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Ca(2+) is required for human Fpn transport activity
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SLC40A1 expression is increased in the intestine of patients with type 2 diabetes in association with iron stores and serum hepcidin levels.
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In this study, we identified three domestic sporadic families of hereditary hemochromatosis in China and demonstrated mutations in HFE and SLC40A1 respectively.
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The 1st 3D model of human ferroportin was used to study disease-associated mutations to determine the role of conserved residues in protein stability and iron transport. Molecular mechanisms critical for ferroportin endocytosis include at least 3 fundamental steps: hepcidin binding, structural reorganization of the N- and C-ter ferroportin lobes, and ferroportin ubiquitination.
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SLC40A1 mutation analysis in 7 Italian families with type 4 hereditary hemochromatosis
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Ferroportin protects erythrocytes against oxidative stress and malaria infection.
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Nrf2 suppresses prostate cancer cells viability, migration, and mitosis by upregulating ferroportin expression.
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Of the non-HFE forms of iron overload, TFR2-, HFE2-, and HAMP-related forms are predicted to be rare, with pathogenic allele frequencies in the range of 0.00007 to 0.0005. Significantly, SLC40A1 variants that have been previously associated with autosomal-dominant ferroportin disease were identified in several populations (pathogenic allele frequency 0.0004), being most prevalent among Africans
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Of the 13 iron-overloaded patients showed that 10 were homozygous for the c.44-24G>C polymorphism located in intron 1, whereas the three remaining patients were heterozygous for this sequence variation. Several reports have suggested that this polymorphism could be linked to IO and/or to the severity of haemochromatosis.
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study followed the dynamics of hepcidin-mediated ferroportin internalization; also showed that the novel p.D84E mutation, associated with the classical form of ferroportin disease, is both iron transport defective and hepcidin insensitive
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Reduced expression of ferroportin mRNA identifies a subset of infertile women and may constitute a target for therapy.
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FPN1 cycles as a monomer within the endocytic/plasma membrane compartment and responds to its physiological inhibitor, Hepc, in both control and ferroportin disease (FD) cells. However, in FD, FPN1 fails to reach the cell surface when cells undergo high iron turnover.
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These results suggest that FPN1 exports iron received from the iron chaperone PCBP2. Therefore, it was found that PCBP2 modulates cellular iron export, which is an important physiological process.
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All these findings suggest that in erythroid cells FPN1 could be part of the signaling pathway through which the erythron communicates iron needs to expand the erythroid compartment regardless of systemic iron level.
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Mir-20a controls expression of the iron exporter ferroportin (FPN1) by binding to highly conserved target sites in its 3'-untranslated region. Expression of miR-20a is inversely correlated to FPN1 in lung cancer.
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The concentration of functional membrane-associated ferroportin is controlled by its ligand, the iron-regulatory hormone hepcidin, and fine-tuned by regulatory mechanisms serving iron homeostasis, oxygen utilization, host defense, and erythropoiesis.
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Low hepcidin and high ferroportin expression by erythroblasts and macrophages were seen in iron deficiency anemia, while the opposite was true in anemia of chronic disorders.
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Erythroblasts from Beta-thalassemia patients showed a significantly reduced expression of total MTP1 protein.
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Several family members had hemochromatosis and hyperferritinemia associated with a SLC40A1 deletion in exon 5(485_487delTTG) resulting in the deletion of a valine residue (p.V162del). This is the 1st Spanish family reported with this European mutation.
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TLR4 dependent macrophage signaling is controlled via hepcidin-ferroportin1 axis by influencing TLR4-lipid raft interactions
