How does hepcidin hinder ferroportin activity?
نویسندگان
چکیده
منابع مشابه
Hepcidin targets ferroportin for degradation in hepatocytes.
Hepcidin, a circulating regulatory hormone peptide produced by hepatocytes, functions as the master regulator of cellular iron export by controlling the amount of ferroportin, an iron exporter present on the basolateral surface of intestinal enterocytes and macrophages. Hepcidin binding to ferroportin induces its internalization and degradation, resulting in cellular iron retention and decrease...
متن کاملPharmacological Targeting of the Hepcidin/Ferroportin Axis
The iron regulatory hormone hepcidin limits iron fluxes to the bloodstream by promoting degradation of the iron exporter ferroportin in target cells. Hepcidin insufficiency causes hyperabsorption of dietary iron, hyperferremia and tissue iron overload, which are hallmarks of hereditary hemochromatosis. Similar responses are also observed in iron-loading anemias due to ineffective erythropoiesis...
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متن کاملHuman mutation D157G in ferroportin leads to hepcidin-independent binding of Jak2 and ferroportin down-regulation.
Mutations in the iron exporter ferroportin (Fpn) result in iron overload in macrophages or hepatocytes depending upon the mutation. Patients with Fpn mutation D157G show high serum ferritin and normal to slightly elevated transferrin saturation. Here, we show that Fpn(D157G)-green fluorescent protein (GFP) is down-regulated independent of hepcidin, and that this down-regulation is due to the co...
متن کاملHepcidin regulates ferroportin expression and intracellular iron homeostasis of erythroblasts.
The iron-regulatory hormone, hepcidin, regulates systemic iron homeostasis by interacting with the iron export protein ferroportin (FPN1) to adjust iron absorption in enterocytes, iron recycling through reticuloendothelial macrophages, and iron release from storage in hepatocytes. We previously demonstrated that FPN1 was highly expressed in erythroblasts, a cell type that consumes most of the s...
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ژورنال
عنوان ژورنال: Blood
سال: 2018
ISSN: 0006-4971,1528-0020
DOI: 10.1182/blood-2018-01-824151