Search results for "Phosphorylation"

showing 10 items of 975 documents

Adaptive antioxidant methionine accumulation in respiratory chain complexes explains the use of a deviant genetic code in mitochondria

2008

Humans and most other animals use 2 different genetic codes to translate their hereditary information: the standard code for nuclear-encoded proteins and a modern variant of this code in mitochondria. Despite the pivotal role of the genetic code for cell biology, the functional significance of the deviant mitochondrial code has remained enigmatic since its first description in 1979. Here, we show that profound and functionally beneficial alterations on the encoded protein level were causative for the AUA codon reassignment from isoleucine to methionine observed in most mitochondrial lineages. We demonstrate that this codon reassignment leads to a massive accumulation of the easily oxidized …

Respiratory chainOxidative phosphorylationMitochondrionBiologyDNA MitochondrialGenomeAntioxidantsElectron Transportchemistry.chemical_compoundMethionineAnimalsIsoleucineInner mitochondrial membraneGeneticschemistry.chemical_classificationGenomeMultidisciplinaryMethionineFungiPlantsBiological SciencesGenetic codeBiological EvolutionAmino acidOxidative StresschemistryGenetic CodeMitochondrial MembranesDatabases Nucleic AcidProceedings of the National Academy of Sciences
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A new vicious cycle involving glutamate excitotoxicity, oxidative stress and mitochondrial dynamics

2011

Glutamate excitotoxicity leads to fragmented mitochondria in neurodegenerative diseases, mediated by nitric oxide and S-nitrosylation of dynamin-related protein 1, a mitochondrial outer membrane fission protein. Optic atrophy gene 1 (OPA1) is an inner membrane protein important for mitochondrial fusion. Autosomal dominant optic atrophy (ADOA), caused by mutations in OPA1, is a neurodegenerative disease affecting mainly retinal ganglion cells (RGCs). Here, we showed that OPA1 deficiency in an ADOA model influences N-methyl-D-aspartate (NMDA) receptor expression, which is involved in glutamate excitotoxicity and oxidative stress. Opa1enu/+mice show a slow progressive loss of RGCs, activation …

Retinal Ganglion CellsCancer ResearchReceptor expressionExcitotoxicityApoptosisNeurodegenerativeMitochondrionEyemedicine.disease_causeGTP PhosphohydrolasesMice0302 clinical medicineReceptorsoxidative stressPhosphorylationbcl-2-Associated X Protein0303 health sciencesbiologyGlutamate receptorMitochondriaUp-RegulationCell biologymitochondrial fusionAutosomal DominantOriginal Articlebcl-Associated Death ProteinMitochondrial fissionN-Methyl-D-AspartateBiotechnologymitochondrial fragmentationOncology and CarcinogenesisImmunologybcl-X ProteinSOD2Glutamic AcidReceptors N-Methyl-D-AspartateNMDA receptorsCell Line03 medical and health sciencesCellular and Molecular NeuroscienceBcl-2-associated X proteinOptic Atrophy Autosomal DominantmedicineAnimalsEye Disease and Disorders of Vision030304 developmental biologySuperoxide DismutaseNeurosciencesCell BiologyMolecular biologyeye diseasesOxidative StressOptic AtrophyMutationbiology.proteinOPA1 mutationBiochemistry and Cell Biologysense organsglutamate excitotoxicity030217 neurology & neurosurgeryCell Death & Disease
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PGC-1α signaling coordinates susceptibility to metabolic and oxidative injury in the inner retina.

2013

Retinal ganglion cells (RGCs), used as a common model of central nervous system injury, are particularly vulnerable to metabolic and oxidative damage. However, molecular mechanisms underlying this sensitivity have not been determined in vivo . PGC-1α (encoded by PPARGC1A ) regulates adaptive metabolism and oxidative stress responses in a tissue- and cell-specific manner. Aberrant PGC-1α signaling is implicated in neurodegeneration, but the mechanism underlying its role in central nervous system injury remains unclear. We provide evidence from a mouse model that PGC-1α expression and activity are induced in adult retina in response to metabolic and oxidative challenge. Deletion of Ppargc1a d…

Retinal Ganglion CellsCentral nervous systemOxidative phosphorylationBiologymedicine.disease_causeRetinal ganglionPathology and Forensic MedicineMicemedicineIn Situ Nick-End LabelingAnimalsHumansIn Situ HybridizationMice KnockoutRetinaReverse Transcriptase Polymerase Chain ReactionNeurodegenerationAnatomyTFAMmedicine.diseaseImmunohistochemistryPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyOxidative Stressmedicine.anatomical_structureAstrocytessense organsOxidative stressAstrocyteSignal TransductionTranscription FactorsThe American journal of pathology
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Oxidative stress in cardiovascular disease: successful translation from bench to bedside?

2007

Over the last decades, sound evidence has been generated that oxidative stress is one of the most potent inductors of endothelial dysfunction and is involved at all stages of atherosclerotic plaque evolution.1,2 Experimental and animal models provide a clear association between the amount of oxidative challenge and reversible vascular dysfunction that can be observed before permanent alterations of the vessel wall occur. Article p 1367 Important for cardiovascular biology is the consumption of nitric oxide (NO) by reactive oxygen species. Endothelium relaxant factor is a central molecule in vascular homeostasis as a modulator of endothelial tone and reactivity.3 It is produced by NO synthas…

RiskEndotheliumOxidative phosphorylation030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeArginineNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)medicineHumansEndothelial dysfunction030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesbiologybusiness.industryThrombosismedicine.diseaseAtherosclerosis3. Good healthVasodilationOxidative Stressmedicine.anatomical_structurechemistryCardiovascular DiseasesMyeloperoxidaseImmunologyHemorheologybiology.proteinEndothelium VascularCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesPeroxynitriteOxidative stressBiomarkersCirculation
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SERCA activity is reduced in DJ-1 mutant flies and human cells due to oxidative modification

2020

ABSTRACTDJ-1 is a causative gene for familial Parkinson’s disease (PD) with different functions, standing out its role against oxidative stress (OS). Accordingly, PD model flies harboring a mutation in the DJ-1β gene (the Drosophila ortholog of human DJ-1) show high levels of OS markers like protein carbonylation, a common post-translational modification that may alter protein function. To increase our understanding of PD pathogenesis as well as to discover potential therapeutic targets for pharmacological intervention, we performed a redox proteomic assay in DJ-1β mutant flies. Among the proteins that showed increased carbonylation levels in PD model flies, we found SERCA, an endoplasmic r…

SERCAChemistryActivator (genetics)Endoplasmic reticulumProtein CarbonylationMutantmedicineOxidative phosphorylationmedicine.disease_causeOxidative stressHomeostasisCell biology
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HSP110 promotes colorectal cancer growth through STAT3 activation.

2017

IF 7.932; International audience; Heat shock protein 110 (HSP110) is induced by different stresses and, through its anti-apoptotic and chaperoning properties, helps cells survive these adverse situations. In colon cancers, HSP110 is abnormally abundant. We have recently shown that colorectal cancer patients with microsatellite instability (MSI) had an improved response to chemotherapy because they harbor an HSP110-inactivating mutation (HSP110DE9). In this work, we used patient biopsies, human colorectal cancer cells grown in vitro and in vivo (xenografts), and intestinal crypts to demonstrate that HSP110 is also involved in colon cancer growth. We showed that HSP110 induces colon cancer ce…

STAT3 Transcription Factor0301 basic medicineCancer ResearchColorectal cancerBiopsyMice Nudecolorectal cancer[SDV.CAN]Life Sciences [q-bio]/CancerMouse model of colorectal and intestinal cancerBiologymedicine.disease_causeMolecular oncology[ SDV.CAN ] Life Sciences [q-bio]/CancerSTAT3Mice03 medical and health sciences0302 clinical medicineGrowth factor receptorCell Line TumorGeneticsmedicineAnimalsHumansHSP110 Heat-Shock ProteinsIntestinal MucosaPhosphorylationSTAT3Molecular BiologyCell ProliferationMicrosatellite instabilityCell cyclemedicine.diseaseMolecular biologydigestive system diseases3. Good health030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleColorectal NeoplasmsCarcinogenesisNeoplasm TransplantationHSP110Protein Binding
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Protein kinase CK2 governs the molecular decision between encephalitogenic T H 17 cell and T reg cell development

2016

T helper 17 (TH17) cells represent a discrete TH cell subset instrumental in the immune response to extracellular bacteria and fungi. However, TH17 cells are considered to be detrimentally involved in autoimmune diseases like multiple sclerosis (MS). In contrast to TH17 cells, regulatory T (Treg) cells were shown to be pivotal in the maintenance of peripheral tolerance. Thus, the balance between Treg cells and TH17 cells determines the severity of a TH17 cell-driven disease and therefore is a promising target for treating autoimmune diseases. However, the molecular mechanisms controlling this balance are still unclear. Here, we report that pharmacological inhibition as well as genetic ablat…

STAT3 Transcription Factor0301 basic medicineEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisCellMice Transgenicchemical and pharmacologic phenomenaBiologySeverity of Illness IndexT-Lymphocytes RegulatoryMice03 medical and health sciences0302 clinical medicineImmune systemmedicineAnimalsHumansIL-2 receptorPhosphorylationCasein Kinase IISTAT3MultidisciplinaryCell growthInterleukin-17Experimental autoimmune encephalomyelitisGranulocyte-Macrophage Colony-Stimulating FactorFOXP3Peripheral toleranceForkhead Transcription Factorshemic and immune systemsReceptors Interleukinmedicine.diseasePeptide FragmentsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureGene Expression RegulationImmunologybiology.proteinCancer researchTh17 CellsMyelin-Oligodendrocyte GlycoproteinSignal Transduction030215 immunologyProceedings of the National Academy of Sciences
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Chronic lymphocytic leukemia nurse-like cells express hepatocyte growth factor receptor (c-MET) and indoleamine 2,3-dioxygenase and display features …

2014

Hepatocyte growth factor, produced by stromal and follicular dendritic cells, and present at high concentrations in the sera of patients with chronic lymphocytic leukemia, prolongs the survival of leukemic B cells by interacting with their receptor, c-MET. It is, however, unknown whether hepatocyte growth factor influences microenvironmental cells, such as nurse-like cells, which deliver survival signals to the leukemic clone. We evaluated the expression of c-MET on nurse-like cells and monocytes from patients with chronic lymphocytic leukemia and searched for phenotypic/functional features supposed to be influenced by the hepatocyte growth factor/c-MET interaction. c-MET is expressed at hi…

STAT3 Transcription FactorC-MetStromal cellmedicine.medical_treatmentGene ExpressionBiologyMonocyteschemistry.chemical_compoundT-Lymphocyte SubsetsmedicineHumansIndoleamine-Pyrrole 23-DioxygenaseGrowth factor receptor inhibitorPhosphorylationIndoleamine 23-dioxygenaseCells CulturedFollicular dendritic cellsMacrophagesGrowth factorArticlesHematologyProto-Oncogene Proteins c-metLeukemia Lymphocytic Chronic B-CellCoculture TechniquesInterleukin-10C-MET; INDOLEAMINE 23-DIOXYGENASEchronic lymphocytic leukemia hepatocyte growth factor c-MET nurse-like cellshepatocyte growth factornurse-like cellschemistryHepatocyte Growth Factor ReceptorCancer researchchronic lymphocytic leukemiaHepatocyte growth factorC-METINDOLEAMINE 23-DIOXYGENASEmedicine.drugHaematologica
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Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
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Parthenolide sensitizes hepatocellular carcinoma cells to trail by inducing the expression of death receptors through inhibition of STAT3 activation

2011

This article shows that HepG2, Hep3B, and SK-Hep1 cells, three lines of human hepatocellular carcinoma (HCC) cells, are resistant to apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Parthenolide, a sesquiterpene lactone found in European feverfew, has been shown to exert both anti-inflammatory and anti-cancer activities. This article demonstrates that co-treatment with parthenolide and TRAIL-induced apoptosis with synergistic interactions in the three lines of HCC cells. In order to explain these effects we ascertained that parthenolide increased either at protein or mRNA level the total content of death receptors TRAIL-R1 and -R2 as well as their surfac…

STAT3 Transcription FactorCarcinoma HepatocellularPhysiologyClinical BiochemistryCellDown-RegulationTRAILApoptosisPharmacologyParthenolideSTAT3TNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundSettore BIO/10 - BiochimicamedicineHumansParthenolidePhosphorylationReceptorSTAT3CaspaseJanus KinasesbiologyLiver NeoplasmsProto-Oncogene Proteins c-mdm2Hep G2 CellsReceptors Death DomainCell BiologyapoptosiEnzyme ActivationGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryCell cultureApoptosisCaspasesbiology.proteinSTAT proteinDrug Screening Assays AntitumorTumor Suppressor Protein p53SesquiterpenesJournal of Cellular Physiology
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