Search results for "mitochondrial fusion"

showing 10 items of 15 documents

Are Mitochondrial Fusion and Fission Impaired in Leukocytes of Type 2 Diabetic Patients?

2016

Mitochondrial fusion/fission alterations have been evaluated in different tissues of type 2 diabetic (T2D) patients. However, it is not known whether mitochondrial dynamics is disturbed in the leukocytes of T2D patients and whether glycemic control affects its regulation. Anthropometric and metabolic parameters in 91 T2D patients (48 with glycated hemoglobin [HbA1c]6.5% and 43 with HbA1c6.5%) were characteristic of the disease when compared with 78 control subjects. We observed increased reactive oxygen species production in leukocytes from diabetic patients, together with a reduced mitochondrial oxygen consumption rate, especially in poorly controlled patients. Mitochondrial fusion was red…

0301 basic medicineAdultMalemedicine.medical_specialtyendocrine system diseasesEndotheliumPhysiologyClinical BiochemistryCell CommunicationBiologymedicine.disease_causeBiochemistryMitochondrial DynamicsMitochondrial Membrane Transport Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDiabetes mellitusmedicineLeukocytesHumansMolecular BiologyGeneral Environmental ScienceGlycemicAgedCase-control studyIncreased reactive oxygen species productionCell BiologyMiddle Agedmedicine.diseaseMitochondriaOxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structuremitochondrial fusionchemistryDiabetes Mellitus Type 2Gene Expression Regulation030220 oncology & carcinogenesisCase-Control StudiesGeneral Earth and Planetary SciencesFemaleGlycated hemoglobinEndothelium VascularReactive Oxygen SpeciesOxidative stressBiomarkersAntioxidantsredox signaling
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A Crucial Role of Mitochondrial Dynamics in Dehydration Resistance in Saccharomyces cerevisiae

2021

Mitochondria are dynamic organelles as they continuously undergo fission and fusion. These dynamic processes conduct not only mitochondrial network morphology but also activity regulation and quality control. Saccharomyces cerevisiae has a remarkable capacity to resist stress from dehydration/rehydration. Although mitochondria are noted for their role in desiccation tolerance, the mechanisms underlying these processes remains obscure. Here, we report that yeast cells that went through stationary growth phase have a better survival rate after dehydration/rehydration. Dynamic defective yeast cells with reduced mitochondrial genome cannot maintain the mitochondrial activity and survival rate o…

0301 basic medicineMitochondrial DNASaccharomyces cerevisiae ProteinsQH301-705.5030106 microbiologySaccharomyces cerevisiaeSaccharomyces cerevisiaeMitochondrionyeastMitochondrial DynamicsCatalysisArticleInorganic ChemistryDesiccation tolerance03 medical and health sciencesmedicineDehydrationPhysical and Theoretical ChemistryBiology (General)DesiccationMolecular BiologyQD1-999SpectroscopyMicrobial ViabilitybiologyDehydrationChemistryOrganic ChemistryCell CycleWild typeGeneral Medicinedynamicsmedicine.diseasebiology.organism_classificationYeastComputer Science ApplicationsCell biologyMitochondriaChemistry030104 developmental biologymitochondrial fusionGenome MitochondrialInternational Journal of Molecular Sciences
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Mitochondrial Dynamics: In Cell Reprogramming as It Is in Cancer

2017

Somatic cells can be reprogrammed into a pluripotent cellular state similar to that of embryonic stem cells. Given the significant physiological differences between the somatic and pluripotent cells, cell reprogramming is associated with a profound reorganization of the somatic phenotype at all levels. The remodeling of mitochondrial morphology is one of these dramatic changes that somatic cells have to undertake during cell reprogramming. Somatic cells transform their tubular and interconnected mitochondrial network to the fragmented and isolated organelles found in pluripotent stem cells early during cell reprogramming. Accordingly, mitochondrial fission, the process whereby the mitochond…

0301 basic medicinelcsh:Internal medicineInduced stem cellsSomatic cellReview ArticleCell BiologyBiologyEmbryonic stem cellCell biology03 medical and health sciences030104 developmental biologymitochondrial fusionMitochondrial fissionlcsh:RC31-1245Induced pluripotent stem cellMolecular BiologyCell potencyReprogrammingStem Cells International
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Nuclear-mitochondrial interaction.

2007

The biogenesis of mitochondria depends on the coordinated expression of nuclear and mitochondrial genomes. Consequently, the control of mitochondrial biogenesis and function depends on extremely complex processes requiring a variety of well orchestrated regulatory mechanisms. It is clear that the interplay of transcription factors and coactivators contributes to the expression of both nuclear and mitochondrial respiratory genes. In addition, the regulation of mitochondria biogenesis depends on proteins that, interacting with messenger RNAs for mitochondrial proteins, influence their metabolism and expression. Moreover, a tight regulation of the import and final assembly of mitochondrial pro…

Cell NucleusRNA-binding proteinRNA-binding proteinsCell BiologyCell CommunicationBiologyMitochondrionCell biologyEpigenesis GeneticMitochondriamitochondrial fusionMitochondrial biogenesisNeoplasmsMolecular MedicineAnimalsHumansMitochondrial fissionMolecular BiologyTranscription factorPost-transcriptional regulationBiogenesistranscriptional factorpost-transcriptional regulationTranscription FactorsMitochondrion
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The ARF GAPs ELMOD1 and ELMOD3 act at the Golgi and cilia to regulate ciliogenesis and ciliary protein traffic

2022

ELMODs are a family of three mammalian paralogs that display GTPase activating protein (GAP) activity towards a uniquely broad array of ADP-ribosylation factor (ARF) family GTPases that includes ARF-like (ARL) proteins. ELMODs are ubiquitously expressed in mammalian tissues, highly conserved across eukaryotes, and ancient in origin, being present in the last eukaryotic common ancestor. We described functions of ELMOD2 in immortalized mouse embryonic fibroblasts (MEFs) in the regulation of cell division, microtubules, ciliogenesis, and mitochondrial fusion. Here, using similar strategies with the paralogs ELMOD1 and ELMOD3, we identify novel functions and locations of these cell regulators a…

Cell divisionGTPase-activating proteinGolgi ApparatusGTPaseBiologyMicrotubulesMitochondrial Dynamicssymbols.namesakeMiceMicrotubuleCiliogenesisAnimalsCiliaMolecular BiologyADP-Ribosylation FactorsCiliumGTPase-Activating ProteinsCorrectionCell BiologyGolgi apparatusFibroblastsCell biologyCytoskeletal Proteinsmitochondrial fusionsymbolsSignal Transduction
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2020

Mitochondrial fusion and fission tailors the mitochondrial shape to changes in cellular homeostasis. Players of this process are the mitofusins, which regulate fusion of the outer mitochondrial membrane, and the fission protein DRP1. Upon specific stimuli, DRP1 translocates to the mitochondria, where it interacts with its receptors FIS1, MFF, and MID49/51. Another fission factor of clinical relevance is GDAP1. Here, we identify and discuss cysteine residues of these proteins that are conserved in phylogenetically distant organisms and which represent potential sites of posttranslational redox modifications. We reveal that worms and flies possess only a single mitofusin, which in vertebrates…

FIS1endocrine systemmitochondrial fusionChemistryMFN2MFN1Cellular homeostasisGeneral MedicineMitochondrionGenomeCysteineCell biologyCells
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Roles for ELMOD2 and Rootletin in ciliogenesis.

2021

AbstractELMOD2 is a GTPase activating protein (GAP) with uniquely broad specificity for ARF family GTPases. We previously showed that it acts with ARL2 in mitochondrial fusion and microtubule stability and with ARF6 during cytokinesis. Mouse embryonic fibroblasts deleted for ELMOD2 also displayed changes in cilia related processes including increased ciliation, multiciliation, ciliary morphology, ciliary signaling, centrin accumulation inside cilia, and loss of rootlets at centrosomes with loss of centrosome cohesion. Increasing ARL2 activity or overexpressing Rootletin reversed these defects, revealing close functional links between the three proteins. This was further supported by the fin…

GTPase-activating proteinBiologyMicrotubulesMitochondrial DynamicsCell Line03 medical and health sciencesMice0302 clinical medicineMicrotubuleGTP-Binding ProteinsCiliogenesisAnimalsHumansCiliaMolecular Biology030304 developmental biologyCytokinesisCentrosome0303 health sciencesADP-Ribosylation FactorsCiliumGTPase-Activating ProteinsCell BiologyArticlesFibroblastsCell biologyMitochondriaCytoskeletal Proteinsmitochondrial fusionCentrosomeCentrinRootletin030217 neurology & neurosurgeryCytokinesisSignal TransductionMolecular biology of the cell
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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The thiol switch C684 in Mitofusin-2 mediates redox-induced alterations of mitochondrial shape and respiration

2017

Mitofusin-2 (MFN2) is a GTPase in the outer mitochondrial membrane involved in the regulation of mitochondrial fusion and bioenergetics. MFN2 also plays a role in mitochondrial fusion induced by changes in the intracellular redox state. Adding oxidized glutathione (GSSG), the core cellular stress indicator, to mitochondrial preparations stimulates mitochondrial fusion by inducing disulphide bond-mediated oligomer formation of MFN2 and its homolog MFN1 which involve cysteine 684 (C684) of MFN2. Mitochondrial hyperfusion represents an adaptive stress response that confers transient protection by increasing mitochondrial ATP production but how this depends on the thiol switch C684 in MFN2 has …

Mice Knockout0301 basic medicineCell RespirationMFN2Cell BiologyOxidative phosphorylationMitochondrionBiologyMitochondrial apoptosis-induced channelGTP PhosphohydrolasesMitochondriaCell biologyMice03 medical and health sciencesCellular and Molecular NeuroscienceMitofusin-2030104 developmental biologymitochondrial fusionAnimalsMFN1Sulfhydryl CompoundsATP–ADP translocaseCell ShapeOxidation-ReductionCells CulturedNeurochemistry International
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Lack of GDAP1 induces neuronal calcium and mitochondrial defects in a knockout mouse model of Charcot-Marie-tooth neuropathy

2015

27 páginas, 9 figuras.

Mitochondrial proteinCancer Researchlcsh:QH426-470Nerve Tissue ProteinsBiologyMitochondrionCharcot-Marie-Tooth diseaseGDAP1 geneMiceGeneticsAutophagyAnimalsCalcium SignalingMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsCytoskeletonCalcium signalingGeneticsVoltage-dependent calcium channelEndoplasmic reticulumAutophagyBiología y Biomedicina / BiologíaAxonsCell biologyMitochondriaMitochondrialMice Inbred C57BLAlpha tubulinlcsh:Geneticsmitochondrial fusionKnockout mouseMitochondrial fissionCalcium ChannelsAnimal cellGene DeletionResearch Article
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