Search results for "Iron-Binding Proteins"

showing 10 items of 19 documents

PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

2020

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is characterized by degeneration of the large sensory neurons and spinocerebellar tracts, cardiomyopathy, and increased incidence in diabetes. The underlying pathophysiological mechanism of FRDA, driven by a significantly decreased expression of frataxin (FXN), involves increased oxidative stress, reduced activity of enzymes containing iron‑sulfur clus-ters (ISC), defective energy production, calcium dyshomeostasis, and impaired mitochondrial biogenesis, leading to mitochondrial dysfunction. The peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcriptional factor playing a key role in mito…

0301 basic medicineAtaxiaCell SurvivalCaspase 3PPAR agonistlcsh:RC321-57103 medical and health sciencesMice0302 clinical medicineIron-Binding ProteinsmedicineNeuritesAnimalsHumansMyocytes CardiacNeurodegenerationDorsal root ganglia neuronslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMembrane Potential MitochondrialNeuronsCardiomyocytesbiologyChemistryFrataxinNeurodegenerationCalpainLipid DropletsPeroxisomemedicine.diseaseCell biologyMitochondriaRatsPPAR gamma030104 developmental biologyNeurologyMitochondrial biogenesisFriedreich AtaxiaFrataxinbiology.proteinThiazolidinedionesmedicine.symptomMitochondrial function030217 neurology & neurosurgery
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Pirin: A novel redox-sensitive modulator of primary and secondary metabolism in Streptomyces

2018

Pirins are evolutionarily conserved iron-containing proteins that are found in all kingdoms of life, and have been implicated in diverse molecular processes, mostly associated with cellular stress. In the present study, we started from the evidence that the insertional inactivation of pirin-like gene SAM23877_RS18305 (pirA) by Phi C31 Att/Int system-based vectors in spiramycin-producing strain Streptomyces ambofaciens ATCC 23877 resulted in marked effects on central carbon and energy metabolism gene expression, high sensitivity to oxidative injury and repression of polyketide antibiotic production. By using integrated transcriptomic, proteomic and metabolite profiling, together with genetic…

0301 basic medicineIn silico030106 microbiologyBioengineeringStreptomycesApplied Microbiology and Biotechnology03 medical and health sciencesPolyketideBacterial ProteinsIron-Binding ProteinsGene expressionActinomycetes; Antibiotics; Beta-oxidation of fatty acids; Pirin; Secondary metabolismSecondary metabolismGenePsychological repressionbiologyChemistryActinomyceteAntibioticbiology.organism_classificationStreptomycesComplementation030104 developmental biologyMetabolic EngineeringBiochemistryPirinPolyketidesSecondary metabolismOxidation-ReductionBeta-oxidation of fatty acidBiotechnology
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Metal homeostasis regulators suppress FRDA phenotypes in a drosophila model of the disease

2016

Friedreich's ataxia (FRDA), the most commonly inherited ataxia in populations of European origin, is a neurodegenerative disorder caused by a decrease in frataxin levels. One of the hallmarks of the disease is the accumulation of iron in several tissues including the brain, and frataxin has been proposed to play a key role in iron homeostasis. We found that the levels of zinc, copper, manganese and aluminum were also increased in a Drosophila model of FRDA, and that copper and zinc chelation improve their impaired motor performance. By means of a candidate genetic screen, we identified that genes implicated in iron, zinc and copper transport and metal detoxification can restore frataxin def…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicineMitochondrionmedicine.disease_causeAntioxidantsIron-Binding ProteinsMedicine and Health SciencesHomeostasislcsh:ScienceGeneticsMultidisciplinarybiologyDrosophila MelanogasterIron-binding proteinsAnimal ModelsPhenotypeMitochondria3. Good healthInsectsDNA-Binding ProteinsChemistryZincPhenotypesPhysical SciencesDrosophilaAnatomymedicine.symptomDrosophila melanogasterResearch ArticleChemical ElementsAtaxiaArthropodaIronResearch and Analysis Methods03 medical and health sciencesModel OrganismsOcular SystemmedicineGeneticsAnimalsHumansGenetikManganeselcsh:ROrganismsBiology and Life SciencesCell Biologybiology.organism_classificationInvertebratesOxidative StressDisease Models Animal030104 developmental biologyFriedreich AtaxiaFrataxinbiology.proteinEyeslcsh:QPhysiological ProcessesCarrier ProteinsHeadCopperOxidative stressAluminumTranscription FactorsGenetic screen
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Biomarkers and clinical characteristics of autoimmune chronic spontaneous urticaria: Results of the PURIST Study.

2019

Background: Autoimmune chronic spontaneous urticaria (aiCSU) is an important subtype of chronic spontaneous urticaria (CSU) in which functional IgG autoantibodies to IgE or its high-affinity receptor (FcεRI) induces mast cell degranulation and subsequent symptom development. However, it has not been tightly characterized. This study aimed to better define the clinical and immunological features and to explore potential biomarkers of aiCSU. Methods: This was a multinational, multicenter study of 182 CSU patients. The clinical features studied included: urticaria activity and impact (UAS7 and quality of life); autologous serum skin test (ASST); IgG anti-FcεRI and IgG anti-IgE; IgG-anti-thyrop…

0301 basic medicinechronic spontaneous urticariaMaleBasophilIgG autoantibodiesImmunoglobulin EAutoantigensHistamine Releasechemistry.chemical_compound0302 clinical medicineIron-Binding ProteinsImmunology and AllergyChronic UrticariaReceptorAutologous serum skin testbiologyDegranulationMiddle AgedChronic spontaneous urticariaAntibodies Anti-IdiotypicBasophilsmedicine.anatomical_structurePhenotypeAutologous serum skin testautologous serum skin testFemaleSymptom AssessmentHistamineAdultAdolescentImmunologyIodide PeroxidaseAutoimmune Diseases03 medical and health sciencesYoung Adultautoimmune CSUmedicineJournal ArticleHumansAgedAutoantibodiesbusiness.industryReceptors IgEAutoantibodyBasophil activation030104 developmental biology030228 respiratory systemchemistryImmunoglobulin GImmunologyBasophil activation assaysbiology.proteinAutoimmune CSUbusinessbasophil activation assaysBiomarkersAllergyREFERENCES
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Genotype and phenotype analysis of Friedreich's ataxia compound heterozygous patients

2000

Friedreich's ataxia is caused by mutations in the FRDA gene that encodes frataxin, a nuclear-encoded mitochondrial protein. Most patients are homozygous for the expansion of a GAA triplet repeat within the FRDA gene, but a few patients show compound heterozygosity for a point mutation and the GAA-repeat expansion. We analyzed DNA samples from a cohort of 241 patients with autosomal recessive or isolated spinocerebellar ataxia for the GAA triplet expansion. Patients heterozygous for the GAA expansion were screened for point mutations within the FRDA coding region. Molecular analyses included the single-strand conformation polymorphism analysis, direct sequencing, and linkage analysis with FR…

AdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAtaxiaGenotypeGenetic LinkageDNA Mutational AnalysisGenes RecessiveCompound heterozygosityLoss of heterozygosityTrinucleotide RepeatsIron-Binding ProteinsGenotypeGeneticsmedicineHumansPoint MutationAge of OnsetAlleleChildAllelesPolymorphism Single-Stranded ConformationalGenetics (clinical)Family HealthGeneticsbiologynutritional and metabolic diseasesmedicine.diseasePedigreePhosphotransferases (Alcohol Group Acceptor)PhenotypeFriedreich AtaxiaChild PreschoolFrataxinbiology.proteinSpinocerebellar ataxiamedicine.symptomTrinucleotide Repeat ExpansionTrinucleotide repeat expansionMicrosatellite Repeats
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Congenital goitrous primary hypothyroidism in two German families caused by novel thyroid peroxidase (TPO) gene mutations.

2013

Congenital hypothyroidism occurs with a prevalence of approximately 1:3 500. Defects in thyroid hormone synthesis which lead to goitrous hypothyroidism account for 10-15% of these cases. Several genetic defects have been characterized and mutations in the thyroid peroxidase (TPO) gene are the most common cause for dyshormonogenesis.So far, more than 80 mutations in the TPO gene have been described, resulting in a variable decrease in TPO bioactivity. Clinically TPO defects manifest with congenital primary goitrous hypothyroidism.We here present 2 children with congenital primary hypothyroidism, who were identified to have compound heterozygous TPO mutations. They both shared the same novel …

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismMutation MissenseGene mutationmedicine.disease_causeCompound heterozygosityAutoantigensIodide Peroxidasefluids and secretionsEndocrinologyThyroid dyshormonogenesisThyroid peroxidaseInternal medicineGermanyIron-Binding ProteinsInternal MedicinemedicineCongenital HypothyroidismMissense mutationHumansFamilyMutationbiologybusiness.industryGoiterPrimary hypothyroidismInfant Newbornfood and beveragesGeneral MedicineExonsmedicine.diseaseCongenital hypothyroidismEndocrinologyembryonic structuresbiology.proteinFemalebusinessExperimental and clinical endocrinologydiabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
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Possible link between Hashimoto's thyroiditis and oral lichen planus: a novel association found

2013

Objectives: Hashimoto's thyroiditis as well as lichen planus has been associated to a number of disorders, generally of auto-immune origin. A novel possible association between oral lichen planus (OLP) and Hashimoto's thyroiditis (HT) is here proposed on the basis of a cross-sectional survey. Materials and methods: One hundred and five unrelated OLP patients were considered. Diagnosis of HT was based on positive serum anti-TPO, anti-Tg, TSH levels and the typical ultrasound pattern of the thyroid gland. Results: In the present survey, the prevalence of HT in the OLP group was 14. 3 % whereas the prevalence of HT-related hypothyroidism in the general population was reported to be equal to 1 …

Adultendocrine systemmedicine.medical_specialtyendocrine system diseasesPopulationThyrotropinAutoimmunityHashimoto Diseasemedicine.disease_causeAutoantigensIodide PeroxidaseGastroenterologyAsymptomaticThyroiditisAutoimmunityHashimoto's thyroiditistomatognathic systemSettore MED/28 - Malattie OdontostomatologicheIron-Binding ProteinsInternal medicinePrevalencemedicineHumansThyroid NoduleOral mucosaeducationGeneral DentistryAutoantibodieseducation.field_of_studybusiness.industryThyroidMiddle AgedCirculating thyroid antibodiesmedicine.diseaseAnti-thyroid autoantibodiesThyroxinestomatognathic diseasesCross-Sectional Studiesmedicine.anatomical_structureItalyOral lichen planuHashimoto's thyroiditis; Oral lichen planus; Autoimmunity; Circulating thyroid antibodiesTriiodothyronineFemaleOral lichen planusmedicine.symptombusinessLichen Planus OralClinical Oral Investigations
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Negative staining across holes: application to fibril and tubular structures.

2007

The negative staining technique, when used with holey carbon support films, presents superior imaging conditions than is the case when samples are adsorbed to continuous carbon films. A demonstration of this negative staining approach is presented, using ammonium molybdate in combination with trehalose, applied to several fibrillar and tubular samples. Fibrils formed from the amyloid-beta peptide and the protease inhibitor pepstain A spread very well unsupported across holes and the different polymorphic fibril forms can be readily assessed. However, tubular forms of amyloid-beta have a tendency to be flattened, due to surface tension forces prior to and during specimen drying. Sub-fibril a…

AmyloidMaterials scienceGeneral Physics and Astronomychemistry.chemical_elementFibrilNegative Stainingchemistry.chemical_compoundFerrihydriteMicroscopy Electron TransmissionStructural BiologyIron-Binding ProteinsPepstatinsAnimalsHumansNanotechnologyGeneral Materials ScienceAmmonium molybdateMolybdenumAmyloid beta-PeptidesProteinsTrehaloseCell BiologyDNATrehaloseNegative stainCarbonStainingRatsCrystallographyCarbon filmchemistryBiophysicsCollagenPeptidesCarbonMicron (Oxford, England : 1993)
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Causative role of oxidative stress in a Drosophila model of Friedreich ataxia

2006

Friedreich ataxia (FA), the most common form of hereditary ataxia, is caused by a deficit in the mitochondrial protein frataxin. While several hypotheses have been suggested, frataxin function is not well understood. Oxidative stress has been suggested to play a role in the pathophysiology of FA, but this view has been recently questioned, and its link to frataxin is unclear. Here, we report the use of RNA interference (RNAi) to suppress the Drosophila frataxin gene (fh) expression. This model system parallels the situation in FA patients, namely a moderate systemic reduction of frataxin levels compatible with normal embryonic development. Under these conditions, fh-RNAi flies showed a shor…

AtaxiaBlotting WesternLongevityGene ExpressionCHO Cellsmedicine.disease_causeBiochemistryAconitaseMitochondrial ProteinsCricetulusRNA interferenceCricetinaeIron-Binding ProteinsGeneticsmedicineAnimalsDrosophila ProteinsRNA MessengerMolecular BiologyGeneAconitate HydrataseHyperoxiaGeneticsElectron Transport Complex IbiologyReverse Transcriptase Polymerase Chain ReactionSuccinate dehydrogenasefungiImmunohistochemistryCell biologySuccinate DehydrogenaseOxidative StressDrosophila melanogasterFriedreich AtaxiaFrataxinbiology.proteinRNA Interferencemedicine.symptomOxidative stressBiotechnologyThe FASEB Journal
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Deferiprone and idebenone rescue frataxin depletion phenotypes in a Drosophila model of Friedreich's ataxia

2013

Friedreich's ataxia (FRDA), the most common inherited ataxia, is a neurodegenerative disease caused by a reduction in the levels of the mitochondrial protein frataxin, the function of which remains a controversial matter. Several therapeutic approaches are being developed to increase frataxin expression and reduce the intramitochondrial iron aggregates and oxidative damage found in this disease. In this study, we tested separately the response of a Drosophila RNAi model of FRDA ( Llorens et al., 2007) to treatment with the iron chelator deferiprone (DFP) and the antioxidant idebenone (IDE), which are both in clinical trials. The FRDA flies have a shortened life span and impaired motor coord…

AtaxiaPyridonesUbiquinoneIronLife spanHyperoxiaBiologyPharmacologyMitochondrionmedicine.disease_causeAconitaseAntioxidantsAconitasechemistry.chemical_compoundIron-Binding ProteinsGeneticsmedicineAnimalsIdebenoneDeferiproneAconitate HydrataseHyperoxiaFrataxinClimbing capabilityGeneral MedicineMitochondriaDisease Models AnimalOxidative StressPhenotypechemistryFriedreich AtaxiaOxidative stressMutationFrataxinbiology.proteinDrosophilamedicine.symptomDeferiproneOxidative stressmedicine.drugGene
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