Search results for "Mitocondris"

showing 4 items of 4 documents

MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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Early ERK1/2 activation promotes DRP1-dependent mitochondrial fission necessary for cell reprogramming.

2016

During the process of reprogramming to induced pluripotent stem (iPS) cells, somatic cells switch from oxidative to glycolytic metabolism, a transition associated with profound mitochondrial reorganization. Neither the importance of mitochondrial remodelling for cell reprogramming, nor the molecular mechanisms controlling this process are well understood. Here, we show that an early wave of mitochondrial fragmentation occurs upon expression of reprogramming factors. Reprogramming-induced mitochondrial fission is associated with a minor decrease in mitochondrial mass but not with mitophagy. The pro-fission factor Drp1 is phosphorylated early in reprogramming, and its knockdown and inhibition…

0301 basic medicineDynaminsSomatic cellMAP Kinase Signaling SystemScienceCèl·lulesCellInduced Pluripotent Stem CellsKruppel-Like Transcription FactorsGeneral Physics and AstronomyBiologyMitochondrionMitochondrial DynamicsGeneral Biochemistry Genetics and Molecular BiologyMitocondrisArticleCell LineProto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4MiceMitophagymedicineAnimalsPhosphorylationInduced pluripotent stem cellGeneticsMultidisciplinarySOXB1 Transcription FactorsQGeneral ChemistryCellular ReprogrammingCell biologyMitochondria030104 developmental biologymedicine.anatomical_structurePhosphorylationMitochondrial fissionReprogrammingOctamer Transcription Factor-3Nature communications
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Mitochondrial DNA Replacement Techniques to Prevent Human Mitochondrial Diseases.

2021

Background: Mitochondrial DNA (mtDNA) diseases are a group of maternally inherited genetic disorders caused by a lack of energy production. Currently, mtDNA diseases have a poor prognosis and no known cure. The chance to have unaffected offspring with a genetic link is important for the affected families, and mitochondrial replacement techniques (MRTs) allow them to do so. MRTs consist of transferring the nuclear DNA from an oocyte with pathogenic mtDNA to an enucleated donor oocyte without pathogenic mtDNA. This paper aims to determine the efficacy, associated risks, and main ethical and legal issues related to MRTs. Methods: A bibliographic review was performed on the MEDLINE and Web of S…

0301 basic medicinePoor prognosisLegal positionMitochondrial DNAFarmacologiaWeb of scienceMEDLINEReviewmitochondrial DNABioinformaticsDNA MitochondrialCatalysisMitocondrisInorganic Chemistrylcsh:Chemistry03 medical and health sciencesmitochondrial donation0302 clinical medicineMedicineHumansPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5Spectroscopymitochondrial diseases030219 obstetrics & reproductive medicinebusiness.industryOrganic ChemistryDonor oocyteGeneral MedicineDNAGenetic TherapyComputer Science ApplicationsNuclear DNAMitochondriaClinical trial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oocytesmitochondrial replacementthree-parent babybusinessInternational journal of molecular sciences
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Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.

2021

Background: Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods: Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigate…

medicine.medical_specialtyAging[SDV]Life Sciences [q-bio]Respiratory chainOxidative phosphorylationDiseases of the musculoskeletal systemGlucosephosphate DehydrogenaseMitocondrisLipid peroxidation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnvellimentPhysiology (medical)Internal medicineAdipocytemedicineNADPHAnimalsOrthopedics and Sports MedicineRespiratory exchange ratio030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesDisabilityFrailtybusiness.industryMusclesQM1-695Skeletal muscleGlucose 1-DehydrogenaseGlutathioneOriginal Articles3. Good healthMitochondriamedicine.anatomical_structureEndocrinologyGlucosechemistryRC925-935Human anatomyHealthspanOriginal ArticleAntioxidantbusinessReactive oxygen species030217 neurology & neurosurgeryJournal of cachexia, sarcopenia and muscle
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