Search results for "Cytochrome-C"

showing 10 items of 11 documents

Mutations of mitochondrial DNA and human death.

1990

In the skeletal muscle of patients with mitochondrial myopathies (Kearns-Sayre syndrome and chronic progressive external ophthalmoplegia) and in the heart and skeletal muscle of healthy persons cells lacking cytochrome c oxidase are found. The respiratory-defective cells have the following features in common: onset of the defect at juvenile or adult age; progressive character of the defect with increasing age; and focal pattern of respiratory-deficient cells (fibers). A statistic mutation of mtDNA in affected cells is suggested to cause the defect of mitochondrial function. It is postulated that the continuous accumulation of respiratory-deficient cells, mainly in the human heart with incre…

Mitochondrial DNAmedicine.medical_specialtyCytochrome-c Oxidase DeficiencyMitochondrionBiologyHuman mitochondrial geneticsDNA MitochondrialMitochondria HeartKearns–Sayre syndromeElectron Transport Complex IVMitochondrial myopathyMuscular DiseasesReference ValuesInternal medicinemedicineAnimalsHumansEcology Evolution Behavior and SystematicsGeneticsMammalsHomoplasmySkeletal muscleGeneral Medicinemedicine.diseaseMitochondria MuscleDeathEndocrinologymedicine.anatomical_structureMutationChronic progressive external ophthalmoplegiaDie Naturwissenschaften
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Myo-, neuro-, gastrointestinal encephalopathy (MNGIE syndrome) due to partial deficiency of cytochrome-c-oxidase

1987

A 42-year-old woman had a 10-year history of external ophthalmoplegia, malabsorption resulting in chronic malnutrition, muscle atrophy and polyneuropathy. Computer tomography revealed hypodensity of her cerebral white matter. A metabolic disturbance consisted of lactic acidosis after moderate glucose loads with increased excretion of hydroxybutyric and fumaric acids. Post-mortem studies revealed gastrointestinal scleroderma as the morphological manifestation of her malabsorption syndrome, ocular and skeletal myopathy with ragged red fibers, peripheral neuropathy, vascular abnormalities of meningeal and peripheral nerve vessels. Biochemical examination of the liver and muscle tissues reveale…

AdultPathologymedicine.medical_specialtyMalabsorptionGastrointestinal DiseasesEncephalopathyRespiratory chainCytochrome-c Oxidase DeficiencyEyePathology and Forensic Medicine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineMuscular DiseasesMitochondrial myopathymedicineHumansMuscular dystrophy030304 developmental biology2. Zero hungerBrain Diseases0303 health sciencesbusiness.industryPeripheral Nervous System DiseasesSyndromemedicine.diseaseMitochondria MusclePeripheral neuropathyLactic acidosisFemaleNeurology (clinical)businessPolyneuropathy030217 neurology & neurosurgeryActa Neuropathologica
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Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon ca…

2017

Erratum inCorrection: Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway. [PLoS One. 2017]; International audience; Dietary polyphenols, derived from natural products, have received a great interest for their chemopreventive properties against cancer. In this study, we investigated the effects of phenolic extract of the oleaster leaves (PEOL) on tumor growth in mouse model and on cell death in colon cancer cell lines. We assessed the effect of oleaster leaf infusion on HCT116 (human colon cancer cell line) xenograft growth in athymic nude mice.…

0301 basic medicineLeavesCarcinoma Cellslcsh:MedicineApoptosisPlant ScienceMitochondrionEndoplasmic ReticulumBiochemistry[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineMedicine and Health SciencesMitochondrial calcium uptakeDiseaselcsh:ScienceEnergy-Producing OrganellesStainingchemistry.chemical_classificationSecretory PathwayMultidisciplinaryCell DeathPlant AnatomyCytochrome cCell StainingAnimal ModelsMitochondriaOlive Leaf ExtractChemistryOncologyExperimental Organism SystemsBiochemistryCell Processes030220 oncology & carcinogenesisPhysical SciencesCellular Structures and OrganellesResearch ArticleProgrammed cell deathActivationMouse Models[SDV.CAN]Life Sciences [q-bio]/CancerBioenergeticsBiologyResearch and Analysis MethodsColorectal-CancerCaspase-Dependent Apoptosis03 medical and health sciencesModel OrganismsPhenolsCytochrome-CColorectal CancerReactive oxygen speciesP53Cell growthProteinlcsh:RChemical CompoundsBiology and Life SciencesCancers and NeoplasmsPolyphenolsCell BiologyMolecular biology030104 developmental biologychemistrySpecimen Preparation and TreatmentApoptosisbiology.proteinCalciumlcsh:QPLoS ONE
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Structure of the Zymomonas mobilis respiratory chain: oxygen affinity of electron transport and the role of cytochrome c peroxidase

2014

The genome of the ethanol-producing bacterium Zymomonas mobilis encodes a bd-type terminal oxidase, cytochrome bc 1 complex and several c-type cytochromes, yet lacks sequences homologous to any of the known bacterial cytochrome c oxidase genes. Recently, it was suggested that a putative respiratory cytochrome c peroxidase, receiving electrons from the cytochrome bc 1 complex via cytochrome c 552, might function as a peroxidase and/or an alternative oxidase. The present study was designed to test this hypothesis, by construction of a cytochrome c peroxidase mutant (Zm6-perC), and comparison of its properties with those of a mutant defective in the cytochrome b subunit of the bc 1 complex (Zm…

ZymomonasbiologyCytochrome bc1Cytochrome c peroxidaseCytochrome cCytochrome dCytochrome-c PeroxidaseMicrobiologyMolecular biologyStandardElectron TransportOxygenBiochemistryCytochrome C1Coenzyme Q – cytochrome c reductasebiology.proteinCytochrome c oxidaseOxidoreductasesPhysiology and BiochemistryGene DeletionPeroxidaseMicrobiology
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Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
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The stability and functional properties of proteoliposomes mixed with dextran derivatives bearing hydrophobic anchor groups

1992

Liposomes composed of Escherichia coli phospholipid were coated with polysaccharides bearing hydrophobic palmitoyl anchors. The effect on the stability of liposomes without or with integral membrane proteins was investigated. A high concentration of hydrophobized dextrans protected the liposomes against detergent degradation, decreased the fluidity of the membranes, prevented fusion of the liposomes and enhanced their stability. Proteoliposomes containing beef heart cytochrome-c oxidase and the lactose transport carrier of E. coli were similarly affected by coating with the dextrans. Under these conditions both membrane proteins were still active. Long-term stability of the coated liposomes…

PROTEINMembrane FusionBiochemistryMembrane Potentialschemistry.chemical_compoundFUSIONINTEGRAL MEMBRANE PROTEINBINDINGIntegral membrane proteinLiposomeSymportersEscherichia coli ProteinsVesiclePROTEOLIPOSOMEDextransDEXTRAN DERIVATIVEBIOLOGICAL-MEMBRANESFluoresceinsMembraneCarbohydrate SequenceESCHERICHIA-COLIMonosaccharide Transport ProteinsCations DivalentMembrane FluidityProteolipidsMolecular Sequence DataBiophysicsPhospholipidFluorescence PolarizationLactose transportOXIDASECYTOCHROME-CVESICLESElectron Transport Complex IVHYDROPHOBIC ANCHOR GROUPEscherichia coliAnimalsKINETICSChromatographyMyocardiumMembrane ProteinsMembrane Transport ProteinsBiological membraneCell BiologyPROTON-MOTIVE FORCEMembrane proteinchemistryLiposomesCalciumCattleBiochimica et Biophysica Acta (BBA) - Biomembranes
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Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ?accidental cell death' (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. "Regulated cell death" (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to…

Biochemical Manifestations of Cell DeathISCHEMIA-REPERFUSION INJURYApoptosisReviewTransduction (genetics)0302 clinical medicineCASPASE INHIBITION SWITCHESAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction610 Medicine & healthCaspaseTUMOR-NECROSIS-FACTOR0303 health sciencesSettore BIO/17biologySettore BIO/11NeurodegenerationSettore BIO/13APOPTOSIS3. Good healthMedicina Básicacell death030220 oncology & carcinogenesiscell death; Morphologic Aspects of Cell Death; Biochemical Manifestations of Cell DeathSignal transductionDOMAIN-LIKE PROTEINIntracellularHumanSignal TransductionNecroptosiCYTOCHROME-C RELEASEOUTER-MEMBRANE PERMEABILIZATIONProgrammed cell deathCIENCIAS MÉDICAS Y DE LA SALUDSettore BIO/06Inmunología610 Medicine & healthCELL DEATHNOQ-VD-OPH03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALEddc:570Terminology as TopicAPOPTOSIS-INDUCING FACTORMIXED LINEAGE KINASEmedicineAnimalsHumansAnimals; Humans; Terminology as Topic; Apoptosis; Signal Transduction; Molecular Biology; Cell BiologyMorphologic Aspects of Cell DeathSettore BIO/10Molecular Biology030304 developmental biologyAnimalCell growthApoptosiBiology and Life SciencesCell Biologymedicine.diseaseMITOCHONDRIAL PERMEABILITY TRANSITIONApoptosisImmunologybiology.proteinNeuroscienceCell death and differentiation
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Identification of a novel compound heterozygote SCO2 mutation in cytochrome c oxidase deficient fatal infantile cardioencephalomyopathy

2006

UNLABELLED Fatal infantile cardioencephalomyopathy (OMIM No. 604377) is a disorder of the mitochondrial respiratory chain and is characterised by neonatal progressive muscular hypotonia and cardiomyopathy because of severe Cytochrome c oxidase deficiency. Here we report a novel mutation in the Cytochrome c oxidase assembly gene SCO2 in an infant with fatal infantile cardioencephalomyopathy despite normal initial metabolic screening. CONCLUSION In newborns with unexplained muscular hypotonia and cardiomyopathy genetic testing of mitochondrial respiratory chain disorders might be helpful to establish a final diagnosis and guide treatment decisions.

Heterozygotemedicine.medical_specialtyPathologyCardiomyopathyCytochrome-c Oxidase DeficiencyCompound heterozygositymedicine.disease_causeMitochondrial ProteinsFatal OutcomeMitochondrial EncephalomyopathiesInternal medicinemedicineHumansCytochrome c oxidaseGeneGenetic testingMutationMuscular hypotoniamedicine.diagnostic_testbiologybusiness.industryInfantGeneral Medicinemedicine.diseaseEndocrinologyMitochondrial respiratory chainMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleCardiomyopathiesCarrier ProteinsbusinessMolecular ChaperonesActa Paediatrica
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Monte Carlo simulation in phylogenies: an application to test the constancy of evolutionary rates.

1994

Monte Carlo simulation has commonly been used in phylogenetic studies to test different tree-reconstruction methods, and consequently, its application for testing evolutionary models can be considered as a natural extension of this usage. Repetitive simulation of a given evolutionary process, under the restrictions imposed by the model to be tested, along a determinate tree topology allow the estimate of probability distributions for the desired parameters. Next, the phylogenetic tree can be reconstructed again without the constraints of the model, and the parameter of interest, derived from this tree, can be compared to the corresponding probability distribution derived from the restricted…

Least-squares methodBiometryMonte Carlo methodCytochrome c GroupBiologySet (abstract data type)Hybrid Monte Carlosymbols.namesakeGeneticsAnimalsHumansComputer SimulationMolecular BiologyEcology Evolution Behavior and SystematicsMonte Carlo simulationPhylogenyPhylogenetic treeModels GeneticMolecular clockEvolutionary ratesMarkov chain Monte CarloTree (data structure)Genetic TechniquesMutationsymbolsProbability distributionCytochrome-cAlgorithmMonte Carlo MethodMonte Carlo molecular modelingParametric bootstrapJournal of molecular evolution
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Novel LRPPRC compound heterozygous mutation in a child with early-onset Leigh syndrome French-Canadian type: Case report of an Italian patient

2020

Abstract Background Mitochondrial diseases, also known as oxidative phosphorylation (OXPHOS) disorders, with a prevalence rate of 1:5000, are the most frequent inherited metabolic diseases. Leigh Syndrome French Canadian type (LSFC), is caused by mutations in the nuclear gene (2p16) leucine-rich pentatricopeptide repeat-containing (LRPPRC). It is an autosomal recessive neurogenetic OXPHOS disorder, phenotypically distinct from other types of Leigh syndrome, with a carrier frequency up to 1:23 and an incidence of 1:2063 in the Saguenay-Lac-St Jean region of Quebec. Recently, LSFC has also been reported outside the French-Canadian population. Patient presentation We report a male Italian (Sic…

MaleHypotonia - developmental delayPediatricsmedicine.medical_specialtyPopulationEncephalopathyCytochrome-c Oxidase DeficiencyCase ReportHypotoniaCompound heterozygosityDiagnosis Differential03 medical and health sciences0302 clinical medicineWhole-genome-sequencingHypotonia; developmental delay; Mitochondrial disease; Whole-exome sequencing; CCT5030225 pediatricsmedicineMissense mutationHumansGlobal developmental delayeducationeducation.field_of_studyComparative Genomic Hybridizationbusiness.industrylcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseHypotoniaHypoplasiaMitochondrial diseaseNeoplasm Proteinsdevelopmental delayNeonatal hypotoniaPhenotypeItalyWhole-exome sequencingMutationLSFCmedicine.symptomLeigh DiseaseCCT5business030217 neurology & neurosurgeryInfant Premature
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