Search results for "DAS"

showing 10 items of 4164 documents

Aβ Induces Excitotoxicity Mediated by APC/C-Cdh1 Depletion That Can Be Prevented by Glutaminase Inhibition Promoting Neuronal Survival

2016

AbstractThe E3 ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) is activated by the fizzy-related protein homolog/CDC20-like protein 1 (cdh1) in post-mitotic neurons. Growing evidence suggests that dysregulation of APC/C-Cdh1 is involved in neurodegenerative diseases. Here we show in neurons that oligomers of amyloid beta (Aβ), a peptide related to Alzheimer’s disease, cause proteasome-dependent degradation of cdh1. This leads to a subsequent increase in glutaminase (a degradation target of APC/C-Cdh1), which causes an elevation of glutamate levels and further intraneuronal Ca2+ dysregulation, resulting in neuronal apoptosis. Glutaminase inhibition prevents glutamate excitotoxi…

0301 basic medicineProteasome Endopeptidase ComplexCell SurvivalAmyloid betaBlotting WesternExcitotoxicityHippocampusmedicine.disease_causeHippocampusArticleAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsAnimals Genetically ModifiedMice03 medical and health sciences0302 clinical medicineGlutaminasemedicineAnimalsRats WistarNeuronsAmyloid beta-PeptidesMultidisciplinarybiologyGlutaminaseCyclin-dependent kinase 5Glutamate receptorCyclin-Dependent Kinase 5Molecular biologyRatsUbiquitin ligase030104 developmental biologyApoptosisbiology.protein030217 neurology & neurosurgeryScientific Reports
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Phosphorylation and proteasome recognition of the mRNA- binding protein Cth2 facilitates yeast adaptation to iron deficiency

2018

Iron is an indispensable micronutrient for all eukaryotic organisms due to its participation as a redox cofactor in many metabolic pathways. Iron imbalance leads to the most frequent human nutritional deficiency in the world. Adaptation to iron limitation requires a global reorganization of the cellular metabolism directed to prioritize iron utilization for essential processes. In response to iron scarcity, the conserved Saccharomyces cerevisiae mRNA-binding protein Cth2, which belongs to the tristetraprolin family of tandem zinc finger proteins, coordinates a global remodeling of the cellular metabolism by promoting the degradation of multiple mRNAs encoding highly iron-consuming proteins.…

0301 basic medicineProteasome Endopeptidase ComplexSaccharomyces cerevisiae ProteinsIronPosttranslational regulationSaccharomyces cerevisiaeMrna bindingMicrobiology03 medical and health sciencesProtein stabilityTristetraprolinGene Expression Regulation FungalVirologyPolitical scienceProtein stabilitySerineRNA MessengerPhosphorylationIron deficiencyAdaptation PhysiologicalQR1-502Yeast030104 developmental biologyMutagenesisChristian ministryProtein Processing Post-TranslationalHumanities
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BAG3 regulates total MAP1LC3B protein levels through a translational but not transcriptional mechanism

2015

Autophagy is mainly regulated by post-translational and lipid modifications of ATG proteins. In some scenarios, the induction of autophagy is accompanied by increased levels of certain ATG mRNAs such as MAP1LC3B/LC3B, ATG5 or ATG12. However, little is known about the regulation of ATG protein synthesis at the translational level. The cochaperone of the HSP70 system BAG3 (BCL2-associated athanogene 3) has been associated to LC3B lipidation through an unknown mechanism. In the present work, we studied how BAG3 controls autophagy in HeLa and HEK293 cells. Our results showed that BAG3 regulates the basal amount of total cellular LC3B protein by controlling its mRNA translation. This effect was …

0301 basic medicineProteasome Endopeptidase ComplexTranscription GeneticATG8ATG5BiologyBAG3ATG1203 medical and health sciences0302 clinical medicineProtein biosynthesisHumansRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingGeneticsGene knockdownAutophagyCell BiologyLipidsBasic Research PaperCell biologyHEK293 Cells030104 developmental biologyProtein BiosynthesisProteolysisApoptosis Regulatory ProteinsLysosomesMicrotubule-Associated ProteinsMAP1LC3B030217 neurology & neurosurgeryHeLa Cells
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Allopurinol partially prevents disuse muscle atrophy in mice and humans

2018

AbstractDisuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The pro…

0301 basic medicineProteasome Endopeptidase Complexmedicine.medical_specialtyScience[SDV]Life Sciences [q-bio]Allopurinolmedicine.medical_treatmentAllopurinolHindlimbBed restArticleMice03 medical and health sciences0302 clinical medicineAtrophyPhysical Conditioning AnimalInternal medicineAnimalsHumansMedicineAnkle InjuriesMuscle SkeletalWastingSoleus muscleMultidisciplinaryUbiquitinbusiness.industryQRmedicine.diseaseMuscular Disorders AtrophicMuscle atrophy3. Good healthGoutMuscular Atrophy030104 developmental biologyEndocrinologyHindlimb SuspensionMedicinemedicine.symptombusiness030217 neurology & neurosurgerymedicine.drugScientific Reports
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Phosphorylation of meprin β controls its cell surface abundance and subsequently diminishes ectodomain shedding

2021

Meprin β is a zinc-dependent metalloprotease exhibiting a unique cleavage specificity with strong preference for acidic amino acids at the cleavage site. Proteomic studies revealed a diverse substrate pool of meprin β including the interleukin-6 receptor (IL-6R) and the amyloid precursor protein (APP). Dysregulation of meprin β is often associated with pathological conditions such as chronic inflammation, fibrosis, or Alzheimer's disease (AD). The extracellular regulation of meprin β including interactors, sheddases, and activators has been intensively investigated while intracellular regulation has been barely addressed in the literature. This study aimed to analyze C-terminal phosphorylat…

0301 basic medicineProtein Kinase C-alphaImmunoprecipitationmedia_common.quotation_subjectBiochemistry03 medical and health sciences0302 clinical medicineProtein Kinase C betaTumor Cells CulturedGeneticsAmyloid precursor proteinHumansPhosphorylationInternalizationMolecular BiologyProtein kinase Cmedia_commonbiologyChemistryCell MembraneMetalloendopeptidasesSheddaseCell biology030104 developmental biologyGene Expression RegulationEctodomainColonic NeoplasmsProteolysisbiology.proteinPhosphorylationExtracellular Space030217 neurology & neurosurgeryIntracellularBiotechnologyThe FASEB Journal
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Generation of three human iPSC lines from PLAN (PLA2G6-associated neurodegeneration) patients

2021

© 2021 The Authors.

0301 basic medicineQH301-705.5Cellular differentiationInduced Pluripotent Stem CellsNeuroaxonal Dystrophies:Cells::Stem Cells::Adult Stem Cells::Induced Pluripotent Stem Cells [ANATOMY]Biologymedicine.disease_cause:células::células madre::células madre adultas::células madre pluripotentes inducidas [ANATOMÍA]Sistema nerviós - DegeneracióCell LineDermal fibroblastGroup VI Phospholipases A203 medical and health sciencesKruppel-Like Factor 40302 clinical medicineSOX2medicineHumans:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Biology (General)Induced pluripotent stem cellMutationNeurodegenerationCell DifferentiationCell BiologyGeneral Medicinemedicine.diseaseCellular Reprogramming030104 developmental biologyKLF4:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]MutationCancer researchMalalties raresReprogramming030217 neurology & neurosurgeryGenèticaDevelopmental BiologyStem Cell Research
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Antiproliferative Effect of Elastin-Derived Peptide VGVAPG on SH-SY5Y Neuroblastoma Cells

2019

Throughout the lifetime of humans, the amount of stem cells and the rate of cell proliferation continue to decrease. Reactive oxygen species (ROS) are one among the many factors that promote stem cell aging. Both a decrease in the level of stem cells and increase in ROS production can lead to the development of different neurodegenerative diseases. This study was conducted to determine how the VGVAPG peptide, liberated from elastin during the aging process and under pathological conditions, affects ROS production and activities of antioxidant enzymes in undifferentiated, proliferating SH-SY5Y cells. SH-SY5Y cells were maintained in Dulbecco’s modified Eagle’s medium/nutrient mixture F-12 su…

0301 basic medicineSH-SY5YProliferationEnzyme-Linked Immunosorbent AssayToxicologySH-SY5YReal-Time Polymerase Chain ReactionSuperoxide dismutase03 medical and health sciencesNeuroblastoma0302 clinical medicineSuperoxide Dismutase-1Cell Line TumorHumansCell Proliferationchemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologyDose-Response Relationship DrugCell growthGeneral NeuroscienceGlutathione peroxidaseROSCatalaseCell biologyElastin-derived peptidesElastinPPAR gamma030104 developmental biologyKi-67 AntigenchemistryVGVAPGbiology.proteinOriginal ArticleStem cellReactive Oxygen SpeciesElastinOligopeptides030217 neurology & neurosurgeryFetal bovine serumNeurotoxicity Research
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The angiotensin‐(1‐7)/Mas receptor axis protects from endothelial cell senescence via klotho and Nrf2 activation

2019

Endothelial cell senescence is a hallmark of vascular aging that predisposes to vascular disease. We aimed to explore the capacity of the renin-angiotensin system (RAS) heptapeptide angiotensin (Ang)-(1-7) to counteract human endothelial cell senescence and to identify intracellular pathways mediating its potential protective action. In human umbilical vein endothelial cell (HUVEC) cultures, Ang II promoted cell senescence, as revealed by the enhancement in senescence-associated galactosidase (SA-β-gal+) positive staining, total and telomeric DNA damage, adhesion molecule expression, and human mononuclear adhesion to HUVEC monolayers. By activating the G protein-coupled receptor Mas, Ang-(1…

0301 basic medicineSenescenceAgingNF-E2-Related Factor 2medicine.medical_treatmentCellBiologyKlothoReceptors G-Protein-Coupled03 medical and health sciences0302 clinical medicineheme oxygenase‐1medicineHuman Umbilical Vein Endothelial CellsHumansReceptorKlothoKlotho ProteinsCells CulturedCellular SenescenceGlucuronidaseangiotensin‐(1‐7)Original PaperNuclear factor (erythroid-derived 2)-like 2nuclear factor (erythroid‐derived 2)‐like 2Vascular agingCell BiologyAngiotensin-(1-7)FarmaciaOriginal PapersPeptide FragmentsEndothelial senescenceCell biologyEndothelial stem cell030104 developmental biologyCytokinemedicine.anatomical_structureHeme oxygenase-1cardiovascular systemHuman umbilical vein endothelial cellAngiotensin I030217 neurology & neurosurgeryIntracellular
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Paracrine effects of human adipose-derived mesenchymal stem cells in inflammatory stress-induced senescence features of osteoarthritic chondrocytes

2016

Aging and exposure to stress would determine the chondrocyte phenotype in osteoarthritis (OA). In particular, chronic inflammation may contribute to stress-induced senescence of chondrocytes and cartilage degeneration during OA progression. Recent studies have shown that adipose-derived mesenchymal stem cells exert paracrine effects protecting against degenerative changes in chondrocytes. We have investigated whether the conditioned medium (CM) from adipose-derived mesenchymal stem cells may regulate senescence features induced by inflammatory stress in OA chondrocytes. Our results indicate that CM down-regulated senescence markers induced by interleukin-1β including senescence-associated β…

0301 basic medicineSenescenceAgingPathologymedicine.medical_specialtyadipose-derived mesenchymal stem cells conditioned mediumsenescenceCaveolin 1chondrocytesAdipose tissueInflammationmedicine.disease_cause03 medical and health sciencesParacrine signalling0302 clinical medicineOsteoarthritisParacrine CommunicationmedicineHumansCellular SenescenceInflammation030203 arthritis & rheumatologybiologySirtuin 1KinaseMesenchymal stem cellMesenchymal Stem CellsCell Biologybeta-GalactosidaseCell biologyOxidative Stress030104 developmental biologyAdipose Tissuebiology.proteinmedicine.symptomOxidative stressResearch PaperAging
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On the origin of BAG(3) and its consequences for an expansion of BAG3's role in protein homeostasis

2021

The B-cell CLL 2-associated athanogene (BAG) protein family in general and BAG3, in particular, are pivotal elements of cellular protein homeostasis, with BAG3 playing a major role in macroautophagy. In particular, in the contexts of senescence and degeneration, BAG3 has exhibited an essential role often related to its capabilities to organize and remove aggregated proteins. Exciting studies in different species ranging from human, murine, zebrafish, and plant samples have delivered vital insights into BAG3s' (and other BAG proteins') functions and their regulations. However, so far no studies have addressed neither BAG3's evolution nor its phylogenetic position in the BAG family.

0301 basic medicineSenescenceProteasome Endopeptidase ComplexProtein family610 MedizinBiologyProtein HomeostasisBAG3BiochemistryEvolution MolecularWW domain03 medical and health sciences0302 clinical medicineProtein Domains610 Medical sciencesAutophagyAnimalsHumansMolecular BiologyZebrafishCellular SenescencePhylogenyAdaptor Proteins Signal TransducingAutophagyFungiCell BiologyPlantsbiology.organism_classificationCell biology030104 developmental biologyProteostasis030220 oncology & carcinogenesisProteolysisProteostasisbiology.proteinApoptosis Regulatory ProteinsSignal TransductionJournal of Cellular Biochemistry
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