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Hereditary hemochromatosis due to resistance to hepcidin: high hepcidin concentrations in a family with C326S ferroportin mutation
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The molecular basis of hepcidin-resistant hereditary hemochromatosis
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Suppression of the hepcidin-encoding gene Hamp permits iron overload in mice lacking both hemojuvelin and matriptase-2/TMPRSS6
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Cross-talk between the mitogen activated protein kinase and bone morphogenetic protein/hemojuvelin pathways is required for the induction of hepcidin by holotransferrin in primary mouse hepatocytes
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Plasma hepcidin levels are elevated but responsive to erythropoietin therapy in renal disease
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Genome-wide association study identifies variants in TMPRSS6 associated with hemoglobin levels
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BMP6 is a key endogenous regulator of hepcidin expression and iron metabolism
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Common variants in TMPRSS6 are associated with iron status and erythrocyte volume
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Suppression of hepcidin during anemia requires erythropoietic activity
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Interleukin induces hepcidin expression through STAT3
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Synthetic hepcidin causes rapid dose-dependent hypoferremia and is concentrated in ferroportin-containing organs
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Time-course analysis of hepcidin, serum iron, and plasma cytokine levels in humans injected with LPS
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Expression of hepcidin is down-regulated in TfR2 mutant mice manifesting a phenotype of hereditary hemochromatosis
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