reduced surface levels of both CXCR4 and vascular cell adhesion marker-1 (VCAM-1). These studies demonstrate that SHIP is critical for normal HSC function, homeostasis, and homing. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Z. Wang, G. Li, W. Tse, and K. D. Bunting Conditional deletion of STAT5 in adult mouse hematopoietic stem cells causes loss of quiescence and permits efficient nonablative stem cell replacement Blood, May 14, 2009; 113(20): 4856 - 4865. [Abstract] [Full Text] [PDF] S. Kang, S. Elf, S. Dong, T. Hitosugi, K. Lythgoe, A. Guo, H. Ruan, S. Lonial, H. J. Khoury, I. R. Williams, et al. Fibroblast Growth Factor Receptor 3 Associates with and Tyrosine Phosphorylates p90 RSK2, Leading to RSK2 Activation That Mediates Hematopoietic Transformation Mol. Cell. Biol., April 15, 2009; 29(8): 2105 - 2117. [Abstract] [Full Text] [PDF] A. L. Hazen, M. J. Smith, C. Desponts, O. Winter, K. Moser, and W. G. Kerr SHIP is required for a functional hematopoietic stem cell niche Blood, March 26, 2009; 113(13): 2924 - 2933. [Abstract] [Full Text] [PDF] M. M. Collazo, D. Wood, K. H. T. Paraiso, E. Lund, R. W. Engelman, C.-T. Le, D. Stauch, K. Kotsch, and W. G. Kerr SHIP limits immunoregulatory capacity in the T-cell compartment Blood, March 26, 2009; 113(13): 2934 - 2944. [Abstract] [Full Text] [PDF] K. H. T. Paraiso, T. Ghansah, A. Costello, R. W. Engelman, and W. G. Kerr Induced SHIP Deficiency Expands Myeloid Regulatory Cells and Abrogates Graft-versus-Host Disease J. Immunol., March 1, 2007; 178(5): 2893 - 2900. [Abstract] [Full Text] [PDF]

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