Search results for "Phosphorylation"

showing 10 items of 975 documents

Trx2p-dependent Regulation of Saccharomyces cerevisiae Oxidative Stress Response by the Skn7p Transcription Factor under Respiring Conditions

2013

The whole genome analysis has demonstrated that wine yeasts undergo changes in promoter regions and variations in gene copy number, which make them different to lab strains and help them better adapt to stressful conditions during winemaking, where oxidative stress plays a critical role. Since cytoplasmic thioredoxin II, a small protein with thiol-disulphide oxidoreductase activity, has been seen to perform important functions under biomass propagation conditions of wine yeasts, we studied the involvement of Trx2p in the molecular regulation of the oxidative stress transcriptional response on these strains. In this study, we analyzed the expression levels of several oxidative stress-related…

Saccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeBlotting WesternMolecular Sequence Datalcsh:MedicineWineOxidative phosphorylationSaccharomyces cerevisiaemedicine.disease_causePolymerase Chain ReactionThioredoxinsGene Expression Regulation FungalGene expressionmedicineImmunoprecipitationPhosphorylationlcsh:ScienceTranscription factorHeat-shock responseDNA PrimersRegulation of gene expressionMultidisciplinarybiologyBase Sequencelcsh:RPromoterbiology.organism_classificationCatalasebeta-GalactosidaseYeastGene regulationDNA-Binding ProteinsOxidative StressBiochemistryOxidative stresslcsh:QGene expressionThioredoxinTranscription factorOxidative stressGene DeletionResearch ArticlePlasmidsTranscription FactorsPLoS ONE
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Saccharomyces cerevisiae Glutaredoxin 5-deficient Cells Subjected to Continuous Oxidizing Conditions Are Affected in the Expression of Specific Sets …

2004

The Saccharomyces cerevisiae GRX5 gene codes for a mitochondrial glutaredoxin involved in the synthesis of iron/sulfur clusters. Its absence prevents respiratory growth and causes the accumulation of iron inside cells and constitutive oxidation of proteins. Null ⌬grx5 mu- tants were used as an example of continuously oxidized cells, as opposed to situations in which oxidative stress is instantaneously caused by addition of external oxi- dants. Whole transcriptome analysis was carried out in the mutant cells. The set of genes whose expression was affected by the absence of Grx5 does not significantly overlap with the set of genes affected in respiratory petite mutants. Many Aft1-dependent ge…

Saccharomyces cerevisiae ProteinsTranscription GeneticIronSaccharomyces cerevisiaeMutantProtein Array AnalysisDown-RegulationSaccharomyces cerevisiaeOxidative phosphorylationmedicine.disease_causeProtein oxidationBiochemistryOxygen ConsumptionGene Expression Regulation FungalIron-Binding ProteinsGlutaredoxinmedicineRNA MessengerMolecular BiologyGlutaredoxinsbiologyMembrane ProteinsNuclear ProteinsProteinsRNA-Binding ProteinsCell BiologyBlotting Northernbiology.organism_classificationCarbonUp-RegulationOxygenOxidative StressRegulonCCAAT-Binding FactorDatabases as TopicBiochemistryMutationFrataxinbiology.proteinOxidoreductasesReactive Oxygen SpeciesOxidative stressTranscription FactorsJournal of Biological Chemistry
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Impact of High pH Stress on Yeast Gene Expression: A Comprehensive Analysis of mRNA Turnover During Stress Responses.

2015

Environmental alkalinisation represents a stress condition for yeast Saccharomyces cerevisiae, to which this organism responds with extensive gene expression remodelling. We show here that alkaline pH causes an overall decrease in the transcription rate (TR) and a fast destabilisation of mRNAs, followed by a more prolonged stabilisation phase. In many cases, augmented mRNA levels occur without the TR increasing, which can be attributed to mRNA stabilisation. In contrast, the reduced amount of mRNAs is contributed by both a drop in the TR and mRNA stability. A comparative analysis with other forms of stress shows that, unlike high pH stress, heat-shock, osmotic and oxidative stresses present…

Saccharomyces cerevisiae ProteinsTranscription GeneticRNA StabilitySaccharomyces cerevisiaeBiophysicsSaccharomyces cerevisiaeOxidative phosphorylationBiochemistryStress (mechanics)Stress PhysiologicalStructural BiologyGene Expression Regulation FungalGene expressionGeneticsRNA MessengerDestabilisationRNA Processing Post-TranscriptionalMolecular BiologyGeneMessenger RNAbiologyHydrogen-Ion Concentrationbiology.organism_classificationYeastCell biologyBiochemistryGene-Environment Interaction
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Hyperphosphorylation of Msn2p and Msn4p in response to heat shock and the diauxic shift is inhibited by cAMP in Saccharomyces cerevisiae.

2000

In response to various stresses, as well as during the diauxic transition, the Msn2p and Msn4p transcription factors of Saccharomyces cerevisiae are activated and induce a large set of genes. This activation is inhibited by the Ras/cAMP/PKA (cAMP-dependent protein kinase) pathway. Here we show by immunoblotting experiments that Msn2p and Msn4p are phosphorylated in vivo during growth on glucose, and become hyperphosphorylated at the diauxic transition and upon heat shock. This hyperphosphorylation is correlated with activation of Msn2/4p-dependent transcription. An increased level of cAMP prevents and reverses these hyperphosphorylations, indicating that kinases other than PKA are involved.…

Saccharomyces cerevisiae ProteinsbiologyKinaseSaccharomyces cerevisiaeImmunoblottingHyperphosphorylationSaccharomyces cerevisiaebiology.organism_classificationAlkaline PhosphataseMicrobiologyCyclic AMP-Dependent Protein KinasesCell biologyDNA-Binding ProteinsBiochemistryTranscription (biology)Gene Expression Regulation FungalCyclic AMPPhosphorylationHeat shockPhosphorylationProtein kinase ATranscription factorHeat-Shock ResponseTranscription FactorsMicrobiology (Reading, England)
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Phosphorylation of the Usher syndrome 1G protein SANS controls Magi2-mediated endocytosis.

2014

Item does not contain fulltext The human Usher syndrome (USH) is a complex ciliopathy with at least 12 chromosomal loci assigned to three clinical subtypes, USH1-3. The heterogeneous USH proteins are organized into protein networks. Here, we identified Magi2 (membrane-associated guanylate kinase inverted-2) as a new component of the USH protein interactome, binding to the multifunctional scaffold protein SANS (USH1G). We showed that the SANS-Magi2 complex assembly is regulated by the phosphorylation of an internal PDZ-binding motif in the sterile alpha motif domain of SANS by the protein kinase CK2. We affirmed Magi2's role in receptor-mediated, clathrin-dependent endocytosis and showed tha…

Scaffold proteinGuanylate kinaseMolecular Sequence DataPrimary Cell CultureNerve Tissue ProteinsBiologyEndocytosisPhotoreceptor cellExocytosisMiceCiliogenesisGeneticsmedicineAnimalsHumansProtein Interaction Domains and MotifsAmino Acid SequencePhosphorylationRNA Small InterferingSensory disorders Radboud Institute for Molecular Life Sciences [Radboudumc 12]Molecular BiologyGenetics (clinical)Adaptor Proteins Signal TransducingBinding SitesGeneral MedicineClathrinEndocytosisCell biologyMice Inbred C57BLRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]medicine.anatomical_structureHEK293 CellsGene Expression RegulationCiliary pocketCarrier ProteinsSterile alpha motifGuanylate KinasesSequence AlignmentUsher SyndromesPhotoreceptor Cells VertebrateProtein BindingSignal TransductionHuman molecular genetics
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Oxidative stress in environmental-induced carcinogenesis.

2009

Reactive oxygen species (ROS) are the more abundant free radicals in nature and have been related with a number of tissue/organ injuries induced by xenobiotics, ischemia, activation of leucocytes, UV exposition, etc. Oxidative stress is caused by an imbalance between ROS production and a biological system's ability to readily detoxify these reactive intermediates or easily repair the resulting damage. Thus, oxidative stress is accepted as a critical pathophysiological mechanism in different frequent human pathologies, including cancer. In fact ROS can cause protein, lipid, and DNA damage, and malignant tumors often show increased levels of DNA base oxidation and mutations. Different lifesty…

SenescenceAgingDNA damageHealth Toxicology and MutagenesisInflammationOxidative phosphorylationBiologymedicine.disease_causeModels BiologicalNeoplasmsGeneticsmedicineAnimalsHumansObesityLife StyleCarcinogenchemistry.chemical_classificationReactive oxygen speciesCarcinogens EnvironmentalOxidative StressCell Transformation NeoplasticBiochemistrychemistryCancer researchmedicine.symptomCarcinogenesisReactive Oxygen SpeciesOxidative stressMutation research
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Characterization of aging-associated up-regulation of constitutive nuclear factor-kappa B binding activity.

2001

Changes occur in gene expression during aging in vivo and in replicative senescence in vitro, suggesting that aging can affect gene regulation. We have recently observed age-related changes in ubiquitously expressed, oxidative stress-responsive nuclear factor-kappa B (NF-kappa B) pathway during aging. Here we report a significant age-related increase in nuclear NF-kappa B binding activity together with increased protein levels of p52 and p65 components in rat liver. An additional, higher molecular weight protein band seen in their western blots suggests that their post-translational modification (but not phosphorylation) occurs in liver, which might affect their nuclear localization and bin…

SenescenceAgingPhysiologyClinical BiochemistryBlotting WesternCell Cycle ProteinsNerve Tissue ProteinsIκB kinaseBiologyTransfectionBiochemistrySynaptotagminsCalcium-binding proteinGene expressionAnimalsRats WistarPromoter Regions GeneticMolecular BiologyCells CulturedGeneral Environmental ScienceRegulation of gene expressionMembrane GlycoproteinsCalcium-Binding ProteinsNF-kappa BCell BiologyBlotting NorthernMolecular biologyRatsUp-RegulationIκBαGene Expression RegulationLiverSynaptotagmin IGeneral Earth and Planetary SciencesPhosphorylationNuclear localization sequenceAntioxidantsredox signaling
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Overexpression of apolipoprotein J in human fibroblasts protects against cytotoxicity and premature senescence induced by ethanol and tert-butylhydro…

2008

Human diploid fibroblasts (HDFs) exposed to subcytotoxic stresses under H2O2, tert-butylhydroperoxide (t-BHP), and ethanol (EtOH) undergo stress-induced premature senescence (SIPS) characterized by many biomarkers of HDFs replicative senescence. Among these biomarkers are a growth arrest, an increase in the senescence-associated β-galactosidase activity, a senescent morphology, an overexpression of p21waf-1 and the subsequent inability to phosphorylate pRb, the presence of the common 4977-bp mitochondrial deletion, and an increase in the steady-state level of several senescence-associated genes such as apolipoprotein J (apo J). Apo J has been described as a survival gene against cytotoxic s…

SenescenceCell SurvivalGene ExpressionSimian virus 40Biologymedicine.disease_causeTritiumBiochemistrytert-ButylhydroperoxideGene expressionmedicineHumansOsteonectinRNA MessengerCytotoxicityCells CulturedCellular SenescenceCell Line TransformedGlycoproteinsClusterinEthanolCentral Nervous System DepressantsCell BiologyTransfectionOriginal ArticlesFibroblastsbeta-GalactosidaseMolecular biologyRecombinant ProteinsFibronectinsOxidative StressClusterinbiology.proteinPhosphorylationMitogensCell agingOxidative stressMolecular ChaperonesThymidineCell Stress and Chaperones
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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Attenuation of NF-κB Signaling Response to UVB Light during Cellular Senescence

1999

The ability of cells to adapt to environmental stresses undergoes a progressive reduction during aging. NF-kappaB-mediated signaling is a major defensive system against various environmental challenges. The aim of this study was to find out whether replicative senescence affects the response of the NF-kappaB signaling pathway to UVB light in human WI-38 and IMR-90 fibroblasts. The exposure of early passage fibroblasts to UVB light inhibited the proliferation and induced a flat phenotype similar to that observed in replicatively senescent fibroblasts not exposed to UVB light. The UVB radiation dose used (153 mJ/cm2) did not induce apoptosis in either early or late passage WI-38 fibroblasts. …

SenescenceP50Ultraviolet RaysLactams MacrocyclicBiologyCell LineBenzoquinonesHumansEnzyme InhibitorsProtein Kinase InhibitorsCellular SenescenceCell Line TransformedNF-kappa BQuinonesCell BiologyFibroblastsTyrphostinsMolecular biologyIκBαRifabutinApoptosisPhosphorylationTumor necrosis factor alphaSignal transductionNuclear localization sequenceSignal TransductionExperimental Cell Research
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