Reference : Inositol trisphosphate 3-kinase B (InsP3KB) as a physiological modulator of myelopoiesis
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Life sciences : Genetics & genetic processes
http://hdl.handle.net/2268/34461
Inositol trisphosphate 3-kinase B (InsP3KB) as a physiological modulator of myelopoiesis
English
Jia, Y. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Loison, F. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Erneux, C. [Université Libre de Bruxelles - ULB > > > >]
Park, S. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Gao, C. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Chai, L. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Silberstein, L. E. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
Schurmans, Stéphane mailto [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire > > >]
Luo, H. R. [Joint Program in Transfusion Medicine, Harvard Medical School, Boston, MA 02115 > > > >]
2008
Proceedings of the National Academy of Sciences of the United States of America
National Academy of Sciences
105
4739-4744
Yes (verified by ORBi)
International
0027-8424
1091-6490
Washington
DC
[en] Hematopoiesis ; Inositol phosphate ; Neutrophils
[en] Inositol trisphosphate 3-kinase B (InsP3KB) belongs to a family of kinases that convert inositol 1,4,5-trisphosphate (Ins(1,4,5)P3 or IP3) to inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4). Previous studies have shown that disruption of InsP3KB leads to impaired T cell and B cell development as well as hyperactivation of neutrophils. Here, we demonstrate that InsP3KB is also a physiological modulator of myelopoiesis. The InsP3KB gene is expressed in all hematopoietic stem/progenitor cell populations. In InsP3KB null mice, the bone marrow granulocyte monocyte progenitor (GMP) population was expanded, and GMP cells proliferated significantly faster. Consequently, neutrophil production in the bone marrow was enhanced, and the peripheral blood neutrophil count was also substantially elevated in these mice. These effects might be due to enhancement of PtdIns(3,4,5)P3/Akt signaling in the InsP3KB null cells. Phosphorylation of cell cycle-inhibitory protein p21(cip1), one of the downstream targets of Akt, was augmented, which can lead to the suppression of the cell cycle-inhibitory effect of p21
Researchers ; Professionals
http://hdl.handle.net/2268/34461

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