Search results for "antisense oligonucleotide"

showing 10 items of 17 documents

CiliaCarta: An integrated and validated compendium of ciliary genes

2019

The cilium is an essential organelle at the surface of mammalian cells whose dysfunction causes a wide range of genetic diseases collectively called ciliopathies. The current rate at which new ciliopathy genes are identified suggests that many ciliary components remain undiscovered. We generated and rigorously analyzed genomic, proteomic, transcriptomic and evolutionary data and systematically integrated these using Bayesian statistics into a predictive score for ciliary function. This resulted in 285 candidate ciliary genes. We generated independent experimental evidence of ciliary associations for 24 out of 36 analyzed candidate proteins using multiple cell and animal model systems (mouse…

ProteomicsSensory ReceptorsNematodaSocial SciencesCiliopathiesBiochemistrySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Transcriptome0302 clinical medicineAnimal CellsPsychologyRETINAL PHOTORECEPTOR CELLSExomeNeurons0303 health sciences030302 biochemistry & molecular biologyEukaryotaGenomicsPRIMARY CILIUMthecilium3. Good healthNucleic acidsGenetic interferenceOsteichthyesMedicineEpigeneticsCellular Structures and OrganellesCellular Typesproteomic databasesSensory Receptor CellsScienceeducationCiliary genesLEBER CONGENITAL AMAUROSISGenomics03 medical and health sciencesGeneticsCiliaCaenorhabditis elegansIDENTIFICATIONMUTATIONSEmbryosciliaOrganismsBiology and Life SciencesBayes TheoremMolecular Sequence Annotationmedicine.diseaseInvertebratesFishciliary proteomeAnimal StudiesCaenorhabditisGene expressionembryos030217 neurology & neurosurgeryDevelopmental BiologyNeurosciencePhotoreceptorsCandidate geneEmbryologyOligonucleotidesMorpholinoDatabase and Informatics MethodsRNA interferenceBayesian classifierTRANSITION ZONEZebrafishAntisense OligonucleotidesZebrafishGeneticsMultidisciplinarySpectrometric Identification of ProteinsProteomic DatabasesNucleotidesCiliumQStable Isotope Labeling by Amino Acids in Cell CultureRphotoreceptorsMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Animal ModelsPhenotypeINTRAFLAGELLAR TRANSPORTDIFFERENTIATIONPhenotypeExperimental Organism SystemsCaenorhabditis ElegansVertebratesSensory PerceptionResearch ArticleSignal TransductionEXPRESSIONStable isotope labeling by amino acids in cell cultureComputational biologyBiologyResearch and Analysis MethodsSOLUTE-CARRIER-PROTEINModel OrganismsmedicineAnimalsdata integration030304 developmental biologyAfferent NeuronsReproducibility of ResultsCell Biologyzebrafishbiology.organism_classificationCiliopathyRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Biological DatabasesCellular NeuroscienceRNAOSCP1CiliaCartaPLoS ONE
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Mongersen, an oral SMAD7 antisense oligonucleotide, and crohn's disease

2015

Crohn's disease-related inflammation is characterized by reduced activity of the immunosuppressive cytokine transforming growth factor β1 (TGF-β1) due to high levels of SMAD7, an inhibitor of TGF-β1 signaling. Preclinical studies and a phase 1 study have shown that an oral SMAD7 antisense oligonucleotide, mongersen, targets ileal and colonic SMAD7.In a double-blind, placebo-controlled, phase 2 trial, we evaluated the efficacy of mongersen for the treatment of persons with active Crohn's disease. Patients were randomly assigned to receive 10, 40, or 160 mg of mongersen or placebo per day for 2 weeks. The primary outcomes were clinical remission at day 15, defined as a Crohn's Disease Activit…

MaleSMAD7 antisense oligonucleotidemedicine.medical_treatmentOligonucleotidesPharmacologyPLACEBO-CONTROLLED TRIALTHERAPYGastroenterologylaw.inventionACTIVATIONImmunosuppressive AgentGlucocorticoidRandomized controlled trialCrohn DiseaselawOligonucleotideMedicineYoung adultCrohn's diseaseSettore MED/12 - GastroenterologiabiologyINDUCTIONMedicine (all)Remission InductionGeneral MedicineMiddle AgedCrohn's diseaseCytokineC-Reactive ProteinCombinationDrug Therapy CombinationFemaleDrugImmunosuppressive AgentsCOLITISHumanAdultmedicine.medical_specialtyAdolescentINFLAMMATORY-BOWEL-DISEASE PLACEBO-CONTROLLED TRIAL NECROSIS-FACTOR-ALPHA TGF-BETA-1-MEDIATED SUPPRESSION COLITIS INDUCTION ACTIVATION EFFICACY THERAPY MICEPlaceboSmad7 ProteinDose-Response RelationshipYoung AdultPharmacotherapyDouble-Blind MethodDrug TherapyInternal medicineHumansAntisenseGlucocorticoidsAgedDose-Response Relationship Drugbusiness.industryC-reactive proteinNECROSIS-FACTOR-ALPHAOligonucleotides AntisenseTGF-BETA-1-MEDIATED SUPPRESSIONEFFICACYmedicine.diseaseClinical trialMICEbiology.proteinbusinessAdolescent; Adult; Aged; C-Reactive Protein; Crohn Disease; Dose-Response Relationship Drug; Double-Blind Method; Drug Therapy Combination; Female; Glucocorticoids; Humans; Immunosuppressive Agents; Male; Middle Aged; Oligonucleotides; Oligonucleotides Antisense; Remission Induction; Smad7 Protein; Young Adult; Medicine (all)INFLAMMATORY-BOWEL-DISEASE
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The future of Extracellular Vesicles as Theranostics – an ISEV meeting report

2020

ABSTRACT The utilization of extracellular vesicles (EVs) in clinical theranostics has rapidly advanced in the past decade. In November 2018, the International Society for Extracellular Vesicles (ISEV) held a workshop on “EVs in Clinical Theranostic”. Here, we report the conclusions of roundtable discussions on the current advancement in the analysis technologies and we provide some guidelines to researchers in the field to consider the use of EVs in clinical application. The main challenges and the requirements for EV separation and characterization strategies, quality control and clinical investigation were discussed to promote the application of EVs in future clinical studies.

0301 basic medicineEngineeringHistologytheranosticMeeting ReportFreeze thawingExtracellular vesiclesCa 19 9 antigen03 medical and health sciences0302 clinical medicineClinical investigationIn vitro studylcsh:QH573-671therapylcsh:Cytologybusiness.industryDietary intakeAntibody affinityCell BiologyExtracellular vesicles030104 developmental biology030220 oncology & carcinogenesisAntisense oligonucleotidesbiomarkerEngineering ethicsbusinessJournal of Extracellular Vesicles
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Silencing of Foxp3 enhances the antitumor efficacy of GM-CSF genetically modified tumor cell vaccine against B16 melanoma

2017

Antonio Miguel,1 Luis Sendra,1 Verónica Noé,2 Carles J Ciudad,2 Francisco Dasí,3,4 David Hervas,5 María José Herrero,1,6 Salvador F Aliño17 1Department of Pharmacology, Faculty of Medicine, University of Valencia, 2Department of Biochemistry and Molecular Biology, Faculty of Pharmacy, University of Barcelona, 3Research University Hospital of Valencia, INCLIVA Health Research Institute, 4Department of Physiology, Faculty of Medicine, University of Valencia Foundation, 5Biostatistics Unit, 6Pharmacogenetics Unit, Instituto de Investigación Sanitaria La Fe (IIS La Fe), 7Clinical Pharmacology Unit, ACM Hospital Univers…

0301 basic medicineantisense oligonucleotidemedicine.medical_treatmentCellImmunoteràpiaIpilimumabchemical and pharmacologic phenomenaImmunotheraphyVacuneslcsh:RC254-282OncoTargets and Therapy03 medical and health sciencesgene silencingCancer immunotherapymedicineGene silencingPharmacology (medical)IL-2 receptorCàncerOriginal ResearchTumorsCancerVaccinescancer immunotherapybiologybusiness.industryFOXP3hemic and immune systemslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensVaccinationTreg030104 developmental biologymedicine.anatomical_structureantitumor vaccineOncologybiology.proteinCancer researchAntibodybusinessmedicine.drugOncoTargets and Therapy
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Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy through miR-7 biogenesis repression

2021

Skeletal muscle symptoms strongly contribute to mortality of myotonic dystrophy type 1 (DM1) patients. DM1 is a neuromuscular genetic disease caused by CTG repeat expansions that, upon transcription, sequester the Muscleblind-like family of proteins and dysregulate alternative splicing of hundreds of genes. However, mis-splicing does not satisfactorily explain muscle atrophy and wasting, and several other contributing factors have been suggested, including hyperactivated autophagy leading to excessive catabolism. MicroRNA ( miR ) -7 has been demonstrated to be necessary and sufficient to repress the autophagy pathway in cell models of the disease, but the origin of its low levels in DM1 was…

autophagyMSI2 antisense oligonucleotides autophagy miR-7 muscle atrophy muscle dysfunction myotonic dystrophy myotubesRM1-950BiologyMyotonic dystrophyMSI2chemistry.chemical_compoundDrug DiscoverymedicineMyocyteGene silencingMBNL1muscle dysfunctionmyotonic dystrophyMyogenesisAutophagymiR-7Skeletal musclemedicine.diseaseMuscle atrophyCell biologymedicine.anatomical_structurechemistryMolecular MedicineTherapeutics. Pharmacologyantisense oligonucleotidesmedicine.symptomMolecular Therapy - Nucleic Acids
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Novel Lipid and Polymeric Materials as Delivery Systems for Nucleic Acid Based Drugs

2015

Nucleic acid based drugs (NADBs) are short DNA/RNA molecules that include among others, antisense oligonucleotides, aptamers, small interfering RNAs and micro-interfering RNAs. Despite the different mechanisms of actions, NABDs have the ability to combat the effects of pathological gene expression in many experimental systems. Thus, nowadays, NABDs are considered to have a great therapeutic potential, possibly superior to that of available drugs. Unfortunately, however, the lack of effective delivery systems limits the practical use of NABDs. Due to their hydrophilic nature, NABDs cannot efficiently cross cellular membrane; in addition, they are subjected to fast degradation by cellular and…

Cellular membranePolymersAntisense oligonucleotides aptamers carbon nanotubes exososomes liposomes miRNA polymers siRNAAptamerClinical BiochemistryNanotechnologyAnimals; Humans; Lipids; Nanoparticles; Nanotubes Carbon; Nucleic Acids; Polymers; Drug Delivery SystemsBiologyNanoparticleDrug Delivery SystemsNucleic AcidsAnimalsHumansAvailable drugsPolymerPharmacologyNanotubesNucleic AcidAnimalNanotubes CarbonCarbon chemistryRNALipidLipidsCarbonSettore CHIM/09 - Farmaceutico Tecnologico ApplicativoAntisense oligonucleotidesNucleic acidNanoparticlesHuman
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MicroRNA-Based Therapeutic Perspectives in Myotonic Dystrophy

2019

Myotonic dystrophy involves two types of chronically debilitating rare neuromuscular diseases: type 1 (DM1) and type 2 (DM2). Both share similarities in molecular cause, clinical signs, and symptoms with DM2 patients usually displaying milder phenotypes. It is well documented that key clinical symptoms in DM are associated with a strong mis-regulation of RNA metabolism observed in patient’s cells. This mis-regulation is triggered by two leading DM-linked events: the sequestration of Muscleblind-like proteins (MBNL) and the mis-regulation of the CUGBP RNA-Binding Protein Elav-Like Family Member 1 (CELF1) that cause significant alterations to their important functions in RNA processing. It ha…

Context (language use)miRNA-based drugReviewBioinformaticsMyotonic dystrophyCatalysislcsh:ChemistryInorganic ChemistryMBNL proteinsCELF1microRNADrug DiscoveryMedicineAnimalsHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCELF1 ProteinRna processingmyotonic dystrophymicroRNAbusiness.industryOrganic ChemistryAlternative splicingmiRNA-targeting drugRNA-Binding ProteinsGeneral MedicineGenetic Therapymedicine.diseasePhenotypeComputer Science ApplicationsAlternative SplicingMicroRNAslcsh:Biology (General)lcsh:QD1-999Drug developmentGene Expression Regulationantisense oligonucleotidesbusinessFunction (biology)International Journal of Molecular Sciences
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Preclinical characterization of antagomiR-218 as a potential treatment for myotonic dystrophy

2021

Myotonic dystrophy type 1 (DM1) is a rare neuromuscular disease caused by expansion of unstable CTG repeats in a non-coding region of the DMPK gene. CUG expansions in mutant DMPK transcripts sequester MBNL1 proteins in ribonuclear foci. Depletion of this protein is a primary contributor to disease symptoms such as muscle weakness and atrophy and myotonia, yet upregulation of endogenous MBNL1 levels may compensate for this sequestration. Having previously demonstrated that antisense oligonucleotides against miR-218 boost MBNL1 expression and rescue phenotypes in disease models, here we provide preclinical characterization of an antagomiR-218 molecule using the HSALR mouse model and patient-d…

antisense oligonucleotidetissue distributionRM1-950BiologyMyotonic dystrophyTranscriptomechemistry.chemical_compoundalternative splicingtranscriptomicsAtrophyDrug DiscoverymicroRNAmedicineMBNL1AntagomirCTG repeat expansionstherapeutic gene modulationCTG repeat expansions MBNL1 protein alternative splicing antisense oligonucleotide microRNAs myotonic dystrophy therapeutic gene modulation tissue distribution transcriptomicsmyotonic dystrophyMyogenesisMyotoniamedicine.diseasemicroRNAschemistryCancer researchMolecular MedicineOriginal ArticleTherapeutics. PharmacologyMBNL1 protein
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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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Allele-specific silencing as therapy for familial amyotrophic lateral sclerosis caused by the p.G376D TARDBP mutation

2022

Abstract Amyotrophic lateral sclerosis is a neurodegenerative disease characterized by the degeneration of motor neurons. There is no treatment for this disease that affects the ability to move, eat, speak and finally breathe, causing death. In an Italian family, a heterozygous pathogenic missense variant has been previously discovered in Exon 6 of the gene TARDBP encoding the TAR DNA-binding protein 43 protein. Here, we developed a potential therapeutic tool based on allele-specific small interfering RNAs for familial amyotrophic lateral sclerosis with the heterozygous missense mutation c.1127G>A. We designed a small interfering RNA that was able to diminish specifically the express…

antisense oligonucleotideCellular and Molecular NeurosciencePsychiatry and Mental healthsiRNA therapyNeurologyallele-specific silencingTDP-43ALS TDP43 siRNA therapy antisense oligonucleotides allele specific silencingSettore MED/26 - NeurologiaALSantisense oligonucleotidesSettore MED/03 - GENETICA MEDICABiological Psychiatry
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