Search results for "messenger"

showing 10 items of 1493 documents

Carbocysteine regulates innate immune responses and senescence processes in cigarette smoke stimulated bronchial epithelial cells

2013

Cigarette smoke represents the major risk factor for chronic obstructive pulmonary disease (COPD). Cigarette smoke extracts (CSE) alter TLR4 expression and activation in bronchial epithelial cells. Carbocysteine, an anti-oxidant and mucolytic agent, is effective in reducing the severity and the rate of exacerbations in COPD patients. The effects of carbocysteine on TLR4 expression and on the TLR4 activation downstream events are largely unknown. This study was aimed to explore whether carbocysteine, in a human bronchial epithelial cell line (16-HBE), counteracted some pro-inflammatory CSE-mediated effects. In particular, TLR4 expression, LPS binding, p21 (a senescence marker), IL-8 mRNA and…

Cyclin-Dependent Kinase Inhibitor p21AgingNeutrophilsPhalloidinAnti-Inflammatory AgentsApoptosisBronchiInflammationBiologyToxicologySettore BIO/09 - FisiologiaAntioxidantsFlow cytometryPulmonary Disease Chronic Obstructivechemistry.chemical_compoundmedicineHumansRNA Messengersenescencebronchial cellscigaretteInnate immune systemmedicine.diagnostic_testCarbocysteineInterleukin-8SmokingEpithelial CellsCell migrationChemotaxisCarbocysteineGeneral MedicineFlow CytometryImmunity InnateCell biologyToll-Like Receptor 4chemistryImmunologyTLR4medicine.symptomInterleukin-1Signal TransductionToxicology Letters
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In vivo studies of altered expression patterns of p53 and proliferative control genes in chronic vitamin A deficiency and hypervitaminosis

2003

Several clinical trials have revealed that individuals who were given beta-carotene and vitamin A did not have a reduced risk of cancer compared to those given placebo; rather, vitamin A could actually have caused an adverse effect in the lungs of smokers [Omenn, G.S., Goodman, G.E., Thornquist, M.D., Balmes, J., Cullen, M.R., Glass, A., Keogh, J.P., Meyskens, F.L., Valanis, B., Williams, J.H., Barnhart, S. & Hammar, S. N. Engl. J. Med (1996) 334, 1150-1155; Hennekens, C.H., Buring, J.E., Manson, J.E., Stampfer, M., Rosner, B., Cook, N.R., Belanger, C., LaMotte, F., Gaziano, J.M., Ridker, P.M., Willet, W. & Peto, R. (1996) N. Engl. J. Med. 334, 1145-1149]. Using differential display techniq…

Cyclin-Dependent Kinase Inhibitor p21VitaminRetinyl Estersmedicine.medical_specialtyMacromolecular SubstancesProto-Oncogene Proteins c-junReceptors Retinoic AcidBlotting WesternRetinoic acidBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundIn vivoCyclinsInternal medicinemedicineAnimalsHypervitaminosis ARNA MessengerRats WistarVitamin AReceptorLungDifferential displayReverse Transcriptase Polymerase Chain ReactionVitamin A DeficiencyGene Expression ProfilingDNAmedicine.diseaseHypervitaminosisPrecipitin TestsRatsVitamin A deficiencyEndocrinologyGene Expression RegulationLiverchemistryChronic DiseaseImmunologyDiterpenesTumor Suppressor Protein p53CarcinogenesisCell DivisionEuropean Journal of Biochemistry
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Roflumilast inhibits respiratory syncytial virus infection in human differentiated bronchial epithelial cells.

2013

Respiratory syncytial virus (RSV) causes acute exacerbations in COPD and asthma. RSV infects bronchial epithelial cells (HBE) that trigger RSV associated lung pathology. This study explores whether the phosphodiesterase 4 (PDE4) inhibitor Roflumilast N-oxide (RNO), alters RSV infection of well-differentiated HBE (WD-HBE) in vitro. WD-HBE were RSV infected in the presence or absence of RNO (0.1-100 nM). Viral infection (staining of F and G proteins, nucleoprotein RNA level), mRNA of ICAM-1, ciliated cell markers (digital high speed videomicroscopy, β-tubulin immunofluorescence, Foxj1 and Dnai2 mRNA), Goblet cells (PAS), mRNA of MUC5AC and CLCA1, mRNA and protein level of IL-13, IL-6, IL-8, T…

CyclopropanesScienceAminopyridinesBronchiCell CountRespiratory Syncytial Virus InfectionsBiologyMucin 5ACImmunofluorescenceVirus ReplicationVirusAntioxidantsChloride ChannelsTubulinGene expressionmedicineHumansCiliaRNA MessengerRespiratory systemRoflumilastMessenger RNAMetaplasiaMultidisciplinarymedicine.diagnostic_testQRvirus diseasesCell DifferentiationEpithelial CellsForkhead Transcription FactorsAxonemal Dyneinsrespiratory systemViral LoadVirologyMolecular biologyRespiratory Syncytial VirusesOxidative StressViral replicationBenzamidesMedicineCytokinesTumor necrosis factor alphaGoblet CellsReactive Oxygen SpeciesBiomarkersmedicine.drugResearch ArticlePloS one
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Enhancement of premature stop codon readthrough in the CFTR gene by Ataluren (PTC124) derivatives.

2015

Abstract Premature stop codons are the result of nonsense mutations occurring within the coding sequence of a gene. These mutations lead to the synthesis of a truncated protein and are responsible for several genetic diseases. A potential pharmacological approach to treat these diseases is to promote the translational readthrough of premature stop codons by small molecules aiming to restore the full-length protein. The compound PTC124 (Ataluren) was reported to promote the readthrough of the premature UGA stop codon, although its activity was questioned. The potential interaction of PTC124 with mutated mRNA was recently suggested by molecular dynamics (MD) studies highlighting the importanc…

Cystic FibrosisNonsense mutationPeptide Chain Elongation TranslationalCystic Fibrosis Transmembrane Conductance RegulatorSettore BIO/11 - Biologia MolecolareMolecular Dynamics SimulationCFTR genechemistry.chemical_compoundStructure-Activity RelationshipPlasmidDrug DiscoveryTumor Cells CulturedCoding regionHumansGreen fluorescent proteinGenePharmacologyGeneticsMessenger RNAOxadiazolesNonsense mutationDose-Response Relationship DrugMolecular StructureDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryTranslational readthroughSettore CHIM/06 - Chimica OrganicaGeneral MedicinePTCs readthroughStop codonAtalurenSettore BIO/18 - GeneticachemistrySettore CHIM/03 - Chimica Generale E InorganicaCodon NonsenseCystic fibrosiMutationFluorinated oxadiazoleHeLa CellsEuropean journal of medicinal chemistry
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The differentiation antigen NY-BR-1 is a potential target for antibody-based therapies in breast cancer

2007

Antibody-based cancer immunotherapy relies on the identification and characterization of target antigens and the development of potent antibodies recognizing the target. Here we report the expression analysis and molecular characterization of the differentiation antigen NY-BR-1, which we previously identified by using the SEREX (serological analysis of recombinant cDNA expression libraries) method. Corroborating methodologies, including mRNA quantitation and immunoblotting show that NY-BR-1 is strongly expressed in >70% of 129 breast tumors. Application of a NY-BR-1 specific antibody demonstrated NY-BR-1 expression in primary and metastastic breast cancers. In contrast, most of the breast c…

CytoplasmCancer ResearchPathologymedicine.medical_specialtyRecombinant Fusion Proteinsmedicine.medical_treatmentCellular differentiationGreen Fluorescent ProteinsImmunoblottingBreast NeoplasmsBiologyTargeted therapyBreast cancerAntigenCancer immunotherapyAntigens NeoplasmCell Line TumormedicineHumansRNA MessengerBinding SitesMicroscopy ConfocalReverse Transcriptase Polymerase Chain ReactionCell MembraneAntibodies MonoclonalMembrane ProteinsFlow Cytometrymedicine.diseaseAntigens DifferentiationImmunohistochemistryTumor antigenGene Expression Regulation NeoplasticOncologyCancer researchbiology.proteinImmunohistochemistryFemaleAntibodyHydrophobic and Hydrophilic InteractionsInternational Journal of Cancer
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Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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Analysis of cytochrome C oxidase subunits III and IV expression in developing rat brain

2004

Abstract Cytochrome c oxidase (COX) complex is built up with both nucleus- and mitochondrion-encoded subunits. Biogenesis and assembly of the complex thus requires fine cross-talk between the two compartments. In order to shed light on the regulation of nuclear–mitochondrial interactions, we studied the expression of COXIII (mitochondrion-encoded) and COXIV (nucleus-encoded) in adult rat tissues and rat developing brain. We found that the levels of COXIV protein and mRNA are not linearly related, thus suggesting a post-transcriptional mode of regulation. In agreement with this observation, we report the presence of a protein that specifically binds to the 3′-untranslated region of COXIV mRN…

CytoplasmRNA-binding proteinProtein subunitBlotting WesternCOX IVRNA-binding proteinMitochondrionBiologyGene Expression Regulation EnzymologicElectron Transport Complex IVAnimalsCytochrome c oxidaseElectrophoresis Gel Two-DimensionalCOX III.RNA MessengerRNA Processing Post-TranscriptionalMessenger RNAGeneral NeuroscienceBrainProteinsRNABlotting NorthernMitochondriaRatsProtein TransportCytosolnucleus-mitochondrion cross-talkBiochemistryCytoplasmbiology.proteinNeuroscience
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Cytoglobin is a respiratory protein in connective tissue and neurons, which is up-regulated by hypoxia.

2004

Cytoglobin is a recently discovered vertebrate globin distantly related to myoglobin, and its function is unknown. Here we present the first detailed analysis of the distribution and expression of cytoglobin. Northern and Western blotting experiments show the presence of cytoglobin mRNA and protein in a broad range of tissues. Quantitative PCR demonstrates an up-regulation of cytoglobin mRNA levels in rat heart and liver under hypoxic conditions (22 and 44 h of 9% oxygen). Immunofluorescence studies with three antibodies directed against different epitopes of the protein consistently show cytoglobin in connective tissue fibroblasts as well as in hepatic stellate cells. Cytoglobin is also pr…

CytoplasmRespiratory SystemFluorescent Antibody TechniqueBiochemistryMiceAntibody SpecificityChlorocebus aethiopsRespiratory functionHypoxiaNeuronsMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionCytoglobinNuclear ProteinsImmunohistochemistryGlobinsRespiratory proteinTracheamedicine.anatomical_structureLiverConnective TissueNeuroglobinRecombinant Fusion ProteinsGreen Fluorescent ProteinsMolecular Sequence DataConnective tissueBiologyTransfectionAntibodiesBone and BonesmedicineAnimalsHumansGlobinAmino Acid SequenceRNA MessengerMolecular BiologyVero CellsCell NucleusMessenger RNAMyocardiumCytoglobinCell BiologyFibroblastsMolecular biologyPeptide FragmentsRatsOxygenLuminescent ProteinsGene Expression RegulationHepatic stellate cellHeLa CellsThe Journal of biological chemistry
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Regulation of ribonucleotide reductase in response to iron deficiency

2011

Ribonucleotide reductase (RNR) is an essential enzyme required for DNA synthesis and repair. Although iron is necessary for class Ia RNR activity, little is known about the mechanisms that control RNR in response to iron deficiency. In this work, we demonstrate that yeast cells control RNR function during iron deficiency by redistributing the Rnr2–Rnr4 small subunit from the nucleus to the cytoplasm. Our data support a Mec1/Rad53-independent mechanism in which the iron-regulated Cth1/Cth2 mRNA-binding proteins specifically interact with the WTM1 mRNA in response to iron scarcity, and promote its degradation. The resulting decrease in the nuclear-anchoring Wtm1 protein levels leads to the re…

CytoplasmSaccharomyces cerevisiae ProteinsDeoxyribonucleoside triphosphateRibonucleoside Diphosphate ReductaseRNA StabilityProtein subunitSaccharomyces cerevisiaeCell Cycle ProteinsSaccharomyces cerevisiaeProtein Serine-Threonine KinasesBiologyResponse ElementsArticleTristetraprolinGene Expression Regulation FungalRibonucleotide ReductasesHumansRNA MessengerMolecular BiologyTranscription factorCell NucleusDNA synthesisIntracellular Signaling Peptides and ProteinsFungal geneticsRNA-Binding ProteinsRNA FungalIron DeficienciesCell Biologybiology.organism_classificationDNA-Binding ProteinsRepressor ProteinsCheckpoint Kinase 2Protein SubunitsProtein TransportRibonucleotide reductaseBiochemistryCytoplasmTranscription Factors
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Gene expression is circular: factors for mRNA degradation also foster mRNA synthesis.

2013

SummaryMaintaining proper mRNA levels is a key aspect in the regulation of gene expression. The balance between mRNA synthesis and decay determines these levels. We demonstrate that most yeast mRNAs are degraded by the cytoplasmic 5′-to-3′ pathway (the “decaysome”), as proposed previously. Unexpectedly, the level of these mRNAs is highly robust to perturbations in this major pathway because defects in various decaysome components lead to transcription downregulation. Moreover, these components shuttle between the cytoplasm and the nucleus, in a manner dependent on proper mRNA degradation. In the nucleus, they associate with chromatin—preferentially ∼30 bp upstream of transcription start-sit…

CytoplasmSaccharomyces cerevisiae ProteinsTranscription GeneticRNA StabilityGenes FungalRNA polymerase IIRNA-binding proteinSaccharomyces cerevisiaeGenètica molecularGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesGene Expression ProcessTranscription (biology)Gene Expression Regulation FungalGene expressionP-bodiesmedicineRNA Messenger030304 developmental biologyRegulation of gene expressionCell Nucleus0303 health sciencesbiologyBiochemistry Genetics and Molecular Biology(all)030302 biochemistry & molecular biologyRNA-Binding ProteinsRNA FungalMolecular biologyCell biologyCell nucleusmedicine.anatomical_structureExoribonucleasesbiology.proteinRNARNA Polymerase IICell
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