Search results for "script"

showing 10 items of 5143 documents

Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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A53T-Alpha-Synuclein Overexpression Impairs Dopamine Signaling and Striatal Synaptic Plasticity in Old Mice

2010

BACKGROUND: Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. METHODOLOGY/PRINCIPAL FINDINGS: Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA…

AgingDopaminelcsh:MedicineMicechemistry.chemical_compoundHomer Scaffolding ProteinsReceptor Cannabinoid CB1lcsh:ScienceLong-term depressionNeurotransmitterChromatography High Pressure LiquidIn Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisMice KnockoutNeuronal PlasticityMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionDopaminergicNeurodegenerationGenetics and Genomics/Gene ExpressionElectrophysiologyalpha-SynucleinResearch ArticleRadioimmunoprecipitation Assaymedicine.medical_specialtyNeuronal Calcium-Sensor ProteinsHOMER1Substantia nigraNeurotransmissionBiologyNeurological DisordersInternal medicinemedicineAnimalsHumansddc:610Cyclic Nucleotide Phosphodiesterases Type 7Activating Transcription Factor 2lcsh:RNeuropeptidesmedicine.diseaseMolecular biologyCorpus StriatumMice Mutant StrainsEndocrinologyGenetics and Genomics/Disease ModelschemistrySynaptic plasticitylcsh:QCarrier ProteinsPLoS ONE
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Long-lived Temnothorax ant queens switch from investment in immunity to antioxidant production with age

2019

Abstract Senescence is manifested by an increase in molecular damage and a deterioration of biological functions with age. In most organisms, body maintenance is traded-off with reproduction. This negative relationship between longevity and fecundity is also evident on the molecular level. Exempt from this negative trait association, social insect queens are both extremely long-lived and highly fecund. Here, we study changes in gene expression with age and fecundity in ant queens to understand the molecular basis of their long lifespan. We analyse tissue-specific gene expression in young founding queens and old fecund queens of the ant Temnothorax rugatulus. More genes altered their express…

AgingEcologyEvolutionAntsGene Expression Profilinglcsh:RFat Bodylcsh:MedicineBrainArticleAntioxidants570 Life sciencesFertilityAnimalslcsh:QFemalelcsh:ScienceTranscriptomicsTranscriptome570 Biowissenschaften
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Influence of gene action across different time scales on behavior.

2002

Genes can affect natural behavioral variation in different ways. Allelic variation causes alternative behavioral phenotypes, whereas changes in gene expression can influence the initiation of behavior at different ages. We show that the age-related transition by honey bees from hive work to foraging is associated with an increase in the expression of the foraging ( for ) gene, which encodes a guanosine 3′,5′-monophosphate (cGMP)–dependent protein kinase (PKG). cGMP treatment elevated PKG activity and caused foraging behavior. Previous research showed that allelic differences in PKG expression result in two Drosophila foraging variants. The same gene can thus exert different types of influe…

AgingForagingGenes InsectHierarchy SocialBiologyGene expressionCyclic GMP-Dependent Protein KinasesAnimalsRNA MessengerAlleleSocial BehaviorGeneCyclic GMPAllelesIn Situ HybridizationMushroom BodiesGeneticsAppetitive BehaviorMultidisciplinaryBehavior AnimalDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingfungiBrainHoney beeFeeding BehaviorBeesPhenotypeUp-RegulationGene expression profilingPhenotypeMushroom bodiesDrosophilaScience (New York, N.Y.)
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Expression of Toll-Like Receptors in the Developing Brain

2012

Toll-like receptors (TLR) are key players of the innate and adaptive immune response in vertebrates. The original protein Toll in Drosophila melanogaster regulates both host defense and morphogenesis during development. Making use of real-time PCR, in situ hybridization, and immunohistochemistry we systematically examined the expression of TLR1-9 and the intracellular adaptor molecules MyD88 and TRIF during development of the mouse brain. Expression of TLR7 and TLR9 in the brain was strongly regulated during different embryonic, postnatal, and adult stages. In contrast, expression of TLR1-6, TLR8, MyD88, and TRIF mRNA displayed no significant changes in the different phases of brain develop…

AgingGene Expressionlcsh:MedicineMiceMolecular Cell BiologyMorphogenesislcsh:ScienceReceptorImmune ResponseRegulation of gene expressionMultidisciplinaryNeocortexToll-Like ReceptorsBrainGene Expression Regulation DevelopmentalAcquired immune systemInnate ImmunityCell biologyInfectious Diseasesmedicine.anatomical_structureMedicineResearch ArticleImmunologyCentral nervous systemMorphogenesisIn situ hybridizationBiologyMolecular GeneticsImmune ActivationDevelopmental NeuroscienceGeneticsmedicineAnimalsHumansRNA MessengerBiologyImmunity to Infectionslcsh:RImmunityComputational BiologyImmune DefenseAxonsHEK293 CellsTRIFImmune SystemCellular NeuroscienceImmunologyClinical Immunologylcsh:QTranscriptomeDevelopmental BiologyNeurosciencePLoS ONE
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Prescription-grade crystalline glucosamine sulfate as an add-on therapy to conventional treatments in erosive osteoarthritis of the hand: results fro…

2022

Abstract Objective To evaluate the efficacy of prescription-grade Crystalline Glucosamine Sulfate (pCGS) as an add-on treatment to conventional therapy, compared to usual therapy alone, in patients with erosive osteoarthritis of the hand (EHOA). Methods This 6-month retrospective case–control study included patients with concomitant knee osteoarthritis and symptomatic EHOA. Participants were stratified into two groups based on whether or not pCGS (1500 mg/day) was added to the conventional therapy (education and training in ergonomic principles, exercise and use on-demand of symptomatic drugs) for hand osteoarthritis. Patients were evaluated at baseline, after 3 and 6 months. Primary outcom…

AgingGlucosamineSymptomatic slow-acting drugs for osteoarthritisPainOsteoarthritis KneePrescription-grade crystalline glucosamine sulfateErosive hand osteoarthritis; Hand osteoarthritis; Pain; Prescription-grade crystalline glucosamine sulfate; Retrospective study; Symptomatic slow-acting drugs for osteoarthritisErosive hand osteoarthritisRetrospective studyPrescriptionsTreatment OutcomeCase-Control StudiesHand osteoarthritisHumansErosive hand osteoarthritis Hand osteoarthritis Pain Prescription-grade crystalline glucosamine sulfate Retrospective study Symptomatic slow-acting drugs for osteoarthritisGeriatrics and GerontologyRetrospective StudiesAging clinical and experimental research
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YAP/TAZ activity in stromal cells prevents ageing by controlling cGAS-STING

2022

Ageing is intimately connected to the induction of cell senescence(1,2), but why this is so remains poorly understood. A key challenge isthe identification of pathways that normally suppress senescence, are lost during ageing and are functionally relevant to oppose ageing(3). Here we connected the structural and functional decline of ageing tissues to attenuated function of the master effectors of cellular mechanosignalling YAP and TAZ. YAP/TAZ activity declines during physiological ageing in stromal cells, and mimicking such decline through genetic inactivation of YAP/TAZ in these cells leads to accelerated ageing. Conversely, sustaining YAP function rejuvenates old cells and opposes the e…

AgingMechanotransductionActin-Related Protein 2; Cellular Senescence; Extracellular Matrix; Healthy Aging; Immunity Innate; Lamin Type B; Mechanotransduction Cellular; Nuclear Envelope; Signal Transduction; Aging; Membrane Proteins; Nucleotidyltransferases; Stromal Cells; Transcriptional Coactivator with PDZ-Binding Motif Proteins; YAP-Signaling ProteinsNuclear EnvelopeSettore MED/08 - Anatomia PatologicaYAP TAZ ageing C-GAS STINGMechanotransduction CellularArticleHealthy AgingInnateCellular SenescenceAdaptor Proteins Signal TransducingMultidisciplinaryLamin Type BImmunityMembrane ProteinsYAP-Signaling ProteinsPhosphoproteinsNucleotidyltransferasesImmunity InnateExtracellular MatrixTranscriptional Coactivator with PDZ-Binding Motif ProteinsActin-Related Protein 2CellularStromal CellsSignal Transduction
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Tif1γ regulates the TGF-β1 receptor and promotes physiological aging of hematopoietic stem cells.

2014

The hematopoietic system declines with age. Myeloid-biased differentiation and increased incidence of myeloid malignancies feature aging of hematopoietic stem cells (HSCs), but the mechanisms involved remain uncertain. Here, we report that 4-mo-old mice deleted for transcription intermediary factor 1γ (Tif1γ) in HSCs developed an accelerated aging phenotype. To reinforce this result, we also show that Tif1γ is down-regulated in HSCs during aging in 20-mo-old wild-type mice. We established that Tif1γ controls TGF-β1 receptor (Tgfbr1) turnover. Compared with young HSCs, Tif1γ(-/-) and old HSCs are more sensitive to TGF-β signaling. Importantly, we identified two populations of HSCs specifical…

AgingMyeloidReceptor Transforming Growth Factor-beta Type IReceptors Cell SurfaceCell SeparationBiologyProtein Serine-Threonine KinasesTransforming Growth Factor beta1MiceSignaling Lymphocytic Activation Molecule Family Member 1Antigens CDmedicineAnimalsMyeloid CellsRNA MessengerPolyubiquitinTranscription factorCellular SenescenceRegulation of gene expressionMultidisciplinaryUbiquitinationhemic and immune systemsBiological SciencesHematopoietic Stem CellsCell biologyHematopoiesisHaematopoiesismedicine.anatomical_structurePhysiological AgingPhenotypeGene Expression RegulationSignal transductionStem cellCell agingReceptors Transforming Growth Factor betaSignal TransductionTranscription FactorsProceedings of the National Academy of Sciences of the United States of America
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BAG3 and friends: co-chaperones in selective autophagy during aging and disease.

2011

There is a reciprocal change in the expression of two members of the BAG (Bcl-2-associated athanogen) family, BAG1 and BAG3, during cellular aging and under acute stress ("BAG1-BAG3-switch"). BAG3 was recently described as a mediator of a novel macroautophagy pathway that uses the specificity of heat shock protein 70 (HSP70) to misfolded proteins and also involves other protein partners, such as HSPB8. Also crucial for induction and execution of autophagy are sequestosome-1/p62 (SQSTM1/p62) and LC3, an autophagosome-associated protein. In this novel pathway, BAG3 mediates the targeting and transport of degradation-prone substrates into aggresomes via the microtubule-motor dynein. Interestin…

AgingProteasome Endopeptidase ComplexDyneinBAG3Models BiologicalJUNQ and IPODUbiquitinAutophagyAnimalsDiseaseMolecular BiologyAdaptor Proteins Signal TransducingbiologyAutophagyUbiquitinationSignal transducing adaptor proteinDyneinsCell BiologyAdaptation PhysiologicalCell biologyHsp70DNA-Binding ProteinsAggresomeBiochemistrybiology.proteinMolecular ChaperonesTranscription FactorsAutophagy
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HSF1-controlled and age-associated chaperone capacity in neurons and muscle cells of C. elegans.

2010

Protein stability under changing conditions is of vital importance for the cell and under the control of a fine-tuned network of molecular chaperones. Aging and age-related neurodegenerative diseases are directly associated with enhanced protein instability. Employing C. elegans expressing GFP-tagged luciferase as a reporter for evaluation of protein stability we show that the chaperoning strategy of body wall muscle cells and neurons is significantly different and that both are differently affected by aging. Muscle cells of young worms are largely resistant to heat stress, which is directly mediated by the stress response controlled through Heat Shock Transcription Factor 1. During recover…

AgingProteomeGreen Fluorescent Proteinslcsh:MedicineBiologyBiochemistryBiochemistry/Protein FoldingAnimals Genetically ModifiedHeat shock proteinAnimalsMyocyteHeat shockCaenorhabditis elegansCaenorhabditis elegans ProteinsHSF1lcsh:ScienceDNA PrimersNeuronsMultidisciplinaryBase SequenceMuscleslcsh:RCell Biology/Cellular Death and Stress ResponsesMolecular biologyCell biologyHeat shock factorMicroscopy FluorescenceChaperone (protein)biology.proteinProtein foldinglcsh:QProtein stabilizationResearch ArticleMolecular ChaperonesTranscription FactorsPLoS ONE
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