Abstract:
: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.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Breda L,Gardenghi S,Guy E,Rachmilewitz EA,Weizer-Stern O,Adamsky K,Amariglio N,Rechavi G,Giardina PJ,Grady RW,Rivella Sdoi
10.1196/annals.1345.069subject
Has Abstractpub_date
2005-01-01 00:00:00pages
417-22eissn
0077-8923issn
1749-6632pii
1054/1/417journal_volume
1054pub_type
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