Search results for "STRESS"

showing 10 items of 6278 documents

Yeast mRNA cap-binding protein Cbc1/Sto1 is necessary for the rapid reprogramming of translation after hyperosmotic shock.

2011

Global translation is inhibited in Saccharomyces cerevisiae cells under osmotic stress; nonetheless, osmostress-protective proteins are synthesized. We found that translation mediated by the mRNA cap-binding protein Cbc1 is stress-resistant and necessary for the rapid translation of osmostress-protective proteins under osmotic stress.

Cell PhysiologySaccharomyces cerevisiae ProteinsOsmotic shockRNA StabilitySaccharomyces cerevisiaeCycloheximideBiology03 medical and health scienceschemistry.chemical_compoundGene Knockout TechniquesEukaryotic translationOsmotic PressureStress PhysiologicalPolysomeGene Expression Regulation FungalProtein biosynthesisRNA MessengerMolecular Biology030304 developmental biologyCell Nucleus0303 health sciencesMicrobial ViabilityOsmotic concentration030302 biochemistry & molecular biologyEIF4ENuclear ProteinsTranslation (biology)Cell BiologyArticlesAdaptation PhysiologicalProtein TransportEukaryotic Initiation Factor-4EchemistryBiochemistryRNA Cap-Binding ProteinsPolyribosomesProtein BiosynthesisProtein BindingMolecular biology of the cell
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Membrane protein oxidation determines neuronal degeneration

2015

Oxidative stress is an early hallmark in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. However, the critical biochemical effector mechanisms of oxidative neurotoxicity have remained surprisingly elusive. In screening various peroxides and potential substrates of oxidation for their effect on neuronal survival, we observed that intramembrane compounds were significantly more active than aqueous or amphiphilic compounds. To better understand this result, we synthesized a series of competitive and site-specific membrane protein oxidation inhibitors termed aminoacyllipids, whose structures were designed on the basis of amino acids frequently found at the protein-lipi…

Cell SurvivalBiologyProtein oxidationmedicine.disease_causeBiochemistryProtein Structure SecondaryRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineAnimalsLipid bilayerCells CulturedNeuronsSphingosineNeurodegenerationNeurotoxicityMembrane Proteinsmedicine.diseaseTransmembrane proteinRatsCell biologyOxidative StressMembrane proteinchemistryNerve DegenerationReactive Oxygen SpeciesOxidation-ReductionOxidative stressJournal of Neurochemistry
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Induction of apoptosis by arachidonic acid in human retinoblastoma Y79 cells: involvement of oxidative stress

2000

Arachidonic acid administration caused apoptosis in Y79 cells, as shown by typical morphological changes, phosphatidylserine externalization, chromatin condensation, processing and activation of caspase-3 and cleavage of the endogenous caspase substrate poly-(ADP-ribose)-polymerase. Arachidonic acid also caused lamin B cleavage, suggesting caspase-6 activation. Arachidonic acid treatment was accompanied by increased formation of the lipid peroxidation end products malondialdehyde and 4-hydroxy-2-nonenal, lowering in reduced glutathione content and in mitochondrial membrane potential. Inhibiting glutathione synthesis sensitized Y79 cells to apoptosis-inducing stimuli, whilst replenishing red…

Cell SurvivalBlotting WesternApoptosisCell Countmedicine.disease_causeMembrane PotentialsLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundPhospholipase A2medicineTumor Cells Culturedarachidonic acidHumansCYP2C8biologyDose-Response Relationship DrugRetinoblastomaGlutathioneTrypan BlueMalondialdehydeFlow CytometryGlutathioneSensory SystemsCell biologyMitochondriaOphthalmologyOxidative StressBiochemistrychemistryMitochondrial permeability transition poreCaspasesbiology.proteinArachidonic acidColorimetryPoly(ADP-ribose) PolymerasesOxidative stress
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Inhibition of stearoyl-CoA desaturase 1 expression induces CHOP-dependent cell death in human cancer cells.

2010

Background Cancer cells present a sustained de novo fatty acid synthesis with an increase of saturated and monounsaturated fatty acid (MUFA) production. This change in fatty acid metabolism is associated with overexpression of stearoyl-CoA desaturase 1 (Scd1), which catalyses the transformation of saturated fatty acids into monounsaturated fatty acids (e.g., oleic acid). Several reports demonstrated that inhibition of Scd1 led to the blocking of proliferation and induction of apoptosis in cancer cells. Nevertheless, mechanisms of cell death activation remain to be better understood. Principal Findings In this study, we demonstrated that Scd1 extinction by siRNA triggered abolition of de nov…

Cell SurvivalEukaryotic Initiation Factor-2lcsh:MedicineApoptosisCHOPBiologyCell Biology/Cell SignalingCell Linechemistry.chemical_compoundCell Line TumorNeoplasmsHumansRNA Small Interferinglcsh:ScienceEndoplasmic Reticulum Chaperone BiPFatty acid synthesisHeat-Shock ProteinsCell ProliferationTranscription Factor CHOPMultidisciplinaryFatty acid metabolismCell DeathCell growthFatty Acidslcsh:RCell Biology/Cellular Death and Stress ResponsesMolecular biologyCell biologychemistryOncologyApoptosisCancer celllipids (amino acids peptides and proteins)lcsh:QStearoyl-CoA desaturase-1Stearoyl-CoA DesaturaseTranscription Factor CHOPResearch ArticleOleic AcidPLoS ONE
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Genotoxicity of 1,4-benzoquinone and 1,4-naphthoquinone in relation to effects on glutathione and NAD(P)H levels in V79 cells.

1989

1,4-Benzoquinone is cytotoxic in V79 Chinese hamster cells and induces gene mutations and micronuclei. The cell-damaging effects of quinones are usually attributed to thiol depletion, oxidation of NAD(P)H, and redox-cycling involving the formation of semiquinone radicals and reactive oxygen species. To elucidate the role of these mechanisms in the genotoxicity of 1,4-benzoquinone, we measured various genotoxic effects, cytotoxicity, and the levels of glutathione, NADPH, NADH, and their oxidized forms all in the same experiment. 1,4-Naphthoquinone, which does not induce gene mutations in V79 cells, was investigated for comparative reasons. The quinones had a similar effect on the levels of c…

Cell SurvivalHealth Toxicology and MutagenesisGlutathione reductaseGene mutationBiologymedicine.disease_causeCell Linechemistry.chemical_compoundBenzoquinonesmedicineAnimalschemistry.chemical_classificationReactive oxygen speciesMutagenicity TestsQuinonesPublic Health Environmental and Occupational HealthGlutathioneNADGlutathioneBiochemistrychemistryMicronucleus testNAD+ kinaseOxidation-ReductionNADPGenotoxicityOxidative stressMutagensNaphthoquinonesResearch ArticleEnvironmental Health Perspectives
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Role of RCAN1 in stress induced cell adaptation

2012

Cell adaptationChemistryPhysiology (medical)Stress inducedBiochemistryCell biologyFree Radical Biology and Medicine
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The yeast mitogen-activated protein kinase Slt2 is involved in the cellular response to genotoxic stress

2012

Abstract Background The maintenance of genomic integrity is essential for cell viability. Complex signalling pathways (DNA integrity checkpoints) mediate the response to genotoxic stresses. Identifying new functions involved in the cellular response to DNA-damage is crucial. The Saccharomyces cerevisiae SLT2 gene encodes a member of the mitogen-activated protein kinase (MAPK) cascade whose main function is the maintenance of the cell wall integrity. However, different observations suggest that SLT2 may also have a role related to DNA metabolism. Results This work consisted in a comprehensive study to connect the Slt2 protein to genome integrity maintenance in response to genotoxic stresses.…

Cell cycle checkpoint<it>Saccharomyces cerevisiae</it>DNA damageSaccharomyces cerevisiaeGenotoxic StressSaccharomyces cerevisiaeBiologyBiochemistrylcsh:RC254-282checkpointlcsh:QH573-671Protein kinase AMolecular BiologyGeneticsDNA integrity checkpointKinaselcsh:CytologyResearchCell BiologyCell cyclebiology.organism_classificationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensgenotoxic stressCell biologyDNA damageSlt2
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Adenine auxotrophy--be aware: some effects of adenine auxotrophy in Saccharomyces cerevisiae strain W303-1A.

2013

Adenine auxotrophy is a commonly used genetic marker in haploid yeast strains. Strain W303-1A, which carries the ade2-1 mutation, is widely used in physiological and genetic research. Yeast extract-based rich medium contains a low level of adenine, so that adenine is often depleted before glucose. This could affect the cell physiology of adenine auxotrophs grown in rich medium. The aim of our study was to assess the effects of adenine auxotrophy on cell morphology and stress physiology. Our results show that adenine depletion halts cell division, but that culture optical density continues to increase due to cell swelling. Accumulation of trehalose and a coincident 10-fold increase in desicc…

Cell physiologyCell divisionAuxotrophyAdenineSaccharomyces cerevisiaeGeneral MedicineSaccharomyces cerevisiaeBiologybiology.organism_classificationCell morphologyApplied Microbiology and BiotechnologyMicrobiologyTrehaloseYeastCulture Mediachemistry.chemical_compoundBiochemistrychemistryStress PhysiologicalBiomassLeucineCell DivisionFEMS yeast research
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Exercise and antioxidant supplements in the elderly

2013

Abstract Both exercise and aging increase reactive oxygen species (ROS), which can result in damage to cells. Aging is the result of damage caused by ROS to the mitochondrial genome in post mitotic cells and numerous studies have demonstrated an increase in ROS or their byproducts with exercise. ROS can cause oxidative stress as they overwhelm the antioxidant cellular defenses. Therefore interventions aimed at limiting or inhibiting ROS production, such as supplementation with antioxidant vitamins, should be able to reduce fatigue during muscle contraction and the rate of formation of aging changes with a consequent reduction of the aging rate and disease pathogenesis. However, it has been …

Cell signalingAgingAntioxidantmedicine.medical_treatmentmedia_common.quotation_subjectPopulationPGC-1αSkeletal musclePhysical Therapy Sports Therapy and RehabilitationPharmacologyBiologymedicine.disease_causeNF-κBchemistry.chemical_compoundmedicineOrthopedics and Sports Medicineeducationmedia_commonchemistry.chemical_classificationeducation.field_of_studyReactive oxygen speciesAdaptationsLongevitySkeletal muscleNF-κBmedicine.anatomical_structurechemistryBiochemistryOxidative stressAntioxidant enzymesOxidative stressJournal of Sport and Health Science
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Delayed ageing through damage protection by the Arf/p53 pathway.

2007

The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These obser…

Cell signalingAgingTime FactorsTumor suppressor geneLongevityBiologymedicine.disease_causeAntioxidantsTranscriptomeMiceCDKN2ANeoplasmsmedicineAnimalsCells CulturedCyclin-Dependent Kinase Inhibitor p16MultidisciplinaryCell cycleFibroblastsCell biologyOxidative StressAgeingDisease SusceptibilitySignal transductionTumor Suppressor Protein p53Oxidative stressNature
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