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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Exploring the Role of Hepcidin, an Antimicrobial and Iron Regulatory Peptide, in Increased Iron Absorption in {beta}-Thalassemia.

To develop new treatments for beta-thalassemia, it is essential to identify the genes involved in the relevant pathophysiological processes. Iron metabolism in thalassemia mice being investigated, focusing on the expression of a gene called hepcidin (Hamp), which is expressed in the liver and whose product (Hamp) is secreted into the bloodstream. In mice, iron overload leads to overexpression of Hamp, while Hamp-knockout mice suffer from hemochromatosis. The aim of this study is to investigate Hamp in the mouse model of beta-thalassemia and to address the potential gene transfer of Hamp to prevent abnormal iron absorption.[1]

References

  1. Exploring the Role of Hepcidin, an Antimicrobial and Iron Regulatory Peptide, in Increased Iron Absorption in {beta}-Thalassemia. Breda, L., Gardenghi, S., Guy, E., Rachmilewitz, E.A., Weizer-Stern, O., Adamsky, K., Amariglio, N., Rechavi, G., Giardina, P.J., Grady, R.W., Rivella, S. Ann. N. Y. Acad. Sci. (2005) [Pubmed]
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