Hfe disruption in the mouse leads to experimental hemochromatosis by a mechanism which remains elusive. Evidence for at least five modifier genes has been obtained. These account for the higher iron load of Hfe-deficient D2 mice compared to B6 mice. Gene expression profling was used to clarify the mechanism of Hfe action and to identify potential modifier genes. Keywords: response to genetic modification
Overall design
Liver and duodenum were obtained from wild-type and Hfe-deficient B6 and D2 mice (three mice per strain/genotype combination).
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