Search results for "Cell line"

showing 10 items of 2924 documents

Fitness Trade-Offs Determine the Role of the Molecular Chaperonin GroEL in Buffering Mutations

2015

Molecular chaperones fold many proteins and their mutated versions in a cell and can sometimes buffer the phenotypic effect of mutations that affect protein folding. Unanswered questions about this buffering include the nature of its mechanism, its influence on the genetic variation of a population, the fitness trade-offs constraining this mechanism, and its role in expediting evolution. Answering these questions is fundamental to understand the contribution of buffering to increase genetic variation and ecological diversification. Here, we performed experimental evolution, genome resequencing, and computational analyses to determine the trade-offs and evolutionary trajectories of Escherich…

PopulationGenetic FitnessBiologyGroELCell LineChaperonin10127 Institute of Evolutionary Biology and Environmental StudiesGenetic drift1311 Geneticsmutational bufferingOperonGenetic variationGenetics1312 Molecular BiologyEscherichia coliexperimental evolutioneducationMolecular BiologyDiscoveriesEcology Evolution Behavior and Systematics2. Zero hungerGeneticseducation.field_of_studyExperimental evolutionGenetic DriftChaperonin 60Gene Expression Regulation BacterialGroEL1105 Ecology Evolution Behavior and SystematicsGenes BacterialMutation570 Life sciences; biology590 Animals (Zoology)bacteriaProtein foldingGenetic FitnessDirected Molecular EvolutionSubcellular Fractions
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Pore-forming toxins activate MAPK p38 by causing loss of cellular potassium.

2009

Mitogen activated protein kinase (MAPK) p38 has emerged as a survival protein in cells that are attacked by bacterial toxins forming small membrane pores. Activation of p38 by pore forming toxins (PFT) has been attributed to osmotic stress, but here we show that loss of K+ is likely to be the critical parameter. Several lines of evidence support this conclusion: first, osmoprotection did not prevent p38-phosphorylation in alpha-toxin-loaded cells. Second, treatment of cells with a K+ ionophore, or simple incubation in K+-free medium sufficed to cause robust p38-phosphorylation. Third, media containing high [K+] prevented p38-activation by Staphylococcus aureus alpha-toxin, Vibrio cholerae c…

Pore Forming Cytotoxic ProteinsOsmotic shockp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologyHemolysin ProteinsBiochemistryp38 Mitogen-Activated Protein KinasesCell LineCell membraneHemolysin ProteinsmedicineHumansPhosphorylationMolecular BiologyPore-forming toxinEscherichia coli ProteinsCell MembraneHemolysinEpithelial CellsCell BiologyCell biologyEnzyme Activationmedicine.anatomical_structureBiochemistryPotassiumStreptolysinCalciumCytolysinBiochemical and biophysical research communications
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Evidence for a direct interaction of Rev protein with nuclear envelop mRNA-translocation system.

1991

The interaction of the Rev protein from human immunodeficiency virus type 1 (HIV-1) with the nucleocytoplasmic mRNA-transport system was investigated. In gel-shift assay, the recombinant Rev protein used in this study selectively bound to the Rev-responsive element (RRE) region of HIV-1 env-specific RNA. Nitrocellulose-filter-binding studies and Northern/Western-blotting experiments revealed an association constant of approximately 1 x 10(10) M-1. The Rev protein also strongly bound to isolated nuclear envelopes from H9 cells, containing the poly(A)-binding site (= mRNA carrier) and the nucleoside triphosphatase (= NTPase), which are thought to be involved in nuclear export of poly(A)-rich …

Pore complexPolyadenylationNuclear EnvelopevirusesBlotting WesternBiologyBiochemistryCell LineAdenosine TriphosphateAnimalsRNA MessengerNuclear porePhosphorylationNuclear export signalMessenger RNAVesicleRNABiological Transportrev Gene Products Human Immunodeficiency VirusBlotting NorthernNucleoside-TriphosphataseMolecular biologyPhosphoric Monoester HydrolasesRecombinant ProteinsCell biologyRatsBlotGene Products revHIV-1RNA ViralPoly AEuropean journal of biochemistry
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A new method to isolate microglia from adult mice and culture them for an extended period of time

2009

As the major immuno-competent cells of the brain, microglia are highly implicated in neuro-protection as well as in neurodegeneration. Therefore, they are of key interest for research on numerous CNS diseases. Currently, to model inflammation in the brain, microglial cell lines or primary microglia prepared from embryonic or neo-natal rodents are widely used. However, these in vitro microglial models are not suitable for research in the field of neuro-degenerative diseases where aging is a crucial parameter. Only a few in vitro studies on aged microglia have been published so far, most of which use ex vivo microglia which cannot be kept in culture for prolonged periods of time. In the prese…

Potassium Channelsmedicine.medical_treatmentPopulationFluorescent Antibody TechniqueInflammationCell SeparationBiologyNitric OxideCell LineMicePhagocytosismedicineAnimalseducationCells Culturededucation.field_of_studyMicrogliaGeneral NeuroscienceCell MembraneNeurodegenerationFlow Cytometrymedicine.diseaseEmbryonic stem cellIn vitroElectrophysiologyMice Inbred C57BLCytokinemedicine.anatomical_structureAnimals NewbornCytokinesFemaleMicrogliamedicine.symptomNeuroscienceEx vivoJournal of Neuroscience Methods
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Functional characterization of two melanocortin (MC) receptors in lamprey showing orthology to the MC1 and MC4 receptor subtypes

2007

Abstract Background The melanocortin (MC) receptors have a key role in regulating body weight and pigmentation. They belong to the rhodopsin family of G protein-coupled receptors (GPCRs). The purpose of this study was to identify ancestral MC receptors in agnathan, river lamprey. Results We report cloning of two MC receptors from river lamprey. The lamprey receptors, designated MCa and MCb, showed orthology to the MC1 and MC4 receptor subtypes, respectively. The molecular clock analysis suggested that lamprey MC receptor genes were not duplicated recently and diverged from each other more than 400 MYR ago. Expression and pharmacological characterization showed that the lamprey MCa receptor …

Pro-OpiomelanocortinSecond Messenger SystemsGene DuplicationProtein Interaction MappingCyclic AMPPetromyzonReceptorPhylogenyCell Line TransformedSkinGeneticsbiologyReceptors MelanocortinMelanocortin 3 receptorCell biologyOrgan SpecificityRhodopsinReceptor Melanocortin Type 4HagfishesMelanocortinReceptor Melanocortin Type 1Protein BindingResearch ArticleEvolutionRecombinant Fusion ProteinsMolecular Sequence DataBinding CompetitivePeptides CyclicEvolution Moleculargamma-MSHAdrenocorticotropic HormoneSpecies SpecificityMelanocortin receptorbeta-MSHQH359-425AnimalsHumansAmino Acid SequenceEcology Evolution Behavior and SystematicsGene LibraryG protein-coupled receptorBinding SitesSequence Homology Amino AcidFuguLampreybiology.organism_classificationPeptide FragmentsVisceraalpha-MSHbiology.proteinCosyntropinSequence Alignmenthuman activitiesBMC Evolutionary Biology
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Cytotoxicity and apoptosis induction by Fumaria officinalis extracts in leukemia and multiple myeloma cell lines

2021

Abstract Ethnopharmacological relevance Fumaria officinalis (Fumariaceae) is recorded in the Kurdish ethnobotany for various health problems. Aim of the study: In this study, the cytotoxic activity of F. officinalis extracts on two leukemia and nine multiple myeloma (MM) cell lines was investigated. Materials and methods: The cytotoxic and ferroptotic activity were examined by resazurin reduction assay. Flow cytometry, immunoblotting assay and fluorescence microscopy were used to measure cell cycle distribution, apoptosis, induction of reactive oxygen species (ROS), loss integrity of mitochondrial membrane potential (MMP) and autophagy. LC-ESI/MS was used to identify chemical constituents p…

Programmed cell deathApoptosisFlow cytometryInhibitory Concentration 5003 medical and health sciences0302 clinical medicineCell Line TumorDrug DiscoveryAutophagymedicineHumansCytotoxicity030304 developmental biologyMembrane Potential MitochondrialPharmacology0303 health sciencesLeukemiamedicine.diagnostic_testbiologyPlant ExtractsChemistryCell growthFumariaFumaria officinalisCell cyclebiology.organism_classificationAntineoplastic Agents PhytogenicMolecular biologyApoptosis030220 oncology & carcinogenesisOfficinalisMultiple MyelomaReactive Oxygen SpeciesJournal of Ethnopharmacology
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Met inhibition revokes IFNγ-induction of PD-1 ligands in MET-amplified tumours

2019

BACKGROUND: Interferon-induced expression of programmed cell death ligands (PD-L1/PD-L2) may sustain tumour immuneevasion. Patients featuring MET amplification, a genetic lesion driving transformation, may benefit from anti-MET treatment. We explored if MET-targeted therapy interferes with Interferon-gamma modulation of PD-L1/PD-L2 in MET-amplified tumours.METHODS: PD-L1/PD-L2 expression and signalling pathways downstream of MET or Interferon-gamma were analysed in MET-amplified tumour cell lines and in patient-derived tumour organoids, in basal condition, upon Interferon-gamma stimulation, and after anti-MET therapy.RESULTS: PD-L1 and PD-L2 were upregulated in MET-amplified tumour cells up…

Programmed cell deathCancer ResearchCancer immunotherapyMET-amplified tumoursB7-H1 AntigenArticleInterferon-gammaTargeted therapiesDownregulation and upregulationInterferonCell Line TumorNeoplasmsHumansMedicineMet inhibitionMolecular Targeted TherapySTAT1Kinase activityReceptorProtein Kinase InhibitorsJanus KinasesReceptors InterferonOncogenebiologyPD-1 ligandsbusiness.industryLiver NeoplasmsOncogenesProto-Oncogene Proteins c-metProgrammed Cell Death 1 Ligand 2 ProteinOrganoidsSTAT1 Transcription FactorOncologybiology.proteinCancer researchOncology; Cancer Research; Met inhibition; IFNγ-induction;PD-1 ligands; MET-amplified tumoursTumor EscapeSignal transductionColorectal NeoplasmsbusinessIFNγ-inductionSignal Transductionmedicine.drug
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The abrogation of the HOXB7/PBX2 complex induces apoptosis in melanoma through the miR-221&222-c-FOS pathway.

2013

Cutaneous melanoma is the fastest increasing cancer worldwide. Although several molecular abnormalities have been associated with melanoma progression, the underlying mechanisms are still largely unknown and few targeted therapies are under evaluation. Here we show that the HOXB7/PBX2 dimer acts as a positive transcriptional regulator of the oncogenic microRNA-221 and -222. In addition, demonstrating c-FOS as a direct target of miR-221&222, we identify a HOXB7/PBX2→miR-221&222 →c-FOS regulatory link, whereby the abrogation of functional HOXB7/PBX2 dimers leads to reduced miR-221&222 transcription and elevated c-FOS expression with consequent cell death. Taking advantage of the treatment wit…

Programmed cell deathCancer ResearchSkin NeoplasmsTranscription GeneticApoptosisSmall Interferingc-FosPolymerase Chain ReactionCell LineGeneticCell Line TumorProto-Oncogene ProteinsHOXB7/PBX2 complexmicroRNATranscriptional regulationmedicinemelanomaHumansPBXRNA Small InterferingDNA PrimersHomeodomain Proteinsc-FOS pathwayTumorbiologymicroRNABase SequenceMelanomaHOXB7; HXR9 peptide; melanoma; microRNA; PBX; Apoptosis; Base Sequence; Cell Line Tumor; DNA Primers; Dimerization; Homeodomain Proteins; Humans; Melanoma; MicroRNAs; Polymerase Chain Reaction; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-fos; RNA Small Interfering; Skin Neoplasms; Transcription Genetic; Cancer Research; Oncologymedicine.diseaseMicroRNAsHXR9 peptideOncologyApoptosisCell cultureCutaneous melanomaHOXB7/PBX2 complex ;melanoma ;c-FOS pathwayCancer researchbiology.proteinHOXB7RNATranscriptionDimerizationProto-Oncogene Proteins c-fosCancer Cell Biology
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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COX-2-dependent and COX-2-independent mode of action of celecoxib in human liver cancer cells.

2011

Celecoxib (Celebrex((R)), Pfizer) is a selective cyclooxygenase-2 (COX-2) inhibitor with chemopreventive and antitumor effects. However, it is now well known that celecoxib has several COX-2-independent activities. To better understand COX-2-independent molecular mechanisms underlying the antitumor activity of celecoxib, we investigated the expression profile of the celecoxib-treated COX-2-positive (Huh7) and COX-2-negative (HepG2) liver cancer cell lines, using microarray analysis. Celecoxib treatment resulted in significantly altered expression levels of 240 and 403 transcripts in Huh7 and HepG2 cells, respectively. Confirmation of the microarray results was performed for selected genes b…

Programmed cell deathCarcinoma HepatocellularMicroarrayTranscription GeneticHepatocellular carcinomaCell SurvivalAntineoplastic AgentsPharmacologyBiologyBiochemistryCell Line TumorGeneticsmedicineHumansMode of actionneoplasmsMolecular BiologySulfonamidesCyclooxygenase 2 InhibitorsCell growthMicroarray analysis techniquesGene Expression ProfilingLiver NeoplasmsCOX-2Gene expression profilingGene Expression Regulation NeoplasticCell cultureCelecoxibCyclooxygenase 2CelecoxibMolecular MedicinePyrazolesBiotechnologymedicine.drugSignal TransductionOmics : a journal of integrative biology
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