Search results for "Small Interfering"

showing 10 items of 249 documents

The Wnt-specific astacin proteinase HAS-7 restricts head organizer formation in Hydra

2021

Abstract Background The Hydra head organizer acts as a signaling center that initiates and maintains the primary body axis in steady state polyps and during budding or regeneration. Wnt/beta-Catenin signaling functions as a primary cue controlling this process, but how Wnt ligand activity is locally restricted at the protein level is poorly understood. Here we report a proteomic analysis of Hydra head tissue leading to the identification of an astacin family proteinase as a Wnt processing factor. Results Hydra astacin-7 (HAS-7) is expressed from gland cells as an apical-distal gradient in the body column, peaking close beneath the tentacle zone. HAS-7 siRNA knockdown abrogates HyWnt3 proteo…

ProteomicsPhysiologyHydraQH301-705.5XenopusPlant ScienceProteinaseGeneral Biochemistry Genetics and Molecular BiologyStructural BiologyAstacinAxis formationAnimalsRNA Small InterferingBiology (General)Wnt Signaling PathwayEcology Evolution Behavior and SystematicsActinbeta CateninBody PatterningGene knockdownBuddingbiologyRegeneration (biology)Wnt signaling pathwayMetalloendopeptidasesCell Biologybiology.organism_classificationWnt signalingCell biologyWnt ProteinsProteolysisLernaean HydraAstacinGeneral Agricultural and Biological SciencesHeadDevelopmental BiologyBiotechnologyResearch ArticleBMC Biology
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Nanocomplexes for gene therapy of respiratory diseases: Targeting and overcoming the mucus barrier

2015

Gene therapy, i.e. the delivery and expression of therapeutic genes, holds great promise for congenital and acquired respiratory diseases. Non-viral vectors are less toxic and immunogenic than viral vectors, although they are characterized by lower efficiency. However, they have to overcome many barriers, including inflammatory and immune mediators and cells. The respiratory and airway epithelial cells, the main target of these vectors, are coated with a layer of mucus, which hampers the effective reaching of gene therapy vectors carrying either plasmid DNA or small interfering RNA. This barrier is thicker in many lung diseases, such as cystic fibrosis. This review summarizes the most impor…

Pulmonary and Respiratory MedicineCystic FibrosisGenetic enhancementContext (language use)Gene deliveryVectors in gene therapyPolyethylene GlycolsViral vectorPolyethyleinimine Poly-L-lysine Ethylene glycol Chitosan PAMAM G0 dendrimer N-(1-(23-Dioleyloxy)propyl)-NNNtrimethylammonium chloride 12-Dioleoylphosphatidylethanolamine N-acetylcystein 12-Dioctadecanoyl-sn-glycero-3-phosphoethanolaminemedicineHumansTechnology PharmaceuticalPharmacology (medical)RNA Small InterferingLungExpectorantsInflammationLungbusiness.industryBiochemistry (medical)Gene Transfer TechniquesGenetic TherapyMucusMucusmedicine.anatomical_structureSettore CHIM/09 - Farmaceutico Tecnologico ApplicativoImmunologyNanoparticlesInflammation MediatorsbusinessPlasmidsRespiratory tract
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Aclidinium inhibits cholinergic and tobacco smoke-induced MUC5AC in human airways.

2010

Mucus hypersecretion and mucin MUC5AC overexpression are pathological features of chronic obstructive pulmonary disease (COPD). This study examines the inhibitory effect of aclidinium, a new long-acting muscarinic antagonist, on MUC5AC expression in human airway epithelial cells. MUC5AC mRNA (RT-PCR) and protein expression (ELISA and immunohistochemistry) were studied in human bronchial tissue and differentiated human airway epithelial cells activated with carbachol (100 μM) or cigarette smoke extract in the absence or presence of aclidinium. Carbachol increased MUC5AC mRNA and protein expression in human bronchus and cultured epithelial cells. Aclidinium inhibited the carbachol-induced MUC…

Pulmonary and Respiratory MedicineMAPK/ERK pathwaymedicine.medical_specialtyCarbacholRespiratory SystemMuscarinic AntagonistsPharmacologyMucin 5ACPulmonary Disease Chronic ObstructiveDownregulation and upregulationInternal medicinemedicineHumansRNA Small InterferingCells CulturedBronchusbusiness.industryMucinSmokingEpithelial Cellsrespiratory systemMucusEpitheliumErbB ReceptorsEndocrinologymedicine.anatomical_structureCarbacholMitogen-Activated Protein KinasesbusinessTyrosine kinasemedicine.drugTropanesThe European respiratory journal
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Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition.

2012

Cigarette smoking contributes to lung remodelling in chronic obstructive pulmonary disease (COPD). As part of this remodelling, peribronchiolar fibrosis is observed in the small airways of COPD patients and contributes to airway obstruction. Fibroblast-to-myofibroblast transition is a key step in peribronchiolar fibrosis formation. This in vitro study examined the effect of cigarette smoke on bronchial fibroblast-to-myofibroblast transition, and whether aclidinium bromide inhibits this process. Human bronchial fibroblasts were incubated with aclidinium bromide (10 −9 –10 −7 M) and exposed to cigarette smoke extract. Collagen type I and α-smooth muscle actin (α-SMA) expression were measured …

Pulmonary and Respiratory MedicineTime FactorsBronchiPharmacologyCholinergic AntagonistsCollagen Type Ichemistry.chemical_compoundAclidinium bromideFibrosisSmokemedicineExtracellularCyclic AMPHumansRNA Small InterferingFibroblastMyofibroblastsLungCells CulturedInflammationbusiness.industrySmokingFibroblastsmedicine.diseaseFluoresceinsAcetylcholinesteraseFibrosisActinsrespiratory tract diseasesmedicine.anatomical_structurechemistryGene Expression RegulationMicroscopy FluorescencebusinessReactive Oxygen SpeciesMyofibroblastAcetylcholineIntracellularmedicine.drugTropanesThe European respiratory journal
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Critical role of fractalkine (CX3CL1) in cigarette smoke-induced mononuclear cell adhesion to the arterial endothelium.

2012

Background Cigarette smoking is an important risk factor for the development of cardiovascular disease, yet the pathways through which this may operate are poorly understood. Therefore, the mechanism underlying cigarette smoke (CS)-induced arterial endothelial dysfunction and the potential link with fractalkine/CX3CL1 upregulation were investigated. Methods and results Stimulation of human arterial umbilical endothelial cells (HUAECs) with pathophysiological concentrations of CS extract (1% CSE) increased CX3CL1 expression. Neutralisation of CX3CL1 activity under dynamic flow conditions significantly inhibited CSE-induced mononuclear cell adhesion to HUAECs (67%). The use of small interferi…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyEndotheliumPeripheral blood mononuclear cellMiceInternal medicineCX3CR1Cell AdhesionMedicineAnimalsHumansEndothelial dysfunctionRNA Small InterferingCell adhesionNADPH oxidasebiologybusiness.industryChemokine CX3CL1MicrocirculationSmokingNOX4Membrane ProteinsNADPH Oxidasesmedicine.diseaseUp-RegulationEndothelial stem cellmedicine.anatomical_structureEndocrinologyNADPH Oxidase 5Immunologybiology.proteinEndothelium VascularbusinessThorax
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p27Kip1participates in the regulation of endoreplication in differentiating chick retinal ganglion cells

2015

Nuclear DNA duplication in the absence of cell division (i.e. endoreplication) leads to somatic polyploidy in eukaryotic cells. In contrast to some invertebrate neurons, whose nuclei may contain up to 200,000-fold the normal haploid DNA amount (C), polyploid neurons in higher vertebrates show only 4C DNA content. To explore the mechanism that prevents extra rounds of DNA synthesis in these latter cells we focused on the chick retina, where a population of tetraploid retinal ganglion cells (RGCs) has been described. We show that differentiating chick RGCs that express the neurotrophic receptors p75 and TrkB while lacking retinoblastoma protein, a feature of tetraploid RGCs, also express p27K…

Retinal Ganglion CellsretinaEndocycleCell divisionCellular differentiationChick EmbryoRetinoblastoma ProteinendoreduplicationMicevertebrateRNA Small InterferingpolyploidyMice KnockoutRGCeducation.field_of_studyCell DifferentiationEndoreduplicationCell cycleImmunohistochemistryNuclear DNAendocycleneurogenesiscell cycleRNA InterferenceCyclin-Dependent Kinase Inhibitor p27NeurogenesisPopulationDown-RegulationCell cycleBiologyRetinal ganglionRetinaPolyploidyReportAnimalsReceptor trkBEndoreduplicationeducationMolecular BiologyPloidiesDNA synthesisVertebrateCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cell BiologyMinichromosome Maintenance Complex Component 7Molecular biologyeye diseasessense organsChickensDevelopmental BiologyCell Cycle
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Dual-targeting siRNAs.

2010

We have developed an algorithm for the prediction of dual-targeting short interfering RNAs (siRNAs) in which both strands are deliberately designed to separately target different mRNA transcripts with complete complementarity. An advantage of this approach versus the use of two separate duplexes is that only two strands, as opposed to four, are competing for entry into the RNA-induced silencing complex. We chose to design our dual-targeting siRNAs as Dicer substrate 25/27mer siRNAs, since design features resembling pre-microRNAs (miRNAs) can be introduced for Dicer processing. Seven different dual-targeting siRNAs targeting genes that are potential targets in cancer therapy have been develo…

STAT3 Transcription FactorSmall interfering RNATranscription GeneticTrans-acting siRNAGenes mycMethodComputational biologyKidneyPolymerase Chain ReactionCell LineSuppression GeneticRNA interferencemicroRNAGene silencingHumansRNA MessengerRNA Small InterferingMolecular BiologyGeneticsGene knockdownbiologyBase SequenceRNAProtein Biosynthesisbiology.proteinProto-Oncogene Proteins c-bcl-6AlgorithmsDicerRNA (New York, N.Y.)
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Phosphorylation of the Usher syndrome 1G protein SANS controls Magi2-mediated endocytosis.

2014

Item does not contain fulltext The human Usher syndrome (USH) is a complex ciliopathy with at least 12 chromosomal loci assigned to three clinical subtypes, USH1-3. The heterogeneous USH proteins are organized into protein networks. Here, we identified Magi2 (membrane-associated guanylate kinase inverted-2) as a new component of the USH protein interactome, binding to the multifunctional scaffold protein SANS (USH1G). We showed that the SANS-Magi2 complex assembly is regulated by the phosphorylation of an internal PDZ-binding motif in the sterile alpha motif domain of SANS by the protein kinase CK2. We affirmed Magi2's role in receptor-mediated, clathrin-dependent endocytosis and showed tha…

Scaffold proteinGuanylate kinaseMolecular Sequence DataPrimary Cell CultureNerve Tissue ProteinsBiologyEndocytosisPhotoreceptor cellExocytosisMiceCiliogenesisGeneticsmedicineAnimalsHumansProtein Interaction Domains and MotifsAmino Acid SequencePhosphorylationRNA Small InterferingSensory disorders Radboud Institute for Molecular Life Sciences [Radboudumc 12]Molecular BiologyGenetics (clinical)Adaptor Proteins Signal TransducingBinding SitesGeneral MedicineClathrinEndocytosisCell biologyMice Inbred C57BLRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]medicine.anatomical_structureHEK293 CellsGene Expression RegulationCiliary pocketCarrier ProteinsSterile alpha motifGuanylate KinasesSequence AlignmentUsher SyndromesPhotoreceptor Cells VertebrateProtein BindingSignal TransductionHuman molecular genetics
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Haem oxygenase-1 counteracts the effects of interleukin-1β on inflammatory and senescence markers in cartilage-subchondral bone explants from osteoar…

2011

IL (interleukin)-1β plays an important role in cartilage extracellular matrix degradation and bone resorption in OA (osteoarthritis) through the induction of degradative enzymes and pro-inflammatory mediators. In the present study, we have determined the consequences of HO-1 (haem oxygenase-1) induction on markers of inflammation and senescence in the functional unit cartilage–subchondral bone stimulated with IL-1β. Cartilage–subchondral bone specimens were obtained from the knees of osteoarthritic patients. Treatment with the HO-1 inducer CoPP (cobalt protoporphyrin IX) counteracted the stimulatory effects of IL-1β on IL-6, nitrite, PGE2 (prostaglandin E2), TGF (transforming growth factor)…

SenescenceCartilage Articularmedicine.medical_treatmentInterleukin-1betaDown-RegulationNitric Oxide Synthase Type IIProtoporphyrinsBone resorptionDinoprostoneOsteoarthritismedicineHumansTelomerase reverse transcriptaseProstaglandin E2Bone ResorptionRNA Small InterferingCellular SenescenceProstaglandin-E SynthasesbiologyInterleukin-6InterleukinGeneral MedicineCOPPMolecular biologyIntramolecular OxidoreductasesCyclooxygenase 2ImmunologyHeme Oxygenase (Decyclizing)Osteocalcinbiology.proteinBiomarkersmedicine.drugProstaglandin EClinical science (London, England : 1979)
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DNA damage causes TP53-dependent coupling of self-renewal and senescence pathways in embryonal carcinoma cells.

2013

Recent studies have highlighted an apparently paradoxical link between self-renewal and senescence triggered by DNA damage in certain cell types. In addition, the finding that TP53 can suppress senescence has caused a re-evaluation of its functional role in regulating these outcomes. To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage. Nuclear POU5F1/OCT4A and P21CIP1 were upregulated in the same cells following etoposide-induced G 2M arrest. However, while accumulating in the karyosol, the amount of OCT4A was reduced in the chromatin fract…

SenescenceCyclin-Dependent Kinase Inhibitor p21OCT4A/POU5F1Embryonal Carcinoma Stem CellssenescenceDNA RepairDNA repairDNA damagetumor cellsBiologyProtein Serine-Threonine Kinasesself-renewalHistonesAurora KinasesCell Line TumorReportAutophagyAurora Kinase BHumansTP53PhosphorylationRNA Small InterferingMolecular BiologyMitosisCellular SenescenceCyclin-Dependent Kinase Inhibitor p16EtoposideOvarian NeoplasmsEmbryonal Carcinoma Stem CellsCell BiologyG2-M DNA damage checkpointbeta-GalactosidasepluripotencyAntineoplastic Agents PhytogenicChromatinUp-RegulationG2 Phase Cell Cycle CheckpointsCheckpoint Kinase 2Cancer researchDNA damageFemaleRNA InterferenceRad51 RecombinaseTumor Suppressor Protein p53Cell agingOctamer Transcription Factor-3Developmental BiologyCell cycle (Georgetown, Tex.)
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