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Blood, 1 March 2006, Vol. 107, No. 5, pp. 1888-1891.
Prepublished online as a Blood First Edition Paper on October 27, 2005; DOI 10.1182/blood-2005-06-2304.
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HEMATOPOIESIS
Brief report
AKT induces erythroid-cell maturation of JAK2-deficient fetal liver progenitor cells and is required for Epo regulation of erythroid-cell differentiation
Saghi Ghaffari,
Claire Kitidis,
Wei Zhao,
Dragan Marinkovic,
Mark D. Fleming,
Biao Luo,
Joseph Marszalek, and
Harvey F. Lodish
From the Department of Gene and Cell Medicine, Brookdale Department of Molecular, Cell, and Developmental Biology, the Department of Medicine, Division of Hematology, Oncology, and the Black Family Stem Cell Institute, Mount Sinai School of Medicine, New York, NY; Whitehead Institute for Biomedical Research, Cambridge, MA; Department of Pathology, Children's Hospital, Harvard Medical School, Boston, MA; and Department of Biology, Massachusetts Institute of Technology, Cambridge.
AKT serine threonine kinase of the protein kinase B (PKB) family plays essential roles in cell survival, growth, metabolism, and differentiation. In the erythroid system, AKT is known to be rapidly phosphorylated and activated in response to erythropoietin (Epo) engagement of Epo receptor (EpoR) and to sustain survival signals in cultured erythroid cells. Here we demonstrate that activated AKT complements EpoR signaling and supports erythroid-cell differentiation in wild-type and JAK2-deficient fetal liver cells. We show that erythroid maturation of AKT-transduced cells is not solely dependent on AKT-induced cell survival or proliferation signals, suggesting that AKT transduces also a differentiation-specific signal downstream of EpoR in erythroid cells. Down-regulation of expression of AKT kinase by RNA interference, or AKT activity by expression of dominant negative forms, inhibits significantly fetal liver–derived erythroid-cell colony formation and gene expression, demonstrating that AKT is required for Epo regulation of erythroid-cell maturation.
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