Search results for "MITO"

showing 10 items of 2513 documents

Análisis de la interacciones parásito-hospedador en el modelo Echinostoma caproni-roedor, con énfasis en los factores que determinan el curso de la i…

2015

En la presente Tesis Doctoral se analizan diferentes parámetros implicados en las relaciones parásito-hospedador en helmintiasis intestinales mediante la utilización del modelo experimental Echinostoma caproni-roedor. Con esta finalidad se estudian diversos aspectos inmunológicos, además de las alteraciones intestinales inducidas por la infección en dos sistemas parásito-hospedador: E. caproni-ratón y E. caproni-rata. Los resultados obtenidos ponen de manifiesto que el IFN-γ y el óxido nítrico son mediadores fundamentales en el desarrollo de infecciones crónicas en ratón, induciendo disfunción mitocondrial en las células del epitelio intestinal e hiperplasia tisular. No obstante, se sugiere…

Nematodainfección superpuestahiperplasia tisularhelminto intestinalEchinostoma caproniOxyuridaeinmunidad protectora:CIENCIAS DE LA VIDA [UNESCO]reactividad cruzadaUNESCO::CIENCIAS DE LA VIDArenovación epitelialproteomarelaciones parásito-hospedadorresistenciaIFN-γEchinostomatidaerataapoptosiscatepsinaSyphacia muris:CIENCIAS MÉDICAS [UNESCO]disfunción mitocondrialiNOSratónexpulsiónUNESCO::CIENCIAS MÉDICAScélulas epiteliales intestinales2D-DIGETrematodaTh17mucinainfección crónica
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Mitochondrial defects and neuromuscular degeneration caused by altered expression of Drosophila Gdap1: implications for the Charcot–Marie–Tooth neuro…

2014

One of the genes involved in Charcot-Marie-Tooth (CMT) disease, an inherited peripheral neuropathy, is GDAP1. In this work, we show that there is a true ortholog of this gene in Drosophila, which we have named Gdap1. By up- and down-regulation of Gdap1 in a tissue-specific manner, we show that altering its levels of expression produces changes in mitochondrial size, morphology and distribution, and neuronal and muscular degeneration. Interestingly, muscular degeneration is tissue-autonomous and not dependent on innervation. Metabolic analyses of our experimental genotypes suggest that alterations in oxidative stress are not a primary cause of the neuromuscular degeneration but a long-term c…

Nerve Tissue ProteinsDiseaseDegeneration (medical)BiologyMitochondrionMitochondrial Sizemedicine.disease_causeRetinaCharcot-Marie-Tooth DiseaseGeneticsmedicineAnimalsDrosophila ProteinsHumansMolecular BiologyGenePhylogenyGenetics (clinical)F-Box ProteinsNeurodegenerationNeuromuscular DiseasesGeneral MedicineAnatomymedicine.diseaseMitochondriaCell biologyTissue DegenerationDisease Models AnimalDrosophila melanogasterGene Expression RegulationMitochondrial SizeOxidative stressHuman Molecular Genetics
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Junctophilin-1 is a modifier gene of GDAP1-related Charcot-Marie-Tooth disease.

2014

Mutations in the GDAP1 gene cause different forms of Charcot-Marie-Tooth (CMT) disease, and the primary clinical expression of this disease is markedly variable in the dominant inheritance form (CMT type 2K; CMT2K), in which carriers of the GDAP1 p.R120W mutation can display a wide range of clinical severity. We investigated the JPH1 gene as a genetic modifier of clinical expression variability because junctophilin-1 (JPH1) is a good positional and functional candidate. We demonstrated that the JPH1-GDAP1 cluster forms a paralogon and is conserved in vertebrates. Moreover, both proteins play a role in Ca(2+) homeostasis, and we demonstrated that JPH1 is able to restore the store-operated Ca…

Nerve Tissue ProteinsDiseaseMitochondrionBiologyCell LineEvolution MolecularMiceCharcot-Marie-Tooth DiseaseGeneticsAnimalsHumansGenetic Predisposition to DiseaseStromal Interaction Molecule 1Molecular BiologyGeneGenetics (clinical)PhylogenyGenes ModifierActivator (genetics)Endoplasmic reticulumMembrane ProteinsSTIM1General MedicinePhenotypeMolecular biologyMitochondriaNeoplasm ProteinsMutationCalciumHomeostasisHuman molecular genetics
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The role of glia, mitochondria, and the immune system in glaucoma.

2009

Author(s): Tezel, Gulgun; Fourth ARVO/Pfizer Ophthalmics Research Institute Conference Working Group

Nerve degenerationRetinal Ganglion Cellsmedicine.medical_specialtyMitochondrial Diseasesbusiness.industryGlaucomaGlaucomaMitochondrionmedicine.diseaseAxonsMitochondriaImmune systemOphthalmologyImmune SystemOptic Nerve DiseasesmedicineHumansbusinessOptic nerve diseasesNeurogliaInvestigative ophthalmologyvisual science
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Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease

2007

Abstract Mutations in the mitochondrial protein GDAP1 are the cause of Charcot-Marie-Tooth type 4A disease (CMT4A), a severe form of peripheral neuropathy associated with either demyelinating, axonal or intermediate pheno-types. GDAP1 is located in the outer mitochondrial membrane and it seems that may be related with the mitochondrial network dynamics. We are interested to define cell expression in the nervous system and the effect of mutations in mitochondrial morphology and pathogenesis of the disease. We investigated GDAP1 expression in the nervous system and dorsal root ganglia (DRG) neuron cultures. GDAP1 is expressed in motor and sensory neurons of the spinal cord and other large neu…

Nervous systemCMT4A mutations and pathogenesisPathologymedicine.medical_specialtyperipheral neuropathyCharcot-Marie-Tooth type 4A diseaseMutation MissenseGene ExpressionImages in Cellular / Molecular MedicineNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_causeNervous SystemPathogenesisMicePurkinje CellsCharcot-Marie-Tooth DiseaseInterneuronsGanglia SpinalChlorocebus aethiopsmedicineAnimalsHumansNeurons AfferentCells CulturedMotor NeuronsMutationfusion and fission pathwayPyramidal CellsCell Biologymedicine.diseaseSpinal cordImmunohistochemistrymitochondrial dynamicsCell biologyOlfactory bulbRatsmedicine.anatomical_structurePeripheral neuropathynervous systemAnimals NewbornSpinal CordCOS CellsMolecular MedicineNeuronHeLa CellsJournal of Cellular and Molecular Medicine
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Expression of Drosophila Cabut during early embryogenesis, dorsal closure and nervous system development.

2010

cabut (cbt) encodes a transcription factor involved in Drosophila dorsal closure (DC), and it is expressed in embryonic epithelial sheets and yolk cell during this process upon activation of the Jun N-terminal kinase (JNK) signaling pathway. Additional studies suggest that cbt may have a role in multiple developmental processes. To analyze Cbt localization through embryogenesis, we generated a Cbt specific antibody that has allowed detecting new Cbt expression patterns. Immunohistochemical analyses on syncytial embryos and S2 cells reveal that Cbt is localized on the surface of mitotic chromosomes at all mitotic phases. During DC, Cbt is expressed in the yolk cell, in epidermal cells and in…

Nervous systemCentral Nervous SystemRecombinant Fusion ProteinsMitosisBiologybehavioral disciplines and activities03 medical and health sciencesGenes ReporterTubulinmental disordersPeripheral Nervous SystemGeneticsmedicineAnimalsDrosophila ProteinsPromoter Regions GeneticMolecular BiologyMitosis030304 developmental biologyRegulation of gene expressionGeneticsCell Nucleus0303 health sciencesSchneider 2 cells030302 biochemistry & molecular biologyEmbryogenesisGene Expression Regulation DevelopmentalEmbryoEmbryonic stem cellDorsal closureChromatin3. Good healthCell biologyProtein Structure Tertiarymedicine.anatomical_structureEpidermal CellsOrgan SpecificityDrosophilaLamininEpidermisDevelopmental BiologyTranscription FactorsGene expression patterns : GEP
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Spatio-temporal expression of Prospero is finely tuned to allow the correct development and function of the nervous system in Drosophila melanogaster.

2007

0012-1606 (Print) Comparative Study Journal Article Research Support, Non-U.S. Gov't; Adaptive animal behaviors depend upon the precise development of the nervous system that underlies them. In Drosophila melanogaster, the pan-neural prospero gene (pros), is involved in various aspects of neurogenesis including cell cycle control, axonal outgrowth, neuronal and glial cell differentiation. As these results have been generally obtained with null pros mutants inducing embryonic lethality, the role of pros during later development remains poorly known. Using several pros-Voila (prosV) alleles, that induce multiple developmental and behavioral anomalies in the larva and in adult, we explored the…

Nervous systemDrosophila melanogaster/*embryologyTranscription Factors/genetics/*metabolismNervous SystemPolymerase Chain Reaction0302 clinical medicineMessenger/*metabolismAntenno-maxillary complexNervous System/*embryologyDrosophila ProteinsProtein IsoformsRegulation of gene expressionGenetics0303 health sciencesbiologyProtein Isoforms/genetics/metabolismNeurogenesisGene Expression Regulation DevelopmentalNuclear ProteinsDrosophila Proteins/genetics/*metabolismPhenotypehumanitiesmedicine.anatomical_structureDrosophila melanogasterPhenotypeDrosophilaDrosophila melanogastereducationContext (language use)ProsperoNerve Tissue ProteinsNerve Tissue Proteins/genetics/*metabolism03 medical and health sciencesNuclear Proteins/genetics/*metabolismmedicineIn Situ Nick-End LabelingAnimalsRNA MessengerMolecular Biology030304 developmental biologyDNA PrimersDevelopmental/*physiologyProsperoCell Biologybiology.organism_classificationGlial cell differentiationMitotic activityGlial cellGene Expression RegulationCentral nervous systemNeuronal cellsRNANeuroscience030217 neurology & neurosurgeryDevelopmental BiologyTranscription FactorsDevelopmental biology
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The Role of Erythropoietin in Neuroprotection: Therapeutic Perspectives

2007

Nervous system diseases are very complex conditions comprising a large variety of local and systemic responses. Several therapeutic agents interfering with all or in part the biochemical steps that ultimately cause neuronal death have been demonstrated to be neuroprotective in preclinical models. However, all the agents so far investigated have inexorably failed in the phase III trials carried out. A large body of evidence suggests that the hormone erythropoietin (EPO), besides its well-known hematopoietic action, exerts beneficial effects in the central nervous system. EPO's effect has been assessed in several experimental models of brain and spinal cord injury thus becoming a serious cand…

Nervous systemEXPERIMENTAL SUBARACHNOID HEMORRHAGECentral nervous systemSIGNAL-TRANSDUCTIONPharmacologyModels BiologicalNeuroprotectionErythropoietin in neuroprotectionNEURONAL APOPTOSISCEREBROSPINAL-FLUIDAnimalsHumansMedicineIN-VIVO EVIDENCEErythropoietinSpinal cord injuryPharmacologyCEREBRAL-ISCHEMIACOMMON BETA-SUBUNITbusiness.industryRECOMBINANT-HUMAN-ERYTHROPOIETIN; GLYCOGEN-SYNTHASE KINASE-3-BETA; EXPERIMENTAL SUBARACHNOID HEMORRHAGE; COMMON BETA-SUBUNIT; IN-VIVO EVIDENCE; CEREBRAL-ISCHEMIA; SIGNAL-TRANSDUCTION; CEREBROSPINAL-FLUID; NEURONAL APOPTOSIS; CYTOKINE RECEPTORSRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseRecombinant ProteinsEnzyme ActivationStrokeClinical trialNeuroprotective AgentsTreatment Outcomemedicine.anatomical_structureErythropoietinGLYCOGEN-SYNTHASE KINASE-3-BETACYTOKINE RECEPTORSBone marrowMitogen-Activated Protein Kinasesbusinessmedicine.drugDrug News & Perspectives
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Hsp60 Friend and Foe of the Nervous System

2019

Hsp60 belongs to the subgroup of molecular chaperones named chaperonins and, typically, resides and functions in the mitochondria but it is also present in extramitochondrial sites. It chaperones client peptides as they fold to achieve the native conformation and also displays anti-stress roles by helping stress-damaged proteins regain a functional shape. Thus, Hsp60 is central to the integrity and functionality of mitochondria and energy production. All cells in the nervous system depend on Hsp60 so when the chaperonin malfunctions the consequences on nervous tissues are usually devastating, causing diverse diseases. These are the Hsp60 chaperonopathies, which can be genetic or acquired wi…

Nervous systemanimal structuresLeucodystrophiesfungiCentral nervous systemMitochondrionBiologyChaperoninCell biologymedicine.anatomical_structurePeripheral nervous systemmedicineHSP60Gene
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Expression analysis of jagged genes in zebrafish embryos

2005

The interaction of transmembrane Delta and Jagged/Serrate ligands with Notch receptors on neighboring cells is critically involved in cell specification during development. In zebrafish, the early expression of delta but not of jagged genes has been investigated in some detail. We have analyzed the sequence and embryonic expression pattern of the three zebrafish genes jagged1a, jagged1b, and jagged2. These genes, whose transcripts are detectable by in situ hybridization from early somitogenesis, are widely and dynamically expressed in embryos. Coexpression is limited, however, to the notochord and lens (jagged1a and jagged1b) and to the otic vesicle and pronephros (jagged1b and jagged2). Co…

Nervous systemanimal structuresNotchNotch signaling pathwayNotochordBiologystomatognathic systemSomitogenesisNotochordmedicineAnimalsPancreaSerrate-Jagged ProteinsSomitePlacodeZebrafishPhylogenyNotch signalingZebrafishGeneticsVertebrateCalcium-Binding ProteinsGene Expression Regulation DevelopmentalMembrane ProteinsCell BiologyZebrafish Proteinsbiology.organism_classificationCell biologyPronephrosmedicine.anatomical_structurezebrafish; Notch; JaggedEmbryoIntercellular Signaling Peptides and ProteinsPronephroOtic vesicleJaggedJagged-2 ProteinOtic PlacodesDevelopmental biologyIn situ hybridizationJagged/serrate geneEmbryo; In situ hybridization; Jagged/serrate genes; Nervous system; Notch signaling; Notochord; Pancreas; Placodes; Pronephros; Somites; Vertebrate; Zebrafish; Developmental Biology; Cell BiologyDevelopmental Biology
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