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 Blood, 26 March 2009, Vol. 113, No. 13, pp. 2924-2933.
Prepublished online as a Blood First Edition Paper on December 12, 2008; DOI 10.1182/blood-2008-02-138008.

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Submitted February 6, 2008
Accepted November 15, 2008

SHIP is required for a functional hematopoietic stem cell niche

Amy L Hazen, Michelle J Smith, Caroline Desponts, Oliver Winter, Katrin Moser, and William G Kerr*

Immunology Program, H. Lee Moffitt Comprehensive Cancer Center and Research Institute, Tampa, FL, United States
Humoral Immunology, German Rheumatism Research Center, Berlin, Germany

* Corresponding author; email: william.kerr{at}moffitt.org.

SH2-domain-containing Inositol 5'-Phosphatase-1 (SHIP) deficiency significantly increases the number of hematopoietic stem cells (HSC) present in the bone marrow (BM). However, the reconstitution capacity of these HSC is severely impaired suggesting that SHIP expression might be an intrinsic requirement for HSC function. To further examine this question, we developed a model in which SHIP expression is ablated in HSC while they are resident in a SHIP-competent milieu. In this setting we find that long-term repopulation by SHIP-deficient HSC is not compromised. Moreover, SHIP-deficient HSC from this model repopulate at levels comparable to wild type (WT) HSC upon serial transfer. However, when HSC from mice with systemic ablation of SHIP are transplanted they are functionally compromised for repopulation. These findings demonstrate SHIP is not an intrinsic requirement for HSC function, but rather that SHIP is required for the BM milieu to support functionally competent HSC. Consistent with these findings, cells that comprise the BM niche express SHIP and SHIP-deficiency profoundly alters their function.


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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.
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