Search results for "Endoplasm"

showing 10 items of 323 documents

The Mitochondria-Targeted Antioxidant MitoQ Modulates Mitochondrial Function and Endoplasmic Reticulum Stress in Pancreatic β Cells Exposed to Hyperg…

2019

Background/aims Mitochondria-targeted antioxidants such as mitoquinone (MitoQ) have demonstrated protective effects against oxidative damage in several diseases. The increase in reactive oxygen species (ROS) production during glucose metabolism in β cells can be exacerbated under hyperglycaemic conditions such as type 2 diabetes (T2D), thus contributing to β cell function impairment. In the present work, we aimed to evaluate the effect of MitoQ on insulin secretion, oxidative stress, endoplasmic reticulum (ER) stress and nuclear factor kappa B (NFκB) signalling in a pancreatic β cell line under normoglycaemic (NG, 11.1 mM glucose), hyperglycaemic (HG, 25 mM glucose) and lipidic (palmitic ac…

0301 basic medicinemedicine.medical_specialtyPhysiologyUbiquinoneCarbohydrate metabolismmedicine.disease_causeMitoQlcsh:PhysiologyPancreatic β cellsAntioxidantsProinflammatory cytokinelcsh:Biochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOrganophosphorus CompoundsInternal medicineCell Line TumorInsulin-Secreting CellsmedicineAnimalslcsh:QD415-436chemistry.chemical_classificationReactive oxygen speciesMitoQlcsh:QP1-981Endoplasmic reticulumGlutathioneEndoplasmic Reticulum StressType 2 DiabetesMitochondriaRatsOxidative Stress030104 developmental biologyEndocrinologyGlucosechemistry030220 oncology & carcinogenesisHyperglycemiaUnfolded protein responseER stressMitochondrial dysfunctionReactive Oxygen SpeciesOxidative stressSignal Transduction
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NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

2021

AbstractBackground and AimsNon-alcoholic fatty liver disease and related hepatic syndromes affect up to one third of the adult population. The molecular mechanisms underlying NAFL etiology remain elusive. Nuclear Protein 1 (NUPR1) expression increases upon cell injury in all organs and recently we report its active participation in the activation of the Unfolded Protein Response (UPR). The UPR typically maintains protein homeostasis, but downstream mediators of the pathway regulate metabolic functions, including lipid metabolism. NUPR1 and UPR increase have been reported in obesity and liver pathologies and the goal of this study was to investigate the roles of NUPR1 in this context.Methods…

0301 basic medicinemedicine.medical_specialtySettore MED/09 - Medicina InternaPPAR-a signalling UPRPeroxisome proliferator-activated receptorContext (language use)UPRDiet High-FatBiochemistry03 medical and health sciencesLiver diseaseMice0302 clinical medicineInternal medicineCell Line TumorGeneticsmedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsHomeostasisHumansMolecular Biologychemistry.chemical_classificationbusiness.industryEndoplasmic reticulumFatty liverNASHLipid metabolismlipotoxicitymedicine.diseaseEndoplasmic Reticulum StressLipid MetabolismNeoplasm Proteins030104 developmental biologyEndocrinologychemistryLipotoxicityLiverNAFLKnockout mouseUnfolded protein responseUnfolded Protein ResponsePPAR-a signallingSteatosisSteatohepatitisbusiness030217 neurology & neurosurgeryNUPR1Biotechnology
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Metabolic syndrome enhances endoplasmic reticulum, oxidative stress and leukocyte–endothelium interactions in PCOS

2017

Polycystic ovary syndrome (PCOS) is associated with insulin resistance, which can lead to metabolic syndrome (MetS). Oxidative stress and leukocyte-endothelium interactions are related to PCOS. Our aim was to evaluate whether the presence of MetS in PCOS patients can influence endoplasmic reticulum (ER) and oxidative stress and leukocyte-endothelium interactions.This was a prospective controlled study conducted in an academic medical center. The study population consisted of 148 PCOS women (116 without/32 with MetS) and 112 control subjects (87 without / 25 with MetS). Metabolic parameters, reactive oxygen species (ROS) production, ER stress markers (GRP78, sXBP1, ATF6), leukocyte-endotheli…

0301 basic medicinemedicine.medical_specialtyXBP1Endocrinology Diabetes and Metabolism030209 endocrinology & metabolismBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineEndocrinologyInsulin resistanceInternal medicineCell AdhesionLeukocytesmedicineHumansProspective StudiesEndoplasmic Reticulum Chaperone BiPMetabolic SyndromeInterleukin-6ATF6Endoplasmic Reticulum StressIntercellular Adhesion Molecule-1medicine.diseasePolycystic ovaryOxidative Stress030104 developmental biologyEndocrinologyUnfolded protein responseHomeostatic model assessmentCytokinesFemaleEndothelium VascularMetabolic syndromeReactive Oxygen SpeciesCell Adhesion MoleculesOxidative stressPolycystic Ovary SyndromeMetabolism
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Insulin Dissociates the Effects of Liver X Receptor on Lipogenesis, Endoplasmic Reticulum Stress, and Inflammation

2016

IF 4.258; International audience; Diabetes is characterized by increased lipogenesis as well as increased endoplasmic reticulum (ER) stress and inflammation. The nuclear hormone receptor liver X receptor (LXR) is induced by insulin and is a key regulator of lipid metabolism. It promotes lipogenesis and cholesterol efflux, but suppresses endoplasmic reticulum stress and inflammation. The goal of these studies was to dissect the effects of insulin on LXR action. We used antisense oligonucleotides to knock down Lxr alpha in mice with hepatocytespecific deletion of the insulin receptor and their controls. We found, surprisingly, that knock-out of the insulin receptor and knockdown of Lxr alpha …

0301 basic medicinemedicine.medical_treatmentLipid-metabolismResistanceBiochemistryHepatitisMESH: HepatitisMESH: Endoplasmic Reticulum Stresspolycyclic compoundsInsulinGene-expressionPhospholipidsLiver X ReceptorsMice KnockoutbiologyMESH : Gene Expression RegulationFatty-acid synthesisfood and beveragesEndoplasmic Reticulum StressOrphan Nuclear ReceptorsCultured-cellsLipidsMESH: Gene Expression RegulationMESH : Endoplasmic Reticulum StressMessenger-rnaLiverMESH: Orphan Nuclear ReceptorsGene Knockdown TechniquesLipogenesisFemalelipids (amino acids peptides and proteins)Signal Transductionliver X receptormedicine.medical_specialtyLxr-alphaMice Transgenicdigestive systemPhospholipid transfer proteinGene Expression Regulation Enzymologic03 medical and health sciencesInsulin resistanceMESH : HepatitisLysophosphatidylcholine acyltransferaseInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyLiver X receptorMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCrosses GeneticLipogenesisEndoplasmic reticulumInsulinElement-binding protein-1cMESH : LiverCell Biologymedicine.diseaseMESH : Orphan Nuclear ReceptorsReceptor InsulinMice Inbred C57BLInsulin receptor030104 developmental biologyEndocrinologyDiabetes Mellitus Type 2Gene Expression RegulationNuclear receptorbiology.proteinUnfolded protein responseInsulin ResistanceMESH: Liver
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Preproinsulin designer antigens excluded from endoplasmic reticulum suppressed diabetes development in nod mice by dna vaccination

2019

DNA vaccines against autoimmune type 1 diabetes (T1D) contain a nonpredictable risk to induce autoreactive T cell responses rather than a protective immunity. Little is known if (and how) antigen expression and processing requirements favor the induction of autoreactive or protective immune responses by DNA immunization. Here, we analyzed whether structural properties of preproinsulin (ppins) variants and/or subcellular targeting of ppins designer antigens influence the priming of effector CD8+ T cell responses by DNA immunization. Primarily, we used H-2b RIP-B7.1 tg mice, expressing the co-stimulator molecule B7.1 in beta cells, to identify antigens that induce or fail to induce autoreacti…

0301 basic medicinepreproinsulin/proinsulin antigensPreproinsulinlcsh:QH426-470type 1 diabetesMouse ModelsBiologyMajor histocompatibility complexArticleDNA vaccinationDNA vaccines03 medical and health sciences0302 clinical medicineImmune systemAntigenImmunityGeneticsmouse models:Science::Medicine [DRNTU]lcsh:QH573-671Molecular BiologyNOD micelcsh:Cytologylcsh:Geneticsendoplasmic reticulum030104 developmental biology030220 oncology & carcinogenesisImmunologybiology.proteinType 1 DiabetesMolecular MedicineCD8
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European contribution to the study of ROS : A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

2017

WOS: 000410470000009

0301 basic medicinereactive oxygen species ; reactive nitrogen species ; redox signaling ; oxidative stress ; antioxidants ; redox therapeuticsRedox signalingInternational CooperationSMOOTH-MUSCLE-CELLS[SDV]Life Sciences [q-bio]Clinical BiochemistryISCHEMIA-REPERFUSION INJURYReviewddc:616.07Bioinformaticsmedicine.disease_causeBiochemistryAntioxidants0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCost actionlcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSmedia_commonlcsh:R5-920Redox therapeuticsReactive nitrogen species3. Good healthVariety (cybernetics)MANGANESE SUPEROXIDE-DISMUTASECHRONIC GRANULOMATOUS-DISEASERisk analysis (engineering)ddc:540lcsh:Medicine (General)Oxidation-ReductionSignal TransductionSocieties ScientificPULMONARY ARTERIAL-HYPERTENSIONMedicinaEstrès oxidatiuBiology03 medical and health sciencesAntioxidants ; Oxidative Stress ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Redox Signaling ; Redox TherapeuticsJournal Articlemedicinemedia_common.cataloged_instanceAnimalsHumans[CHIM]Chemical SciencesEuropean UnionEuropean unionNITRIC-OXIDE SYNTHASETANDEM MASS-SPECTROMETRYMolecular BiologyMITOCHONDRIAL OXIDATIVE STRESSGROWTH-FACTOR-BETAOrganic ChemistryDisease progressionBiology and Life SciencesOxidation reductionManganese Superoxide Dismutase030104 developmental biologylcsh:Biology (General)Oxidative stressReactive oxygen species030217 neurology & neurosurgeryOxidative stressRedox biology
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alpha 2-COP is involved in early secretory traffic in Arabidopsis and is required for plant growth

2017

[EN] COP (coat protein) I-coated vesicles mediate intra-Golgi transport and retrograde transport from the Golgi to the endoplasmic reticulum. These vesicles form through the action of the small GTPase ADP-ribosylation factor 1 (ARF1) and the COPI heptameric protein complex (coatomer), which consists of seven subunits (alpha-, beta-, beta' -, gamma-, delta-, epsilon- and xi-COP). In contrast to mammals and yeast, several isoforms for coatomer subunits, with the exception of gamma and delta, have been identified in Arabidopsis. To understand the role of COPI proteins in plant biology, we have identified and characterized a loss-of-function mutant of alpha 2-COP, an Arabidopsis alpha-COP isofo…

0301 basic medicineα2-COPPhysiologyUbiquitin-Protein LigasesProtein subunitMutantSEC31ArabidopsisPlant ScienceEndoplasmic ReticulumCoatomer ProteinP24 family protein03 medical and health sciencessymbols.namesakeBotanyBIOQUIMICA Y BIOLOGIA MOLECULARCOPIICOPIISecretory pathwayCOPICoat proteinArabidopsis ProteinsChemistryEndoplasmic reticulumAlpha 2-COPBiological TransportCOPIGolgi apparatusSEC31.Cell biologyAlpha 1-COPα1-COP030104 developmental biologyCoatomerGolgi apparatussymbolsCOPII Golgi apparatusResearch Paper
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The Yeast eIF2 Kinase Gcn2 Facilitates H 2 O 2 -Mediated Feedback Inhibition of Both Protein Synthesis and Endoplasmic Reticulum Oxidative Folding du…

2021

Recombinant protein production is a known source of oxidative stress. However, knowledge of which reactive oxygen species are involved or the specific growth phase in which stress occurs remains lacking. Using modern, hypersensitive genetic H2O2-specific probes, microcultivation, and continuous measurements in batch culture, we observed H2O2 accumulation during and following the diauxic shift in engineered Saccharomyces cerevisiae, correlating with peak α-amylase production. In agreement with previous studies supporting a role of the translation initiation factor kinase Gcn2 in the response to H2O2, we find that Gcn2-dependent phosphorylation of eIF2α increases alongside translational atten…

0303 health sciencesEcologyChemistryEndoplasmic reticulumOxidative folding030302 biochemistry & molecular biologyApplied Microbiology and BiotechnologyCell biology03 medical and health sciencesCytosolProtein biosynthesisUnfolded protein responseProtein disulfide-isomeraseProtein kinase ATranslational attenuation030304 developmental biologyFood ScienceBiotechnologyApplied and Environmental Microbiology
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Disarrangement of Endoplasmic reticulum-mitochondria communication impairs Ca2+ homeostasis in FRDA

2020

AbstractFriedreich ataxia (FRDA) is a neurodegenerative disorder characterized by neuromuscular and neurological manifestations. It is caused by mutations in gene FXN, which results in loss of the mitochondrial protein frataxin. Endoplasmic Reticulum-mitochondria associated membranes (MAMs) are inter-organelle structures involved in the regulation of essential cellular processes, including lipid metabolism and calcium signaling. In the present study, we have analyzed in both, unicellular and multicellular models of FRDA, an analysis of calcium management and of integrity of MAMs. We observed that function of MAMs is compromised in our cellular model of FRDA, which was improved upon treatmen…

0303 health sciencesbiologyEndoplasmic reticulumLipid metabolismMitochondrionbiology.organism_classification3. Good healthCell biology03 medical and health sciences0302 clinical medicineFrataxinbiology.proteinMitochondrial calcium uptakeCellular modelDrosophila melanogaster030217 neurology & neurosurgery030304 developmental biologyCalcium signaling
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Genomic organization and promoter characterization of the gene encoding a putative endoplasmic reticulum chaperone, ERp29

2002

Abstract ERp29 is a soluble protein localized in the endoplasmic reticulum (ER) of eukaryotic cells, which is conserved in all mammalian species. The N-terminal domain of ERp29 displays sequence and structural similarity to the protein disulfide isomerase despite the lack of the characteristic double cysteine motif. Although the exact function of ERp29 is not yet known, it was hypothesized that it may facilitate folding and/or export of secretory proteins in/from the ER. ERp29 is induced by ER stress, i.e. accumulation of unfolded proteins in the ER. To gain an insight into the mechanisms regulating ERp29 expression we have cloned and characterized the rat ERp29 gene and studied in details …

5' Flanking RegionRecombinant Fusion ProteinsMolecular Sequence DataCHO CellsBiologyCell LineMiceCricetinaeSequence Homology Nucleic AcidGene expressionTumor Cells CulturedGeneticsAnimalsHumansRNA MessengerLuciferasesPromoter Regions GeneticProtein disulfide-isomeraseGeneHeat-Shock ProteinsPhylogenyBase SequenceGene Expression ProfilingEndoplasmic reticulumPromoter3T3 CellsDNAExonsSequence Analysis DNAGeneral MedicineMolecular biologyIntronsRatsHousekeeping geneSecretory proteinGenesUnfolded protein responseFemaleTranscription Initiation SiteSequence AlignmentHeLa CellsGene
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