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 Blood, 15 November 2007, Vol. 110, No. 10, pp. 3780-3783.
Prepublished online as a Blood First Edition Paper on August 28, 2007; DOI 10.1182/blood-2007-07-100248.

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RED CELLS

Brief Report

Zebrafish as a model for defining the functional impact of mammalian ferroportin mutations

Ivana De Domenico1, Michael B. Vaughn1, Donghoon Yoon2, James P. Kushner2, Diane M. Ward1, and Jerry Kaplan1

1 Department of Pathology and 2 Division of Hematology and Bone Marrow Transplantation, Department of Medicine, School of Medicine, University of Utah, Salt Lake City

The term hemochromatosis represents a group of inherited disorders leading to iron overload. Mutations in HFE, HJV, and TfR2 cause autosomal-recessive forms of hemochromatosis. Mutations in ferroportin, however, result in dominantly inherited iron overload. Some mutations (H32R and N174I) in ferroportin lead to macrophage iron loading, while others (NI44H) lead to hepatocyte iron loading. Expression of H32R or N174I ferroportin cDNA in zebrafish leads to severe iron-limited erythropoiesis. Expression of wild-type ferroportin or hepcidin-resistant ferroportin (N144H) does not affect erythropoiesis. Zebrafish provides a facile way of identifying which ferroportin mutants may lead to macrophage iron loading.


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I. De Domenico, E. Lo, D. M. Ward, and J. Kaplan
Hepcidin-induced internalization of ferroportin requires binding and cooperative interaction with Jak2
PNAS, March 10, 2009; 106(10): 3800 - 3805.
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