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The gene encoding the iron regulatory peptide hepcidin is regulated by anemia, hypoxia, and inflammation.
Modifications of hepcidin gene expression suggest a key role for hepciridin in iron homeostasis under various pathophysiological conditions, which may support the pharmaceutical use of hePCidin agonists and antagonists in various ironHomeostasis disorders.
Lack of hepcidin gene expression and severe tissue iron overload in upstream stimulatory factor 2 (USF2) knockout mice
A peculiar phenotype of Usf2−/− mice that progressively develop multivisceral iron overload is reported; plasma iron overcomes transferrin binding capacity, and nontransferrin-bound iron accumulates in various tissues including pancreas and heart.
Ferritin heavy chain upregulation by NF-kappaB inhibits TNFalpha-induced apoptosis by suppressing reactive oxygen species.
Modulation of FHC or, more broadly, of iron metabolism as a potential approach for anti-inflammatory therapy is suggested and a basis for the NF-kappaB-mediated control of ROS induction is established.
Function and regulation of transferrin and ferritin.
Iron represents a paradox for living systems by being essential for a wide variety of metabolic processes but also having the potential to cause deleterious effects, and a feedback control mechanism prevents the expansion of a catalytically active intracellular iron pool, while maintaining sufficient concentrations of the metal for metabolic needs.
Severe iron deficiency anemia in transgenic mice expressing liver hepcidin
The results strongly support the proposed role of hepcidin as a putative iron-regulatory hormone and the animal models devoid of or overexpressing the peptide represent valuable tools for investigating iron homeostasis in vivo and for deciphering the molecular mechanisms of hePCidin action.
Hepcidin, a new iron regulatory peptide.
The advances toward the understanding of function and regulation of hepcidin in iron metabolism are summarized and new data is provided on theregulation of hePCidin gene expression by erythropoietin, the major regulator of mammalian eryanthropoiesis.
Iron metabolism, free radicals, and oxidative injury.
Mutation in the iron responsive element of the L ferritin mRNA in a family with dominant hyperferritinaemia and cataract
The identification of a single point mutation in the IRE of the L-ferritin mRNA in members from a family affected with dominantly inherited hyperferritinaemia and cataract is reported, the first mutation affecting the IRP–IRE interaction and the iron-mediated regulation of ferritin synthesis.