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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.

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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.


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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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