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Publication : SHIP deficiency enhances HSC proliferation and survival but compromises homing and repopulation.

First Author  Desponts C Year  2006
Journal  Blood Volume  107
Issue  11 Pages  4338-45
PubMed ID  16467196 Mgi Jnum  J:132870
Mgi Id  MGI:3777068 Doi  10.1182/blood-2005-12-5021
Citation  Desponts C, et al. (2006) SHIP deficiency enhances HSC proliferation and survival but compromises homing and repopulation. Blood 107(11):4338-45
abstractText  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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