Search results for " Models"

showing 10 items of 4240 documents

Triptans and CGRP blockade - impact on the cranial vasculature.

2017

Abstract The trigeminovascular system plays a key role in the pathophysiology of migraine. The activation of the trigeminovascular system causes release of various neurotransmitters and neuropeptides, including serotonin and calcitonin gene-related peptide (CGRP), which modulate pain transmission and vascular tone. Thirty years after discovery of agonists for serotonin 5-HT1B and 5-HT1D receptors (triptans) and less than fifteen after the proof of concept of the gepant class of CGRP receptor antagonists, we are still a long way from understanding their precise site and mode of action in migraine. The effect on cranial vasculature is relevant, because all specific anti-migraine drugs and mig…

0301 basic medicineMigraine DisordersCalcitonin gene related peptide – CGRPNeuropeptidelcsh:MedicineMigraine modelsReviewTriptansReview ArticleCalcitonin gene-related peptide03 medical and health sciences0302 clinical medicineJournal ArticlemedicineHumansMigraine treatmentReceptorbusiness.industryTriptans Calcitonin gene related peptide – CGRP Anti-CGRP (receptor) monoclonal antibodies – mAbs Middle meningeal artery Middle cerebral arteries Migraine models Magnetic resonance angiography (MRA)Anti-CGRP (receptor) monoclonal antibodies – mAbsTrigeminovascular systemlcsh:RTriptansGeneral MedicineMiddle meningeal arterymedicine.diseaseTryptamines3. Good healthMagnetic resonance angiography (MRA)Middle cerebral arteries030104 developmental biologyAnesthesiology and Pain MedicineMigraineAnesthesiaNeurology (clinical)SerotoninbusinessNeuroscience030217 neurology & neurosurgerymedicine.drugReceptors Calcitonin Gene-Related PeptideThe journal of headache and pain
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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rbFOX1/MBNL1 competition for CCUG RNA repeats binding contributes to myotonic dystrophy type 1/type 2 differences

2018

Myotonic dystrophy type 1 and type 2 (DM1, DM2) are caused by expansions of CTG and CCTG repeats, respectively. RNAs containing expanded CUG or CCUG repeats interfere with the metabolism of other RNAs through titration of the Muscleblind-like (MBNL) RNA binding proteins. DM2 follows a more favorable clinical course than DM1, suggesting that specific modifiers may modulate DM severity. Here, we report that the rbFOX1 RNA binding protein binds to expanded CCUG RNA repeats, but not to expanded CUG RNA repeats. Interestingly, rbFOX1 competes with MBNL1 for binding to CCUG expanded repeats and overexpression of rbFOX1 partly releases MBNL1 from sequestration within CCUG RNA foci in DM2 muscle ce…

0301 basic medicineModels MolecularProtein Conformation alpha-Helical[SDV]Life Sciences [q-bio]General Physics and AstronomyGene ExpressionRNA-binding proteinCrystallography X-Raychemistry.chemical_compoundMOLECULAR-BASISGene expressionMBNL1Myotonic DystrophyComputingMilieux_MISCELLANEOUSMultidisciplinaryCHLORIDE CHANNELQRNA-Binding ProteinsRecombinant Proteins3. Good healthCell biologyCONGENITAL HEART-DISEASEDrosophila melanogasterThermodynamicsSKELETAL-MUSCLERNA Splicing FactorsCUG REPEATSProtein BindingRNA Splicing Factorsmusculoskeletal diseasesSTEADY-STATEcongenital hereditary and neonatal diseases and abnormalitiesScienceRBFOX1BiologyMyotonic dystrophyBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesmedicineEscherichia coliAnimalsHumansProtein Interaction Domains and MotifsBinding siteNucleotide MotifsMuscle SkeletalSPLICING REGULATOR RBFOX2MUSCLEBLIND PROTEINSBinding SitesPRE-MESSENGER-RNARNAGeneral Chemistrymedicine.diseaseDisease Models AnimalKinetics030104 developmental biologychemistryTRIPLET REPEATRNAProtein Conformation beta-Strand3111 Biomedicine
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Evolving Notch polyQ tracts reveal possible solenoid interference elements.

2016

ABSTRACTPolyglutamine (polyQ) tracts in regulatory proteins are extremely polymorphic. As functional elements under selection for length, triplet repeats are prone to DNA replication slippage and indel mutations. Many polyQ tracts are also embedded within intrinsically disordered domains, which are less constrained, fast evolving, and difficult to characterize. To identify structural principles underlying polyQ tracts in disordered regulatory domains, here I analyze deep evolution of metazoan Notch polyQ tracts, which can generate alleles causing developmental and neurogenic defects. I show that Notch features polyQ tract turnover that is restricted to a discrete number of conserved “polyQ …

0301 basic medicineModels MolecularProtein Structure ComparisonProtein FoldingHuntingtinlcsh:MedicineCarboxamideAnkyrin Repeat DomainBiochemistryProtein Structure SecondaryDatabase and Informatics Methods0302 clinical medicineProtein structureMacromolecular Structure AnalysisDrosophila Proteinslcsh:ScienceGeneticsHuntingtin ProteinMultidisciplinaryReceptors NotchChemistryDrosophila MelanogasterAnimal ModelsCell biologyInsectsExperimental Organism SystemsProtein foldingDrosophilaSequence AnalysisResearch ArticleMultiple Alignment CalculationProtein StructureArthropodamedicine.drug_classBioinformaticsProtein domainSequence alignmentBiologyIntrinsically disordered proteinsResearch and Analysis MethodsTerminal loopEvolution Molecular03 medical and health sciencesModel OrganismsProtein DomainsSequence Motif AnalysisComputational TechniquesmedicineHuntingtin ProteinAnimalsIndelMolecular BiologyRepetitive Sequences Nucleic AcidModels GeneticSequence Homology Amino Acidlcsh:RDNA replicationOrganismsBiology and Life SciencesProteinsHydrogen BondingInvertebratesSplit-Decomposition MethodIntrinsically Disordered Proteins030104 developmental biologyAnkyrin repeatlcsh:QPeptidesSequence Alignment030217 neurology & neurosurgeryPLoS ONE
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Ursolic acid enhances stress resistance, reduces ROS accumulation and prolongs life span in C. elegans serotonin-deficient mutants.

2021

Introduction: Depression and anxiety disorders contribute to the global disease burden. Ursolic acid (UA), a natural compound present in many vegetables, fruits and medicinal plants, was tested in vivo for its effect on (1) enhancing resistance to stress and (2) its effect on life span. Methods: The compound was tested for its antioxidant activity in C. elegans. Stress resistance was tested in the heat and osmotic stress assay. Additionally, the influence on normal life span was examined. RT-PCR was used to assess possible serotonin targets. Results: UA prolonged the life span of C. elegans. Additionally, UA significantly lowered reactive oxygen species (ROS). Molecular docking studies, PCR…

0301 basic medicineModels MolecularSerotoninAntioxidantHot TemperatureOsmotic shockmedicine.medical_treatmentLongevityPharmacologyAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicineUrsolic acidIn vivoOsmotic PressureStress PhysiologicalmedicineAnimalsReceptorCaenorhabditis elegans5-HT receptorchemistry.chemical_classificationReactive oxygen speciesDepressionGeneral MedicineTriterpenesMolecular Docking SimulationDisease Models Animal030104 developmental biologychemistryReceptors SerotoninMutationSerotoninReactive Oxygen Species030217 neurology & neurosurgeryFood ScienceNaphthoquinonesFoodfunction
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In silico discovery of substituted pyrido[2,3-d]pyrimidines and pentamidine-like compounds with biological activity in myotonic dystrophy models

2016

Myotonic dystrophy type 1 (DM1) is a rare multisystemic disorder associated with an expansion of CUG repeats in mutant DMPK (dystrophia myotonica protein kinase) transcripts; the main effect of these expansions is the induction of pre-mRNA splicing defects by sequestering muscleblind-like family proteins (e.g. MBNL1). Disruption of the CUG repeats and the MBNL1 protein complex has been established as the best therapeutic approach for DM1, hence two main strategies have been proposed: targeted degradation of mutant DMPK transcripts and the development of CUG-binding molecules that prevent MBNL1 sequestration. Herein, suitable CUG-binding small molecules were selected using in silico approach…

0301 basic medicineMolecular biologyPhysiologyMutantMyotonic dystrophyDruggabilitylcsh:Medicine01 natural sciencesBiochemistryPhysical ChemistryMyoblastschemistry.chemical_compoundAnabolic AgentsMedicaments--InteraccióAnimal CellsDrug DiscoveryMedicine and Health SciencesMBNL1Drosophila ProteinsMyotonic Dystrophylcsh:ScienceRNA structureConnective Tissue CellsMultidisciplinaryMolecular StructureOrganic CompoundsStem CellsPhysicsRNA-Binding ProteinsBiological activityPhenotypeClimbingMolecular Docking SimulationNucleic acidsChemistryDrosophila melanogasterBiochemistryGenetic DiseasesConnective TissueRNA splicingPhysical SciencesCellular TypesAnatomyLocomotion57 - BiologiaSignal TransductionResearch ArticleBiotechnologyHydrogen bondingcongenital hereditary and neonatal diseases and abnormalitiesIn silicoPrimary Cell CultureComputational biologyBiology010402 general chemistryMyotonic dystrophyMyotonin-Protein KinaseDrug interactionsSmall Molecule Libraries03 medical and health sciencesStructure-Activity RelationshipmedicineAnimalsHumansRNA MessengerEnllaços d'hidrogenClinical GeneticsChemical PhysicsBiology and life sciencesChemical BondingBiological Locomotionlcsh:ROrganic ChemistryEstructura molecularChemical CompoundsHydrogen BondingCell BiologyFibroblastsmedicine.disease0104 chemical sciencesBenzamidinesAlternative SplicingDisease Models AnimalMacromolecular structure analysis030104 developmental biologyPyrimidinesBiological TissuechemistrySmall MoleculesRNAlcsh:QTrinucleotide Repeat ExpansionMolecular structure
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Drosophila SMN2minigene reporter model identifies moxifloxacin as a candidate therapy for SMA

2018

Spinal muscular atrophy is a rare and fatal neuromuscular disorder caused by the loss of alpha motor neurons. The affected individuals have mutated the ubiquitously expressed SMN1 gene resulting in the loss or reduction in the survival motor neuron (SMN) protein levels. However, an almost identical paralog exists in humans: SMN2. Pharmacological activation of SMN2 exon 7 inclusion by small molecules or modified antisense oligonucleotides is a valid approach to treat SMA. Here we describe an in vivo SMN2 minigene reporter system in Drosophila motor neurons that serves as a cost-effective, feasible, and stringent primary screening model for identifying chemicals capable of crossing the conser…

0301 basic medicineMoxifloxacinDrug Evaluation PreclinicalSMN1BiologyBiochemistryAnimals Genetically ModifiedMuscular Atrophy Spinal03 medical and health sciencesExon0302 clinical medicineGenes ReporterGeneticsmedicineAnimalsHumansMolecular BiologyExonsSpinal muscular atrophyMotor neuronSMA*medicine.diseasenervous system diseasesCell biologySurvival of Motor Neuron 2 ProteinAlternative SplicingDisease Models AnimalDrosophila melanogaster030104 developmental biologymedicine.anatomical_structureCajal bodyBlood-Brain BarrierRNA splicing030217 neurology & neurosurgeryBiotechnologyMinigeneThe FASEB Journal
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Myeloid cell populations and fibrogenic parameters in bleomycin- and HOCl-induced fibrosis

2016

Mouse models resembling systemic sclerosis can be chemically induced by application of bleomycin or hypochloric acid (HOCl). To date, little is known about inflammatory cells and their potential role in scleroderma (Scl)-related fibrosis. Therefore, we compared both Scl models to define the early immune cell subsets in relation to fibrosis-related parameters. Both agents induced a significant increase in dermal thickness and collagen deposition after 4 weeks, as hallmarks of Scl. However, clinical skin thickness, densely packed, sirius red-stained collagen bundles and collagen cross-links were more pronounced in HOCl-induced Scl. In parallel, there was a significant upregulation of procolla…

0301 basic medicineMyeloidCD11cDermatologyBleomycinBiochemistryCD19Bleomycin03 medical and health scienceschemistry.chemical_compoundImmune systemFibrosishemic and lymphatic diseasesmedicineAnimalsMyeloid CellsMolecular BiologySkinScleroderma Systemicbiologymedicine.diseaseFibrosisMolecular biologyHypochlorous AcidMice Inbred C57BLDisease Models AnimalProcollagen peptidase030104 developmental biologymedicine.anatomical_structurechemistryIntegrin alpha Mbiology.proteinFemaleExperimental Dermatology
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Approaching Sex Differences in Cardiovascular Non-Coding RNA Research

2020

International audience; Cardiovascular disease (CVD) is the biggest cause of sickness and mortality worldwide in both males and females. Clinical statistics demonstrate clear sex differences in risk, prevalence, mortality rates, and response to treatment for different entities of CVD. The reason for this remains poorly understood. Non-coding RNAs (ncRNAs) are emerging as key mediators and biomarkers of CVD. Similarly, current knowledge on differential regulation, expression, and pathology-associated function of ncRNAs between sexes is minimal. Here, we provide a state-of-the-art overview of what is known on sex differences in ncRNA research in CVD as well as discussing the contributing biol…

0301 basic medicineNcRNAER-BETARNA Untranslatedexperimental modelsreceptorsReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular Systemlcsh:Chemistry0302 clinical medicineSex hormone-binding globulinlncRNAestrogenMedicinePROMOTER METHYLATIONlcsh:QH301-705.5DNA METHYLATIONSpectroscopyGENE-EXPRESSIONSex CharacteristicsbiologyMortality rateGeneral MedicineMOUSE MODELNon-coding RNA[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthComputer Science ApplicationsHEART-FAILUREESTROGEN-RECEPTOR-ALPHAandrogenvascular cells.vascular cellsCatalysisMICRORNA THERAPEUTICSInorganic Chemistry03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemmicroRNAAnimalsHumansEpigeneticsPhysical and Theoretical ChemistryX-INACTIVATIONMolecular BiologySocioeconomic statusmiRNAbusiness.industryOrganic ChemistryPOSTMENOPAUSAL HORMONE-THERAPYcardiovascular diseasesSexual dimorphism030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinbusinessBiomarkersInternational journal of molecular sciences
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