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Human Polyclonal SLC40A1 Primary Antibody for ICC, FACS - ABIN439384
Vanoaica, Darshan, Richman, Schümann, Kühn: Intestinal ferritin H is required for an accurate control of iron absorption. in Cell metabolism 2010
Show all 45 Pubmed References
Human Polyclonal SLC40A1 Primary Antibody for IF (p), IHC (p) - ABIN1387819
Rychtarcikova, Lettlova, Tomkova, Korenkova, Langerova, Simonova, Zjablovskaja, Alberich-Jorda, Neuzil, Truksa: Tumor-initiating cells of breast and prostate origin show alterations in the expression of genes related to iron metabolism. in Oncotarget 2016
Show all 2 Pubmed References
Human Polyclonal SLC40A1 Primary Antibody for ELISA, WB - ABIN4311379
Qiao, Sugianto, Fung, Del-Castillo-Rueda, Moran-Jimenez, Ganz, Nemeth: Hepcidin-induced endocytosis of ferroportin is dependent on ferroportin ubiquitination. in Cell metabolism 2012
Human Polyclonal SLC40A1 Primary Antibody for FACS - ABIN4311374
Marques, Porto, Rêma, Faria, Cruz Paula, Gomez-Lazaro, Silva, Martins da Silva, Lopes: Local iron homeostasis in the breast ductal carcinoma microenvironment. in BMC cancer 2016
Ca(2+) is required for human Fpn transport activity
SLC40A1 expression is increased in the intestine of patients with type 2 diabetes in association with iron stores and serum hepcidin levels.
In this study, we identified three domestic sporadic families of hereditary hemochromatosis in China and demonstrated mutations in HFE and SLC40A1 respectively.
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.
SLC40A1 mutation analysis in 7 Italian families with type 4 hereditary hemochromatosis
Ferroportin protects erythrocytes against oxidative stress and malaria infection.
Nrf2 suppresses prostate cancer cells viability, migration, and mitosis by upregulating ferroportin expression.
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
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.
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
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, 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. Therefore, it was found that PCBP2 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-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.
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.
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.
Erythroblasts from Beta-thalassemia patients showed a significantly reduced expression of total MTP1 protein.
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.
TLR4 dependent macrophage signaling is controlled via hepcidin-ferroportin1 axis by influencing TLR4-lipid raft interactions
Functional impact of mammalian ferroportin mutations studied in zebrafish.
HEP/FPN axis seems to have a central role in infections, with microorganisms within macrophages or that survive in the bloodstream or other cellular spaces. FPN may also have a significant role for embryonic development, growth and organogenesis.
Expression of solute carrier family 9 (sodium/hydrogen exchanger) member 2 (Slc9a2) within the mammary gland can mediate the effect of milk mineral concentration quantitative trait loci 9 (Mmcq9) on milk iron concentration.
The Slc40a1 deletion mildly increased iron levels in both precursor and mature osteoclasts, and its loss in precursors, but not in mature cells, increased osteoclastogenesis and decreased bone mass in vivo Of note, these phenotypes were more pronounced in female than in male mice.
study indicates that copper is an important player in the regulation of the Slc40a1 gene expression.
Pulmonary iron overload is associated with oxidative stress, restrictive lung disease with decreased total lung capacity and reduced blood oxygen saturation in homozygous Slc40a1(C326S/C326S) mice compared to wild-type controls.
ferroportin mRNA downregulation depends on M2 subtype polarization of macrophage
Fasting upregulates Fpn1 expression in spleen and peritoneal macrophages, probably via a ghrelin/GHSR1a/MAPK signaling pathway.
Expression of Hepcidin and Ferroportin in the Placenta, and Ferritin and Transferrin Receptor 1 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
these results indicate that Fpn deficiency decreases Mn trafficking out of the brain, alters body Fe, Mn, Zn and Cu levels, and promotes metal accumulation in olfactory bulbs.
The results suggest that physiologic hepcidin 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 and ferroportin expression levels were increased and hepatic hepcidin mRNA expression and serum hepcidin concentration were reduced.
Fpn plays a central role in Mn transport and flatiron (ffe/+) mice provide an excellent genetic model to explore the role of this exporter in Mn homeostasis.
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, and the Slc40a1 locus are involved in iron metabolism.
Hypoxia signal, stimulated erythropoietin, which affected iron absorption by stabilizing duodenal ferroportin.
A model is proposed that suggests that unlike proteases, which are irreversibly bound to activated alpha2M, hepcidin remains labile and available to down-regulate Fpn1.
The infection of M.tuberculosis can lead to increased Fn expression and decreased FPN expression in macrophages, and the levels of Fn and FPN in the infected macrophages are both related to the strength of the virulence of M.tuberculosis.
Nitric oxide up-regulated the expression of ferroportin-1 (Fpn1), the major cellular iron exporter, in mouse and human cells.
IRT1 directly senses elevated non-iron metal concentrations and integrates multiple substrate-dependent regulations to optimize iron uptake and protect plants from highly reactive metals.
Data suggest that NRAMP1 plays a pivotal role in Fe transport by cooperating with IRT1 to take up Fe in roots under replete conditions.
role of ABCG37, IRT1 and FRO2 in root Fe2+ transport systems
role of IRT1 in iron uptake
Our results reveal a role of SNX1 for the correct trafficking of IRT1 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 and the transport of its substrates, and identifies a molecular mechanism driving polar localization of a cell surface protein in plants.
IDF1 directly regulates IRT1 degradation through its RING-type E3 ligase activity.
Data indicate that steady-state mRNA abundance for three representative Fe homeostasis genes, IRT1, bHLH39, and FER1, oscillated in light/dark (LD) cycles or warm/cold environmental cycles.
AtIRT1 transports nicekl (Ni(2+)) 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 low to ensure proper iron uptake and to prevent metal toxicity.
IRT1 and FRO2 genes are upregulated under iron starvation.
Application of the lipoxygenase inhibitor ibuprofene to plants caused an up-regulation of IRT1 gene expression.
Although ferrous ions and other IRT1-transported metal ions do not bind very tightly, the Histidine-rich sequence has a very high entropy-driven affinity for Fe3+, which may have biological significance.
ferric-chelate reductase FRO2 and ferrous-transporter IRT1 are the targets of the three transcription factors and the transcription of FRO2 and IRT1 is directly regulated by a complex of FIT/AtbHLH38 or FIT/AtbHLH39.
Expression of each of the IRT1 variants in plants from the 35S promoter revealed that K146 or K171 is required for iron-induced protein turnover, and 35S-IRT1K146R,K171R plants contain higher levels of iron compared to 35S-IRT1 and wild type
Results show that IRT2 appears strictly co-regulated with FRO2 and IRT1, supporting the view that IRT2 is an integral component of the root response to iron deficiency in root epidermal cells.
Acidification capacity varied among Arabidopsis accessions and was associated with a high induction of AHA2 and IRT1...
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 gene 1
, putative ferroportin 1 variant IIIB
, solute carrier family 11 (proton-coupled divalent metal ion transporters), member 3
, solute carrier family 40 member 1
, iron-regulated transporter
, solute carrier family 39 (iron-regulated transporter), member 1
, solute carrier family 40 (iron-regulated transporter), member 1
, cell adhesion regulator
, ferroportin 1
, solute carrier family 40 member 1-like
, SLC11A3 iron transporter
, iron-regulated transporter 1
, metal transporter protein 1
, metal transporting protein 1