Search results for "Cystic Fibrosis Transmembrane Conductance Regulator"

showing 10 items of 24 documents

Evidence of Absorptive Function in vivo in a Neo-Formed Bio-Artificial Intestinal Segment Using a Rodent Model.

2015

A promising therapeutic approach for intestinal failure consists in elongating the intestine with a bio-engineered segment of neo-formed autologous intestine. Using an acellular biologic scaffold (ABS), we, and others, have previously developed an autologous bio-artificial intestinal segment (BIS) that is morphologically similar to normal bowel in rodents. This neo-formed BIS is constructed with the intervention of naïve stem cells that repopulate the scaffold in vivo, and over a period of time, are transformed in different cell populations typical of normal intestinal mucosa. However, no studies are available to demonstrate that such BIS possesses functional absorptive characteristics nece…

0301 basic medicineMalePathologymedicine.medical_specialtyCell typeLumen (anatomy)Bio-artificial intestineBio-engineered intestineIntestinal absorption03 medical and health sciences0302 clinical medicineIntestinal mucosaIn vivoIntestine SmallmedicineAnimalsIntestinal MucosabiologyBioartificial OrgansTissue EngineeringTissue ScaffoldsIn vivo absorptionGastroenterologyCystic fibrosis transmembrane conductance regulatorRatsFunctional analysis of bio-artificial intestine030104 developmental biologyIntestinal Absorptionbiology.proteinUltrastructure030211 gastroenterology & hepatologySurgeryStem cellJournal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
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Rescuing the CFTR protein function: Introducing 1,3,4-oxadiazoles as translational readthrough inducing drugs.

2018

Nonsense mutations in the CFTR gene prematurely terminate translation of the CFTR mRNA leading to the production of a truncated protein that lacks normal function causing a more severe form of the cystic fibrosis (CF) disease. About 10% of patients affected by CF show a nonsense mutation. A potential treatment of this alteration is to promote translational readthrough of premature termination codons (PTCs) by Translational Readthrough Inducing Drugs (TRIDs) such as PTC124. In this context we aimed to compare the activity of PTC124 with analogues differing in the heteroatoms position in the central heterocyclic core. By a validated protocol consisting of computational screening, synthesis an…

0301 basic medicineModels MolecularCell SurvivalNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorSettore BIO/11 - Biologia MolecolareContext (language use)OxadiazoleSettore BIO/09 - FisiologiaCystic fibrosis03 medical and health sciencesStructure-Activity Relationship0302 clinical medicineDrug DiscoverymedicineHumansRNA MessengerGenetic disorderPharmacologyMessenger RNAOxadiazolesNonsense mutationDose-Response Relationship DrugMolecular StructureChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryTranslational readthroughPremature termination codonTranslation (biology)Settore CHIM/06 - Chimica OrganicaGeneral Medicinemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSmall moleculeCell biologySettore BIO/18 - Genetica030104 developmental biologyBiological targetCystic fibrosi030220 oncology & carcinogenesisHeLa CellsEuropean journal of medicinal chemistry
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Exploring the readthrough of nonsense mutations by non-acidic Ataluren analogues selected by ligand-based virtual screening

2016

Abstract Ataluren, also known as PTC124, is a 5-(fluorophenyl)-1,2,4-oxadiazolyl-benzoic acid suggested to suppress nonsense mutations by readthrough of premature stop codons in the mRNA. Potential interaction of PTC124 with mRNA has been recently studied by molecular dynamics simulations highlighting the importance of H-bonding and stacking π−π interactions. A series of non-acidic analogues of PTC124 were selected from a large database via a ligand-based virtual screening approach. Eight of them were synthesized and tested for their readthrough activity using the Fluc reporter harboring the UGA premature stop codon. The most active compound was further tested for suppression of the UGA non…

0301 basic medicineNonsense mutationDrug Evaluation PreclinicalMolecular ConformationCystic Fibrosis Transmembrane Conductance RegulatorMolecular Dynamics SimulationOxadiazolemedicine.disease_causeCftr geneCFTR gene03 medical and health scienceschemistry.chemical_compoundDrug DiscoverymedicineHumansRNA MessengerPharmacologyGeneticsOxadiazolesMessenger RNAVirtual screeningMutationNonsense mutationChemistryDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineLigand (biochemistry)PTCs readthroughMolecular biologyStop codonAtaluren030104 developmental biologyCodon NonsenseCystic fibrosiHeLa CellsEuropean Journal of Medicinal Chemistry
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Multicenter validation study for the certification of a CFTR gene scanning method using next generation sequencing technology.

2018

AbstractBackground:Many European laboratories offer molecular genetic analysis of theCFTRgene using a wide range of methods to identify mutations causative of cystic fibrosis (CF) and CFTR-related disorders (CFTR-RDs). Next-generation sequencing (NGS) strategies are widely used in diagnostic practice, and CE marking is now required for most in vitro diagnostic (IVD) tests in Europe. The aim of this multicenter study, which involved three European laboratories specialized in CF molecular analysis, was to evaluate the performance of Multiplicom’s CFTR MASTR Dx kit to obtain CE-IVD certification.Methods:A total of 164 samples, previously analyzed with well-established “reference” methods for t…

0301 basic medicineValidation studycongenital hereditary and neonatal diseases and abnormalitiesCertification[SDV]Life Sciences [q-bio]Clinical BiochemistrySequencing dataCFTR molecular diagnosiCystic Fibrosis Transmembrane Conductance RegulatorComputational biology030105 genetics & heredityBiologyCFTR molecular diagnosisDNA sequencingIn vitro diagnosticCftr genecystic fibrosis03 medical and health sciencesHumanscystic fibrosiCE-IVD certificationBiochemistry (medical)Reproducibility of ResultsIllumina miseqSequence Analysis DNAGeneral MedicineMolecular analysisEurope030104 developmental biologyMulticenter studycomparative sequencing analysicomparative sequencing analysisMutationnext-generation sequencingMultiplex Polymerase Chain Reaction
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Targeting Nonsense: Optimization of 1,2,4-Oxadiazole TRIDs to Rescue CFTR Expression and Functionality in Cystic Fibrosis Cell Model Systems

2020

Cystic fibrosis (CF) patients develop a severe form of the disease when the cystic fibrosis transmembrane conductance regulator (CFTR) gene is affected by nonsense mutations. Nonsense mutations are responsible for the presence of a premature termination codon (PTC) in the mRNA, creating a lack of functional protein. In this context, translational readthrough-inducing drugs (TRIDs) represent a promising approach to correct the basic defect caused by PTCs. By using computational optimization and biological screening, we identified three new small molecules showing high readthrough activity. The activity of these compounds has been verified by evaluating CFTR expression and functionality after…

0301 basic medicineYellow fluorescent proteinCystic Fibrosisnonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorCystic fibrosislcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5SpectroscopyCells CulturedbiologyChemistryGeneral MedicineSmall moleculeCystic fibrosis transmembrane conductance regulatorComputer Science ApplicationsCell biologyCodon Nonsense030220 oncology & carcinogenesisNonsense mutationContext (language use)Settore BIO/11 - Biologia MolecolareCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineHumansRNA MessengerPhysical and Theoretical ChemistryMolecular BiologyGeneMessenger RNAOrganic ChemistryoxadiazolesSettore CHIM/06 - Chimica Organicapremature termination codonmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999translational readthrough inducing drugsProtein BiosynthesisMutationbiology.proteingenetic disorderInternational Journal of Molecular Sciences
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Non-classic cystic fibrosis associated with D1152HCFTR mutation

2010

Burgel P-R, Fajac I, Hubert D, Grenet D, Stremler N, Roussey M, Siret D, Languepin J, Mely L, Fanton A, Labbe A, Domblides P, Vic P, Dagorne M, Reynaud-Gaubert M, Counil F, Varaigne F, Bienvenu T, Bellis G, Dusser D. Non-classic cystic fibrosis associated with D1152H CFTR mutation. Background: Limited knowledge exists on phenotypes associated with the D1152H cystic fibrosis transmembrane conductance regulator (CFTR) mutation. Methods: Subjects with a D1152H allele in trans with another CFTR mutation were identified using the French Cystic Fibrosis Registry. Phenotypic characteristics were compared with those of pancreatic insufficient (PI) and pancreatic sufficient (PS) cystic fibrosis (CF)…

AdultMalemedicine.medical_specialtyConsensusPancreatic diseaseAdolescentCystic FibrosisGENETICSmedicine.medical_treatmentCystic Fibrosis Transmembrane Conductance RegulatorCystic fibrosisGastroenterologyMembrane PotentialsCohort StudiesYoung AdultChloridesInterquartile rangeForced Expiratory VolumeInternal medicineCYSTIC_FIBROSISHumansMedicineLung transplantationGenetic Predisposition to DiseaseChildSweatExocrine pancreatic insufficiencyMUTATIONGenetics (clinical)AgedBronchiectasisbiologybusiness.industryHomozygoteMiddle Agedmedicine.diseaseCongenital absence of the vas deferensCystic fibrosis transmembrane conductance regulatorNasal MucosaEndocrinologyAmino Acid SubstitutionChild Preschoolbiology.proteinFemalebusiness
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Genetic, andrological and clinical characteristics of patients with congenital bilateral absence of vas deferens

2001

Summary The possibility of retrieving spermatozoa from the epididymis allows patients with congenital bilateral absence of the vas deferens (CBAVD) to father a child by means of assisted reproduction techniques. This has, however, increased the chance of transmitting a mutated allele of the cystic fibrosis transmembrane conductance regulator (CFTR) gene which increases the risk of generating offspring with cystic fibrosis (CF). Because of the increased heterogeneity of the CFTR locus, the study of a discrete number of mutations, as usually carried out in a diagnostic work-up, is unable to ascertain the presence of a mutation in a relatively high proportion of the patients screened. In an at…

AdultMalemedicine.medical_specialtyGenotypeCystic Fibrosis Transmembrane Conductance Regulator/genetics; Vas Deferens/abnormalities; Urogenital Abnormalities/geneticsUrologyEndocrinology Diabetes and MetabolismPopulationCystic Fibrosis Transmembrane Conductance RegulatorGastroenterologyCystic fibrosisVas DeferensPregnancyInternal medicinemedicineHumansRespiratory functionSperm Injections IntracytoplasmicAlleleeducationSweat testeducation.field_of_studybiologymedicine.diagnostic_testbusiness.industryVas deferensPregnancy Outcomemedicine.diseaseEpididymisSpermatozoaCystic fibrosis transmembrane conductance regulatorVas Deferens/abnormalitiesEndocrinologymedicine.anatomical_structureReproductive MedicineUrogenital Abnormalities/geneticsUrogenital Abnormalitiesbiology.proteinCystic Fibrosis Transmembrane Conductance Regulator/geneticsFemalebusiness
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The CFTR associated protein CAP70 interacts with the apical Cl-/HCO3- exchanger DRA in rabbit small intestinal mucosa.

2005

DRA (down regulated in adenoma) is an intestinal anion exchanger, acting in parallel with NHE3 to facilitate ileal and colonic NaCl absorption. Furthermore it is involved in small intestinal bicarbonate secretion. Because DRA has a PDZ interaction motif, which may influence its properties, we searched for DRA-interacting PDZ adapter proteins in the small intestine. Using an overlay assay with the recombinant DRA C-terminus as a ligand, a 70 kDa protein was labeled, which was restricted to the brush border membrane in rabbit duodenal and ileal mucosa and was not detected in the colon. Destruction of the C-terminal PDZ interaction motif abolished this band, suggesting a specific protein-prote…

Brush borderColonPDZ domainAmino Acid MotifsMolecular Sequence DataCystic Fibrosis Transmembrane Conductance RegulatorIleumBiologyBiochemistryAntiportersCell LineIntestine SmallmedicineAnimalsHumansSecretionAmino Acid SequenceChloride-Bicarbonate AntiportersRNA MessengerIntestinal MucosaMessenger RNAHEK 293 cellsSignal transducing adaptor proteinMembrane ProteinsMolecular biologySmall intestinePeptide Fragmentsmedicine.anatomical_structureSulfate TransportersRabbitsCarrier ProteinsBiochemistry
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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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Inhalable nano into micro dry powders for ivacaftor delivery: The role of mannitol and cysteamine as mucus-active agents.

2020

In this paper the innovative approach of Nano into micro (NiM9 was developed to produce Nanoparticles loaded Ivacaftor to incorporate into mannitol or mannitol/cysteamine micromatrices for drug pulmonary administration in CF. Nanoparticles composed by a mixture of two polyhydrohydroxyethtylaspartamide copolymers containing a loading of Ivacaftor of 15.5 % w/w were produced. These Nanoparticles were incorporated into microparticles to obtain NiM that were characterized in terms of size and size distribution, interaction with CF-AM by rheological and turbidimetric studies as well as by aerodynamic diameter measurements. Finally the activity of Ivacaftor into these NiM was evaluated by in vitr…

Cystic Fibrosisαβ-poly-(N-2-hydroxyethyl)-DL-aspartamide (PHEA) copolymer PHEA ivacaftor mucus-penetrating nanoparticle cell penetrating peptide nano into micro strategy. CysteamineDrug CompoundingPharmaceutical ScienceNanoparticleCystic Fibrosis Transmembrane Conductance Regulator02 engineering and technologyQuinolonesAminophenols030226 pharmacology & pharmacyIvacaftor03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNano-Administration InhalationMucus-penetrating nanoparticlemedicineCopolymerAnimalsMannitolChloride Channel AgonistsCells CulturedExpectorantsCell penetrating peptideNano into micro strategyChemistry021001 nanoscience & nanotechnologyMucusRats Inbred F344IvacaftorCopolymer PHEADrug LiberationSettore CHIM/09 - Farmaceutico Tecnologico ApplicativoMutationNanoparticlesCysteamineMannitolPowders0210 nano-technologyPeptidesαβ-poly-(N-2-hydroxyethyl)-DL-aspartamide (PHEA)medicine.drugNuclear chemistryInternational journal of pharmaceutics
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