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Functional impact of mammalian ferroportin mutations studied in zebrafish.
role of ABCG37, IRT1 and FRO2 in root Fe2+ transport systems
role of IRT1 (zeige PARP3 Proteine) in iron uptake
these results suggest that the His-loop of MTP1 acts as a sensor of cytosolic zinc to maintain an essential level in the cytosol and that the dysfunction of the loop results in an uncontrolled accumulation of zinc in the vacuoles of root cells.
Our results reveal a role of SNX1 (zeige SNX1 Proteine) for the correct trafficking of IRT1 (zeige PARP3 Proteine) and, thus, for modulating the activity of the iron uptake machinery
This work establishes a functional link between the dynamics and the lateral polarity of IRT1 (zeige PARP3 Proteine) and the transport of its substrates, and identifies a molecular mechanism driving polar localization of a cell surface protein (zeige CD28 Proteine) in plants.
IDF1 directly regulates IRT1 (zeige PARP3 Proteine) degradation through its RING-type E3 ligase activity.
Data indicate that steady-state mRNA abundance for three representative Fe homeostasis genes, IRT1 (zeige PARP3 Proteine), bHLH39, and FER1 (zeige FTH1 Proteine), oscillated in light/dark (LD) cycles or warm/cold environmental cycles.
AtIRT1 transports nicekl (Ni(2 (zeige VMP1 Proteine)+)) in roots, and strongly suggest that Ni accumulation is further accelerated by AtIRT1 that is expressed in response to excess Ni.
These data suggest a model in which monoubiquitin-dependent internalization/sorting and turnover keep the plasma membrane pool of IRT1 (zeige PARP3 Proteine) low to ensure proper iron uptake and to prevent metal toxicity.
IRT1 and FRO2 genes are upregulated under iron starvation.
study followed the dynamics of hepcidin (zeige HAMP Proteine)-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 (zeige HAMP Proteine) insensitive
Reduced expression of ferroportin mRNA identifies a subset of infertile women and may constitute a target for therapy.
FPN1 cycles as a monomer within the endocytic/plasma membrane compartment and responds to its physiological inhibitor, Hepc (zeige HAMP Proteine), in both control and ferroportin disease (FD) cells. However, in FD, FPN1 fails to reach the cell surface when cells undergo high iron turnover.
These results suggest that FPN1 exports iron received from the iron chaperone PCBP2 (zeige PCBP2 Proteine). Therefore, it was found that PCBP2 (zeige PCBP2 Proteine) modulates cellular iron export, which is an important physiological process.
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.
Mir (zeige MLXIP Proteine)-20a controls expression of the iron exporter ferroportin (FPN1) by binding to highly conserved target sites in its 3'-untranslated region. Expression of miR (zeige MLXIP Proteine)-20a is inversely correlated to FPN1 in lung cancer.
The concentration of functional membrane-associated ferroportin is controlled by its ligand, the iron-regulatory hormone hepcidin (zeige HAMP Proteine), and fine-tuned by regulatory mechanisms serving iron homeostasis, oxygen utilization, host defense, and erythropoiesis.
Low hepcidin (zeige HAMP Proteine) and high ferroportin expression by erythroblasts and macrophages were seen in iron deficiency anemia, while the opposite was true in anemia of chronic disorders.
Erythroblasts from Beta-thalassemia patients showed a significantly reduced expression of total MTP1 protein.
Several family members had hemochromatosis (zeige HFE Proteine) 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.
Fasting upregulates Fpn1 expression in spleen and peritoneal macrophages, probably via a ghrelin (zeige GHRL Proteine)/GHSR1a/MAPK (zeige MAPK1 Proteine) signaling pathway.
Expression of Hepcidin (zeige HAMP Proteine) and Ferroportin in the Placenta, and Ferritin (zeige FTL Proteine) and Transferrin Receptor 1 (zeige TFR Proteine) Levels in Maternal and Umbilical Cord Blood in Pregnant Women with and without Gestational Diabetes
findings show that ferroportin expression by macrophages at the site of injury represents a requirement for appropriate activation of myogenic precursors and eventual healing of injured skeletal muscle
The results suggest that physiologic hepcidin (zeige HAMP Proteine) levels are insufficient to alter Fpn levels within the retinal pigment epithelium and Muller cells, but may limit iron transport into the retina from vascular endothelial cells.
In Angiotensin II treated mice, duodenal divalent metal transporter-1 (zeige SLC11A2 Proteine) and ferroportin expression levels were increased and hepatic hepcidin (zeige HAMP Proteine) mRNA expression and serum hepcidin (zeige HAMP Proteine) concentration were reduced.
Mice infected with Salmonella typhimurium have increased duodenal expression of the iron exporter ferroportin-1, consistent with increased uptake of dietary iron.
Results suggest that reduction in ferroportin levels in Alzheimer's disease brains are likely associated with cerebral ischaemia, inflammation, loss of neurons due to protein misfolding, senile plaque formation and possibly ageing process itself
Oral iron failed to be utilized by Fpn-KO mice and was retained in enterocytes, irrespective of the iron source. Ferroportin-dependent efflux from enterocytes controls duodenal iron absorption.
Genetic interactions between Cp, Mon1a (zeige MON1A Proteine), and the Slc40a1 locus are involved in iron metabolism.
Hypoxia signal, stimulated erythropoietin (zeige EPO Proteine), which affected iron absorption by stabilizing duodenal ferroportin.
The protein encoded by this gene is a cell membrane protein that may be involved in iron export from duodenal epithelial cells. Defects in this gene are a cause of hemochromatosis type 4 (HFE4).
, iron-regulated transporter
, solute carrier family 39 (iron-regulated transporter), member 1
, solute carrier family 40 member 1
, solute carrier family 40 (iron-regulated transporter), member 1
, solute carrier family 40 member 1-like
, iron regulated gene 1
, putative ferroportin 1 variant IIIB
, solute carrier family 11 (proton-coupled divalent metal ion transporters), member 3
, SLC11A3 iron transporter
, ferroportin 1
, iron-regulated transporter 1
, metal transporter protein 1
, metal transporting protein 1
, cell adhesion regulator