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A more recent version of this article appeared on September 30, 2005
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M505208200v1
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Papers In Press, published online ahead of print July 14, 2005
J. Biol. Chem, 10.1074/jbc.M505208200
Submitted on May 11, 2005
Accepted on July 14, 2005

Calmodulin-dependent protein kinase IV regulates hematopoietic stem cell maintenance

Christine M. Kitsos, Uma Sankar, Maddalena Illario, Josep M. Colomer-Font, Andrew W. Duncan, Thomas J. Ribar, Tannishtha Reya, and Anthony R. Means

Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27707

Corresponding Author: means001{at}mc.duke.edu

The hematopoietic stem cell (HSC) gives rise to all mature, terminally differentiated cells of the blood. Here we show that calmodulin-dependent protein kinase IV (CaMKIV) is present in c-Kit+ Sca1+ Lin-/low hematopoietic progenitor cells (KLS cells) and that its absence results in hematopoietic failure, characterized by a diminished KLS cell population and by an inability of these cells to reconstitute blood cells upon serial transplantation. KLS cell failure in the absence of CaMKIV is correlated with increased apoptosis and proliferation of these cells in vivo and in vitro. In turn, these cell biological defects are correlated with decreases in CREB-serine133 phosphorylation as well as in CBP and Bcl-2 levels. Re-expression of CaMKIV in Camk4-/- KLS cells results in the rescue of the proliferation defects in vitro as well as in the restoration of CBP and Bcl-2 to wild type levels. These studies show that CaMKIV is a regulator of HSC homeostasis and suggest that its effects may be in part mediated via CBP and Bcl-2.


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