Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A purified polyclonal antiserum directed against the isolated main 80 kD IROMP (iron-regulated outer-membrane protein) from Pseudomonas aeruginosa PAO1 detected only the 80 kD polypeptide of outer-membrane proteins from PAO1 cells grown in iron deficiency in Western blots. It was also shown to inhibit the uptake of 59Fe pyoverdin by PAO1 cells as well as its binding to purified outer membranes. Immunofluorescence experiments with intact PAO1 cells confirmed that the receptor is present only at the surface of cells grown under conditions of iron deficiency. All these data allow us to conclude that the 80 kD main IROMP of P. aeruginosa is indeed the receptor for the siderophore ferripyoverdin.
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PMID:Pyoverdin-facilitated iron uptake in Pseudomonas aeruginosa: immunological characterization of the ferripyoverdin receptor. 212 27

Treatment with iron chelators mimics hypoxic induction of the hypoxia inducible factor (HIF-1) which activates transcription by binding to hypoxia responsive elements (HRE). We investigated whether HIF-1 is involved in transcriptional activation of the transferrin receptor (TfR), a membrane protein which mediates cellular iron uptake, in response to iron deprivation. The transcription rate of the TfR gene in isolated nuclei was up-regulated by treatment of Hep3B human hepatoma cells with the iron chelator desferrioxamine (DFO). The role of HIF-1 in the activation of TfR was indicated by the following observations: (i) DFO-dependent activation of a luciferase reporter gene in transfected Hep3B cells was mediated by a fragment of the human TfR promoter containing a putative HRE sequence; (ii) mutation of this sequence prevented stimulation of luciferase activity; (iii) binding to this sequence of HIF-1alpha, identified by competition experiments and supershift assays, was induced by DFO. Furthermore, in mouse hepatoma cells unable to assemble functional HIF-1, inducibility of TfR transcription by DFO was lost and TfR mRNA up-regulation was reduced. These results, which show the role of HIF-1 in the control of TfR gene expression in conditions of iron depletion, give insights into the mechanisms of transcriptional regulation which concur with the well-characterized post-transcriptional control of TfR expression to expand the extent of response to iron deficiency.
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PMID:HIF-1-mediated activation of transferrin receptor gene transcription by iron chelation. 1051 14

We present the cloning and characterization of an Arabidopsis gene, FRD3, involved in iron homeostasis. Plants carrying any of the three alleles of frd3 constitutively express three strategy I iron deficiency responses and misexpress a number of iron deficiency-regulated genes. Mutant plants also accumulate approximately twofold excess iron, fourfold excess manganese, and twofold excess zinc in their shoots. frd3-3 was first identified as man1. The FRD3 gene is expressed at detectable levels in roots but not in shoots and is predicted to encode a membrane protein belonging to the multidrug and toxin efflux family. Other members of this family have been implicated in a variety of processes and are likely to transport small organic molecules. The phenotypes of frd3 mutant plants, which are consistent with a defect in either iron deficiency signaling or iron distribution, indicate that FRD3 is an important component of iron homeostasis in Arabidopsis.
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PMID:FRD3, a member of the multidrug and toxin efflux family, controls iron deficiency responses in Arabidopsis. 1217 22

The Escherichia coli zupT (formerly ygiE) gene encodes a cytoplasmic membrane protein (ZupT) related to members of the eukaryotic ZIP family of divalent metal ion transporters. Previously, ZupT was shown to be responsible for uptake of zinc. In this study, we show that ZupT is a divalent metal cation transporter of broad substrate specificity. An E. coli strain with a disruption in all known iron uptake systems could grow in the presence of chelators only if zupT was expressed. Heterologous expression of Arabidopsis thaliana ZIP1 could also alleviate iron deficiency in this E. coli strain, as could expression of indigenous mntH or feoABC. Transport studies with intact cells showed that ZupT facilitates uptake of 55Fe2+ similarly to uptake of MntH or Feo. Other divalent cations were also taken up by ZupT, as shown using 57Co2+. Expression of zupT rendered E. coli cells hypersensitive to Co2+ and sensitive to Mn2+. ZupT did not appear to be metal regulated: expression of a Phi(zupT-lacZ) operon fusion indicated that zupT is expressed constitutively at a low level.
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PMID:The metal permease ZupT from Escherichia coli is a transporter with a broad substrate spectrum. 1571 30

Dietary heme iron is an important nutritional source of iron in carnivores and omnivores that is more readily absorbed than non-heme iron derived from vegetables and grain. Most heme is absorbed in the proximal intestine, with absorptive capacity decreasing distally. We utilized a subtractive hybridization approach to isolate a heme transporter from duodenum by taking advantage of the intestinal gradient for heme absorption. Here we show a membrane protein named HCP 1 (heme carrier protein 1), with homology to bacterial metal-tetracycline transporters, mediates heme uptake by cells in a temperature-dependent and saturable manner. HCP 1 mRNA was highly expressed in duodenum and regulated by hypoxia. HCP 1 protein was iron regulated and localized to the brush-border membrane of duodenal enterocytes in iron deficiency. Our data indicate that HCP 1 is the long-sought intestinal heme transporter.
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PMID:Identification of an intestinal heme transporter. 1614 96

Iron acquisition in Arabidopsis depends mainly on AtIRT1, a Fe2+ transporter in the plasma membrane of root cells. However, substrate specificity of AtIRT1 is low, leading to an excess accumulation of other transition metals in iron-deficient plants. In the present study we describe AtIREG2 as a nickel transporter at the vacuolar membrane that counterbalances the low substrate specificity of AtIRT1 and possibly other iron transport systems in iron-deficient root cells. AtIREG2 is co-regulated with AtIRT1 by the transcription factor FRU/FIT1, encodes a membrane protein, which has 10 putative transmembrane domains and shares homology with vertebrate Fe2+ exporters. Heterologous expression of AtIREG2 in various yeast mutants, however, did not demonstrate an iron transport function. Instead, expression in wild-type and nickel-sensitive cot1 yeast cells conferred enhanced tolerance to elevated concentrations of nickel at acidic pH. A role in vacuolar substrate transport was further supported by localization of AtIREG2-GFP fusion proteins to the tonoplast in Arabidopsis suspension cells and root cells of intact plants. Transgenic plants overexpressing AtIREG2 showed an increased tolerance to elevated concentrations of nickel, whereas T-DNA insertion lines lacking AtIREG2 expression were more sensitive to nickel, particularly under iron deficiency, and accumulated less nickel in roots. We therefore propose a role of AtIREG2 in vacuolar loading of nickel under iron deficiency and thus identify it as a novel component in the iron deficiency stress response.
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PMID:AtIREG2 encodes a tonoplast transport protein involved in iron-dependent nickel detoxification in Arabidopsis thaliana roots. 1679 Apr 30

Delusional parasitosis (DP) is a psychotic condition in which a person has the unshakeable and mistaken belief (delusion) and/or aberrant perception (hallucination) of being infested with parasites. The disorder will be usually classified in a primary DP-group without a detectable cause (so-called pure forms), while secondary DP-groups are associated with general organic conditions, psychiatric illnesses and drugs (substance induced). Etiology and pathophysiology of DP remain however unknown. In the present paper we hypothesize for the first time a decreased striatal dopamine transporter (DAT)-functioning (corresponding with an increased extracellular dopamine-level) as etiologic condition for DP (primary and secondary groups). The DAT as key regulator of the dopamine-reuptake in the human brain is well known (regulation of the extracellular dopamine concentration). It is a presynaptic plasma membrane protein highly dense represented in the striatum. The hypothesis of a decreased DAT-functioning as etiologic condition by DP is revealed in case reports which show that DAT-inhibitors, such as cocaine, pemoline, methylphenidate and other amphetamine-derivatives can induce the clinical expression of DP. Several other associated causes of secondary DP-groups (medications, parkinson, chorea huntington, multiple system atrophy, diabetes, cerebrovascular diseases, alcoholism, traumatic brain injury, hyperuricemia, human immunodeficiency virus, iron deficiency, schizophrenia, depression) suggest that the clinical expression of DP may be related to a decreased striatal DAT-functioning (blocking, reduced ligand binding, reduced density, reduced activity). Our examined DP-cases (2-females) show means of magnetic resonance imaging a structurally damaged striatum. Furthermore, we presume that by the primary DP-group, the physiologically age-related decline of the DAT-density is pathologically elevated. Based on this hypothesis we show in the present paper the relation between DP and decreased striatal DAT-functioning, trying to give a new insight into the pathophysiologically mechanism involved. The hypothesis provides supporting evidence that increased levels of extracellular dopamine in the striatum of DP-patients is likely to be the result of decreased DAT-functioning and not increased rates of release. The hypothesis can be investigated simply by dopamine transporter imaging in patients with DP.
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PMID:Delusional parasitosis and the dopamine transporter. A new insight of etiology? 1713 47

Iron deficiency-induced chlorosis in peanut during anthesis was alleviated when peanut was intercropped with maize in field and pot experiments. Iron acquisition of graminaceous plants is characterized by the synthesis and secretion of the iron-chelating phytosiderophores. Compared to the roots of monocropped maize, the roots of maize intercropped with peanut always secreted higher amounts of phytosiderophores during peanut anthesis. For non-graminaceous plants, reduction of ferric to ferrous iron on the root surface is the rate-limiting step for mobilizing iron from soil. The full-length cDNA, AhFRO1, which is encoding an Fe(III)-chelate reductase, was isolated from peanut. AhFRO1 expression in yeast conferred Fe(III)-chelate reductase activity to the cells. Consistent with its function in iron uptake, AhFRO1 was determined to be a membrane protein by transient expression analysis. AhFRO1 mRNA accumulated under iron deficiency conditions. During pre-anthesis, the Fe(III)-chelate reductase activity and the transcript levels of AhFRO1 were similar in monocropped and intercropped peanut. When the iron deficiency-induced chlorosis developed in the monocropped peanuts, both the Fe(III)-chelate reductase activity of peanut and the transcript levels of AhFRO1 were higher in intercropped than in monocropped peanuts, which is consistent with the secretion of phytosiderophores by maize roots. We conclude that AhFRO1 in peanut and phytosiderophores from maize co-operate to improve the iron nutrition of peanut when intercropped with maize.
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PMID:Regulation of AhFRO1, an Fe(III)-chelate reductase of peanut, during iron deficiency stress and intercropping with maize. 1945

In previous research, iron-deficiency symptoms in peanut (Arachis hypgaea) were alleviated during anthesis by intercropping with maize. This benefit was associated with increased phytosiderophore secretion by maize and increased Fe(III)-chelate reductase activity by peanut. In the present study, we isolated the full-length cDNA of AhIRT1 (iron-regulated transporter 1) from peanut and characterized how iron deficiency and intercropping affected its iron-transporting ability. Functional complementation with AhIRT1 restored normal growth of the yeast mutant fet3fet4 (defective in both high- and low-affinity iron-uptake systems) under iron-deficiency conditions. Based on transient expression analysis, AhIRT1 was determined to be a membrane protein, which was consistent with a function in iron uptake. In peanut, transcript levels of AhIRT1 increased in both root and shoot under iron-deficiency conditions. In a pot experiment, AhIRT1 transcript levels in intercropped peanut were 10 times greater during anthesis than pre-anthesis, and transcript levels during anthesis were 40% greater in intercropped than in monocropped peanut.
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PMID:Cloning and functional analysis of the peanut iron transporter AhIRT1 during iron deficiency stress and intercropping with maize. 2043 Apr 76

Membrane lipid and protein composition was compared in erythrocytes from iron deficiency anemia (IDA) and heterozygous beta thalassemia patients. The study was planned to correlate the influence of iron deficiency with the intrinsic defect of the heterozygous condition on the membrane structural integrity as well as to investigate whether there are differences in membrane changes between the two conditions. Results indicate high levels of saturated fatty acids and low unsaturated fatty acids in both disorders although arachidonic acid and the unsaturation index were lower in heterozygous thalassemia than IDA. Nevertheless, neither of the conditions provoked any alterations in membrane protein or glycophorin suggesting alterations in the lipid moiety only. Present findings indicate that irrespective to the etiology, both, iron deficiency and the heterozygous condition show a common pattern of lipid derangement, which may in turn result in increased membrane rigidity and decreased cellular deformability.
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PMID:Comparative analysis of RBC membrane fatty acids, proteins and glycophorin in patients with heterozygous beta thalassemia and iron deficiency anemia. 2310 9


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