Search results for "glutaredoxins"

showing 8 items of 8 documents

Stimulation of Fe-S cluster insertion into apoFNR by Escherichia coli glutaredoxins 1, 2 and 3 in vitro.

2004

Abstract The oxygen sensor fumarate nitrate reductase regu-lator (FNR) of Escherichia coli contains in the active (anaerobic)state a [4Fe–4S] 2þ cluster which is lost after exposure to O 2 .Inaerobically prepared apoFNR, or in FNR obtained by treatmentof [4Fe–4S] FNR with O 2 in vitro, intramolecular cysteinedisulfides are found, including the cysteine residues which serveas ligands for the Fe–S cluster. It is shown here that thereconstitution of [4Fe–4S] FNR from this form of aerobicapoFNR was preceded by a long lag phase when glutathione wasused as the reducing agent. Addition of E. coli glutaredoxins(Grx) 1, 2 or 3 decreased the lag phase greatly and stimulatedthe reconstitution rate slig…

Iron-Sulfur ProteinsTime FactorsReducing agentFNRGlutaredoxinBiophysicsBiologyReductaseSulfidesmedicine.disease_causeNitrate reductaseBiochemistryOxygen sensorchemistry.chemical_compoundStructural BiologyGlutaredoxinGeneticsmedicineEscherichia coliCysteineDisulfidesThioredoxinMolecular BiologyEscherichia coliGlutaredoxinsDisulfide reductaseEscherichia coli ProteinsProteinsCell BiologyGlutathioneGlutathioneOxygenBiochemistrychemistryMultigene FamilyThioredoxinOxidoreductasesCysteineTranscription FactorsFEBS letters
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Redox Proteomics of the Inflammatory Secretome Identifies a Common Set of Redoxins and Other Glutathionylated Proteins Released in Inflammation, Infl…

2015

Protein cysteines can form transient disulfides with glutathione (GSH), resulting in the production of glutathionylated proteins, and this process is regarded as a mechanism by which the redox state of the cell can regulate protein function. Most studies on redox regulation of immunity have focused on intracellular proteins. In this study we have used redox proteomics to identify those proteins released in glutathionylated form by macrophages stimulated with lipopolysaccharide (LPS) after pre-loading the cells with biotinylated GSH. Of the several proteins identified in the redox secretome, we have selected a number for validation. Proteomic analysis indicated that LPS stimulated the releas…

LipopolysaccharidesProteomicsglutaredoxins; glutathione; redox signalingBlotting Westernlcsh:MedicineDown-RegulationInflammationBiologyProteomicsmedicine.disease_causeAntioxidantsDexamethasoneCell LineMiceProfilinschemistry.chemical_compoundThioredoxinsInfluenza HumanmedicineExtracellularAnimalsHumansVimentinSulfhydryl Compoundsglutathionelcsh:Scienceredox signalingglutaredoxinsInflammationMultidisciplinarylcsh:RRProteinsPeroxiredoxinsGlutathioneCell biologyBlotOxidative StressRAW 264.7 CellschemistryQR180lcsh:QTumor necrosis factor alphamedicine.symptomPeroxiredoxinOxidation-ReductionOxidative stressResearch ArticlePLOS ONE
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Microarray mRNA expression analysis of Fanconi anemia fibroblasts.

2007

Fanconi anemia (FA) cells are generally hypersensitive to DNA cross-linking agents, implying that mutations in the different <i>FANC</i> genes cause a similar DNA repair defect(s). By using a customized cDNA microarray chip for DNA repair- and cell cycle-associated genes, we identified three genes, cathepsin B (<i>CTSB</i>), glutaredoxin (<i>GLRX</i>), and polo-like kinase 2 (<i>PLK2</i>), that were misregulated in untreated primary fibroblasts from three unrelated FA-D2 patients, compared to six controls. Quantitative real-time RT PCR was used to validate these results and to study possible molecular links between FA-D2 and other FA subtypes.…

Fanconi anemia complementation group CMicroarrayDNA RepairDNA repairMrna expressionBiologyProtein Serine-Threonine KinasesCathepsin Bchemistry.chemical_compoundCytogeneticsFanconi anemiahemic and lymphatic diseasesGeneticsmedicineHumansRNA MessengerMolecular BiologyGeneGenetics (clinical)GlutaredoxinsOligonucleotide Array Sequence AnalysisGeneticsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleFibroblastsmedicine.diseaseMolecular biologyFanconi AnemiachemistryCase-Control StudiesDNACytogenetic and genome research
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Lack of a peroxiredoxin suppresses the lethality of cells devoid of electron donors by channelling electrons to oxidized ribonucleotide reductase

2017

The thioredoxin and glutaredoxin pathways are responsible of recycling several enzymes which undergo intramolecular disulfide bond formation as part of their catalytic cycles such as the peroxide scavengers peroxiredoxins or the enzyme ribonucleotide reductase (RNR). RNR, the rate-limiting enzyme of deoxyribonucleotide synthesis, is an essential enzyme relying on these electron flow cascades for recycling. RNR is tightly regulated in a cell cycle-dependent manner at different levels, but little is known about the participation of electron donors in such regulation. Here, we show that cytosolic thioredoxins Trx1 and Trx3 are the primary electron donors for RNR in fission yeast. Unexpectedly,…

0301 basic medicineCancer ResearchThioredoxin reductaseSynthesis PhaseYeast and Fungal ModelsBiochemistryElectron DonorsSchizosaccharomyces PombeThioredoxinsGlutaredoxinCell Cycle and Cell DivisionGenetics (clinical)Chemical ReactionsOxidesPeroxidesNucleic acidsChemistryRibonucleotide reductaseBiochemistryExperimental Organism SystemsCell ProcessesSchizosaccharomyces pombePhysical SciencesSynthesis phaseThioredoxinOxidation-ReductionResearch ArticleDNA Replicationlcsh:QH426-470DNA transcriptionElectron donorsBiologyDNA replicationResearch and Analysis MethodsCatalysisElectron Transport03 medical and health sciencesModel OrganismsSchizosaccharomycesRibonucleotide ReductasesOxidationGeneticsMolecular BiologyEcology Evolution Behavior and SystematicsGlutaredoxinsCell growthDNA replicationChemical CompoundsOrganismsFungiBiology and Life SciencesCell BiologyDNAPeroxiredoxinsbiology.organism_classificationYeastCell cycle and cell divisionCheckpoint Kinase 2lcsh:Genetics030104 developmental biologySchizosaccharomyces pombeGene expressionSchizosaccharomyces pombe ProteinsPeroxiredoxin
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Saccharomyces cerevisiae Glutaredoxin 5-deficient Cells Subjected to Continuous Oxidizing Conditions Are Affected in the Expression of Specific Sets …

2004

The Saccharomyces cerevisiae GRX5 gene codes for a mitochondrial glutaredoxin involved in the synthesis of iron/sulfur clusters. Its absence prevents respiratory growth and causes the accumulation of iron inside cells and constitutive oxidation of proteins. Null ⌬grx5 mu- tants were used as an example of continuously oxidized cells, as opposed to situations in which oxidative stress is instantaneously caused by addition of external oxi- dants. Whole transcriptome analysis was carried out in the mutant cells. The set of genes whose expression was affected by the absence of Grx5 does not significantly overlap with the set of genes affected in respiratory petite mutants. Many Aft1-dependent ge…

Saccharomyces cerevisiae ProteinsTranscription GeneticIronSaccharomyces cerevisiaeMutantProtein Array AnalysisDown-RegulationSaccharomyces cerevisiaeOxidative phosphorylationmedicine.disease_causeProtein oxidationBiochemistryOxygen ConsumptionGene Expression Regulation FungalIron-Binding ProteinsGlutaredoxinmedicineRNA MessengerMolecular BiologyGlutaredoxinsbiologyMembrane ProteinsNuclear ProteinsProteinsRNA-Binding ProteinsCell BiologyBlotting Northernbiology.organism_classificationCarbonUp-RegulationOxygenOxidative StressRegulonCCAAT-Binding FactorDatabases as TopicBiochemistryMutationFrataxinbiology.proteinOxidoreductasesReactive Oxygen SpeciesOxidative stressTranscription FactorsJournal of Biological Chemistry
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Cloning and sequencing of the cDNA encoding human glutaredoxin.

1994

Glutaredoxin (thioltransferase) is a small, heat-stable protein, which is involved in thiol/disulfide exchange reactions. We have isolated a cDNA that encodes glutaredoxin from a human brain cDNA library. The encoded protein contains 106 amino acids with a calculated molecular mass of 11.76 kDa and an isoelectric point of 8.09. The amino acid sequence deduced from the cDNA is more than 80% identical to those of other mammalian glutaredoxins.

DNA ComplementaryMolecular Sequence DataBiophysicsSequence alignmentMolecular cloningBiologyBiochemistryStructural BiologyGlutaredoxinComplementary DNAGeneticsHumansAmino Acid SequenceCloning MolecularPeptide sequenceGlutaredoxinschemistry.chemical_classificationBase SequencecDNA libraryNucleic acid sequenceBrainProteinsMolecular biologyAmino acidchemistryBiochemistryOxidoreductasesBiochimica et biophysica acta
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Decreased cell proliferation and higher oxidative stress in fibroblasts from Down Syndrome fetuses. Preliminary study

2013

Abstract Down Syndrome is the most common chromosomal disease and is also known for its decreased incidence of solid tumors and its progeroid phenotype. Cellular and systemic oxidative stress has been considered as one of the Down Syndrome phenotype causes. We correlated, in a preliminary study, the fibroblast proliferation rate and different cell proliferation key regulators, like Rcan1 and the telomere length from Down Syndrome fetuses, with their oxidative stress profile and the Ribonucleic acid and protein expression of the main antioxidant enzymes together with their activity. Increased oxidized glutathione/glutathione ratio and high peroxide production were found in our cell model. Th…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentPrimary Cell CultureSuperoxide dismutasemedicine.disease_causeSuperoxide dismutasechemistry.chemical_compoundFetusSuperoxide Dismutase-1ThioredoxinsInternal medicineGlutaredoxinmedicineHumansThioredoxinMolecular BiologyGlutaredoxinsCell ProliferationSkinchemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseTelomere lengthbiologyGlutathione peroxidaseTelomere HomeostasisGlutathioneRcan1FibroblastsTelomereCatalaseGlutathioneProgeroidOxidative StressEndocrinologychemistryBiochemistryGene Expression Regulationbiology.proteinMolecular MedicineFemaleThioredoxinDown SyndromeOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Thioredoxin and Glutaredoxin Systems as Potential Targets for the Development of New Treatments in Friedreich’s Ataxia

2020

The thioredoxin family consists of a small group of redox proteins present in all organisms and composed of thioredoxins (TRXs), glutaredoxins (GLRXs) and peroxiredoxins (PRDXs) which are found in the extracellular fluid, the cytoplasm, the mitochondria and in the nucleus with functions that include antioxidation, signaling and transcriptional control, among others. The importance of thioredoxin family proteins in neurodegenerative diseases is gaining relevance because some of these proteins have demonstrated an important role in the central nervous system by mediating neuroprotection against oxidative stress, contributing to mitochondrial function and regulating gene expression. Specifical…

0301 basic medicinePhysiologyClinical BiochemistryFriedreich’s ataxiaContext (language use)ReviewMitochondrionBiologyBiochemistrythioredoxins03 medical and health sciences0302 clinical medicineGlutaredoxinGene expressionTranscriptional regulationoxidative stressMolecular BiologyGeneglutaredoxinslcsh:RM1-950Cell BiologyCell biologylcsh:Therapeutics. Pharmacology030104 developmental biologyThioredoxin030217 neurology & neurosurgeryFunction (biology)Antioxidants
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