Search results for "mTOR"

showing 10 items of 275 documents

2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy

2012

Despite recent advances in the development of new cancer therapies, the treatment options for glioma remain limited, and the survival rate of patients has changed little over the past three decades. Here, we show that 2-hydroxyoleic acid (2OHOA) induces differentiation and autophagy of human glioma cells. Compared to the current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficiently and, unlike TMZ, tumor relapse was not observed following 2OHOA treatment. The novel mechanism of action of 2OHOA is associated with important changes in membrane-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glioma cells bef…

MaleProgrammed cell deathTime FactorsCell SurvivalMAP Kinase Signaling SystemCellular differentiationMice NudeAntineoplastic AgentsOleic AcidsBiologyglioma biomarkerfatty acidsMembrane LipidsMicePhosphatidylinositol 3-Kinases2-Hydroxyoleic AcidGliomaCell Line TumormedicineAutophagyTemozolomideAnimalsHumansPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinaryTemozolomideMicroscopy ConfocalDose-Response Relationship DrugCell growthCell MembraneRetinoblastoma proteinCell DifferentiationGliomaBiological Sciencesmedicine.diseaseXenograft Model Antitumor AssaysCell biologyDacarbazineProtein TransportCancer researchbiology.proteinras Proteinssphingomyelin synthaseProto-Oncogene Proteins c-aktcancer drug targetmedicine.drug
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Lysosomal Signaling Licenses Embryonic Stem Cell Differentiation via Inactivation of Tfe3

2019

International audience; Self-renewal and differentiation of pluripotent murine embryonic stem cells (ESCs) is regulated by extrinsic signaling pathways. It is less clear whether cellular metabolism instructs developmental progression. In an unbiased genome-wide CRISPR/Cas9 screen, we identified components of a conserved amino-acid-sensing pathway as critical drivers of ESC differentiation. Functional analysis revealed that lysosome activity, the Ragulator protein complex, and the tumor-suppressor protein Folliculin enable the Rag GTPases C and D to bind and seclude the bHLH transcription factor Tfe3 in the cytoplasm. In contrast, ectopic nuclear Tfe3 represses specific developmental and met…

MaleTranscription GeneticGTPaseGTP PhosphohydrolasesPATHWAYMice0302 clinical medicineNeural Stem CellsCRISPRTUMOR-SUPPRESSORCell Self RenewalPhosphorylationSPECIFICATIONdevelopmental disorder0303 health sciencesGenomeBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell DifferentiationMouse Embryonic Stem CellsFlcndifferentiationCell biologymedicine.anatomical_structuremTORMolecular MedicineFemaleSignal transductionProtein BindingSignal TransductionRECRUITMENTBiology03 medical and health sciencesRag GTPasesLysosomeGeneticsmedicineAnimalsHumansPoint MutationNAIVE PLURIPOTENCYAMINO-ACID LEVELSTranscription factorAllelesPI3K/AKT/mTOR pathway030304 developmental biologyCOMPLEXFOLLICULINRagulatorCell Biologypluripotencyembryonic stem cellEmbryonic stem cellTfe3[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsCytoplasmLysosomes030217 neurology & neurosurgeryCell Stem Cell
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Inducible NO synthase confers chemoresistance in head and neck cancer by modulating survivin

2009

The dual role of the inducible NO synthase (iNOS) and NO signaling in head and neck squamous cell carcinoma (HNSCC) is a complex and can both promote or inhibit tumor progression. However, the underlying molecular mechanisms are not yet resolved in detail. We show for the first time that conditions, favoring low NO levels conferred resistance against cisplatin/taxol-induced apoptosis in HNSCC cell lines. Cytoprotection was mediated by survivin, because we observed its upregulation subsequent to low doses of the NO donors S-nitroso-N-acetyl-penicillamine (SNAP) and sodium nitroprusside (SNP) or ectopic expression of physiologic amounts of iNOS. Also, RNAi-mediated depletion of survivin block…

MaleUmbilical VeinsCancer ResearchSurvivinFluorescent Antibody TechniqueNitric Oxide Synthase Type IIApoptosisp38 Mitogen-Activated Protein KinasesInhibitor of Apoptosis ProteinsImmunoenzyme TechniquesPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundLY294002Enzyme InhibitorsRNA Small InterferingAged 80 and overReverse Transcriptase Polymerase Chain ReactionCell CycleMiddle AgedCell cycleOncologyHead and Neck NeoplasmsCarcinoma Squamous CellFemaleMicrotubule-Associated ProteinsNitroprussidePaclitaxelImmunoblottingAntineoplastic AgentsS-Nitroso-N-AcetylpenicillamineBiologyCell LineDownregulation and upregulationSurvivinmedicineHumansNitric Oxide DonorsRNA MessengerneoplasmsProtein kinase BNitritesPI3K/AKT/mTOR pathwayAgedmedicine.diseaseAntineoplastic Agents PhytogenicHead and neck squamous-cell carcinomachemistryDrug Resistance NeoplasmTumor progressionImmunologyCancer researchEndothelium VascularCisplatinProto-Oncogene Proteins c-aktInternational Journal of Cancer
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Role of mTOR-regulated autophagy in spine pruning defects and memory impairments induced by binge-like ethanol treatment in adolescent mice.

2021

Abstract Adolescence is a brain maturation developmental period during which remodeling and changes in synaptic plasticity and neural connectivity take place in some brain regions. Different mechanism participates in adolescent brain maturation, including autophagy that plays a role in synaptic development and plasticity. Alcohol is a neurotoxic compound and its abuse in adolescence induces neuroinflammation, synaptic and myelin alterations, neural damage and behavioral impairments. Changes in synaptic plasticity and its regulation by mTOR have also been suggested to play a role in the behavioral dysfunction of binge ethanol drinking in adolescence. Therefore, by considering the critical ro…

MaleautophagyDendritic spineSynaptic pruningPeriod (gene)synaptic pruningBiologyPathology and Forensic MedicineBinge Drinkingbinge ethanol treatmentMyelinMicemedicineAnimalsPI3K/AKT/mTOR pathwayNeuroinflammationResearch Articlescognitive functionMemory DisordersNeuronal PlasticityGeneral NeuroscienceTOR Serine-Threonine KinasesAutophagyBraindendritic spinesMice Inbred C57BLmedicine.anatomical_structureSynaptic plasticitymTORFemaleadolescenceNeurology (clinical)NeuroscienceResearch ArticleBrain pathology (Zurich, Switzerland)
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Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
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Cannabinoid receptor 1 and acute resistance exercise – In vivo and in vitro studies in human skeletal muscle

2015

Abstract Aim This study aimed to determine whether Cannabinoid receptor 1 (CB1) is involved in mammalian target of rapamycin (mTOR) signaling and skeletal muscle protein synthesis. Methods This study used human vastus lateralis skeletal muscle biopsies obtained before and after a resistance exercise (RE) bout in young men (n = 18). The signaling mechanisms were studied in vitro in human myotubes. Protein expression was determined by Western blot and confocal microscopy, and gene expression by quantitative PCR. Protein synthesis was measured in vitro using puromycin-based SuNSET technique. Results In human skeletal muscle, an anabolic stimulus in the form of RE down-regulated CB1 expression.…

Malemedicine.medical_specialtyPhysiologyMAP Kinase Signaling SystemMuscle Fibers SkeletalGene ExpressionSkeletal muscleP70-S6 Kinase 1Cell Cycle ProteinsBiochemistryCell LineCellular and Molecular NeuroscienceYoung AdultEndocrinologyPiperidinesReceptor Cannabinoid CB1Internal medicinemedicineCannabinoid receptor type 2HumansCannabinoid receptor 1PhosphorylationMuscle Skeletalta315PI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingChemistryMyogenesista1184Eukaryotic initiation factor 4E bindingSkeletal muscleRibosomal Protein S6 Kinases 70-kDaResistance TrainingPhosphoproteinsResistance exerciseCell biologymedicine.anatomical_structureEndocrinologyRibosomal protein s6Protein BiosynthesismTOR signalingPhosphorylationPyrazolesProtein synthesisProtein Processing Post-TranslationalPeptides
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DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non-Atopic Asthma

2019

A high body mass (BMI) index has repeatedly been associated with non-atopic asthma, but the biological mechanism linking obesity to asthma is still poorly understood. We aimed to test the hypothesis that inflammation and/or innate immunity plays a role in the obesity-asthma link. DNA methylome was measured in blood samples of 61 non-atopic participants with asthma and 146 non-atopic participants without asthma (non-smokers for at least 10 years) taking part in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) study. Modification by DNA methylation of the association of BMI or BMI change over 10 years with adult-onset asthma was examined at each CpG sit…

MaleobesityNon-atopic asthmaHealth Toxicology and Mutagenesislcsh:MedicineToxicologyBody Mass IndexCohort StudiesMice0302 clinical medicineMedicineinnate immunitynon-atopic asthmaInnate immunity0303 health sciencesDNA methylationNF-kappa Bepigenome-wide association study3. Good healthCpG siteDNA methylationFemaleEpigeneticsmedicine.symptomGlucocorticoidmedicine.drugAdultMAP Kinase Signaling SystemInflammationArticle03 medical and health sciencesEpigenome-wide association studyMD MultidisciplinaryAnimalsHumansObesityEpigeneticsadult-onset asthmaPI3K/AKT/mTOR pathway030304 developmental biologyAsthmaInflammationepigeneticsbusiness.industrylcsh:RPublic Health Environmental and Occupational Healthmedicine.diseaseObesityAsthmarespiratory tract diseasesPPAR gamma030228 respiratory systeminflammationImmunologybusinessAdult-onset asthmaInternational Journal of Environmental Research and Public Health
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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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β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8+ T cells through regulation of IL-10

2015

Recent studies have demonstrated that β-catenin in DCs serves as a key mediator in promoting both CD4(+) and CD8(+) T-cell tolerance, although how β-catenin exerts its functions remains incompletely understood. Here we report that activation of β-catenin in DCs inhibits cross-priming of CD8(+) T cells by up-regulating mTOR-dependent IL-10, suggesting blocking β-catenin/mTOR/IL-10 signaling as a viable approach to augment CD8(+) T-cell immunity. However, vaccination of DC-β-catenin(-/-) (CD11c-specific deletion of β-catenin) mice surprisingly failed to protect them against tumor challenge. Further studies revealed that DC-β-catenin(-/-) mice were deficient in generating CD8(+) T-cell immunit…

Mice KnockoutImmunity CellularMultidisciplinaryTOR Serine-Threonine KinasesPriming (immunology)Dendritic CellsBiologyBiological SciencesCD8-Positive T-LymphocytesCancer VaccinesCell biologyInterleukin-10Interleukin 10MiceMediatorImmunityCateninNeoplasmsImmunologyCytotoxic T cellAnimalsPI3K/AKT/mTOR pathwayCD8beta Catenin
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Blocking of myostatin and activins increase muscle protein synthesis and mTORC1 signaling but decreases capillary density

2012

Muscle proteinbiologyMtorc1 signalingCapillary densityBlocking (radio)ChemistryGeneticsbiology.proteinMyostatinMolecular BiologyBiochemistryBiotechnologyCell biologyThe FASEB Journal
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