Search results for "Nonsense mutation"

showing 10 items of 86 documents

Pharmacophore-Based Design of New Chemical Scaffolds as Translational Readthrough-Inducing Drugs (TRIDs)

2020

[Image: see text] Translational readthrough-inducing drugs (TRIDs) rescue the functional full-length protein expression in genetic diseases, such as cystic fibrosis, caused by premature termination codons (PTCs). Small molecules have been developed as TRIDs to trick the ribosomal machinery during recognition of the PTC. Herein we report a computational study to identify new TRID scaffolds. A pharmacophore approach was carried out on compounds that showed readthrough activity. The pharmacophore model applied to screen different libraries containing more than 87000 compounds identified four hit-compounds presenting scaffolds with diversity from the oxadiazole lead. These compounds have been s…

010405 organic chemistryChemistryOrganic ChemistryTranslational readthroughNonsense mutationHTVSnonsense mutationOxadiazoleBenzoxazoleRibosomal RNA01 natural sciencesBiochemistrySmall molecule0104 chemical sciencescystic fibrosis010404 medicinal & biomolecular chemistrychemistry.chemical_compoundBiochemistryDrug Discoverypremature termination codonsPharmacophoreDerivative (chemistry)Pharmacophore modeling
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β-Amyrin Synthase1 Controls the Accumulation of the Major Saponins Present in Pea (Pisum sativum)

2021

Abstract The use of pulses as ingredients for the production of food products rich in plant proteins is increasing. However, protein fractions prepared from pea or other pulses contain significant amounts of saponins, glycosylated triterpenes that can impart an undesirable bitter taste when used as an ingredient in foodstuffs. In this article, we describe the identification and characterization of a gene involved in saponin biosynthesis during pea seed development, by screening mutants obtained from two Pisum sativum TILLING (Targeting Induced Local Lesions IN Genomes) populations in two different genetic backgrounds. The mutations studied are located in a gene designated PsBAS1 (β-amyrin s…

0106 biological sciencesTILLINGPhysiologyMutantNonsense mutationPlant Sciencemedicine.disease_cause01 natural sciencesPisum03 medical and health sciencesSpatio-Temporal AnalysisSativumGene Expression Regulation PlantLoss of Function Mutationmedicine[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyIntramolecular TransferasesGenePlant Proteins030304 developmental biology2. Zero hunger[SDV.EE]Life Sciences [q-bio]/Ecology environment0303 health sciencesMutationbiologyPeasfood and beveragesCell BiologyGeneral MedicineSaponinsbiology.organism_classificationBiochemistrySeedsFunctional genomics010606 plant biology & botany
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Effect of ABC transporter expression and mutational status on survival rates of cancer patients

2020

ATP-binding cassette (ABC) transporters mediate multidrug resistance in cancer. In contrast to DNA single nucleotide polymorphisms in normal tissues, the role of mutations in tumors is unknown. Furthermore, the significance of their expression for prediction of chemoresistance and survival prognosis is still under debate. We investigated 18 tumors by RNA-sequencing. The mutation rate varied from 27,507 to 300885. In ABCB1, three hotspots with novel mutations were in transmembrane domains 3, 8, and 9. We also mined the cBioPortal database with 11,814 patients from 23 different tumor entities. We performed Kaplan-Meier survival analyses to investigate the effect of ABC transporter expression …

0301 basic medicineAdultMaleMutation rateNonsense mutationSingle-nucleotide polymorphismATP-binding cassette transporterRM1-950BiologyMultidrug resistanceP-glycoproteinPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineNeoplasmsmedicineMissense mutationHumansSurvival analysisAgedCancerPharmacologyAged 80 and overPrognostic factorSequence Analysis RNACancerABCB5General MedicineMiddle AgedSurvival analysismedicine.diseaseMolecular Docking SimulationSurvival Rate030104 developmental biologyABC transporters030220 oncology & carcinogenesisMutationCancer researchATP-Binding Cassette TransportersFemaleTherapeutics. PharmacologyBiomedicine & Pharmacotherapy
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Whole-exome sequencing and targeted gene sequencing provide insights into the role ofPALB2as a male breast cancer susceptibility gene

2016

BACKGROUND Male breast cancer (MBC) is a rare disease whose etiology appears to be largely associated with genetic factors. BRCA1 and BRCA2 mutations account for about 10% of all MBC cases. Thus, a fraction of MBC cases are expected to be due to genetic factors not yet identified. To further explain the genetic susceptibility for MBC, whole-exome sequencing (WES) and targeted gene sequencing were applied to high-risk, BRCA1/2 mutation–negative MBC cases. METHODS Germ-line DNA of 1 male and 2 female BRCA1/2 mutation–negative breast cancer (BC) cases from a pedigree showing a first-degree family history of MBC was analyzed with WES. Targeted gene sequencing for the validation of WES results w…

0301 basic medicineCancer genome sequencingProbandGeneticsCancer ResearchPALB2Nonsense mutationCancerBiologymedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineBreast cancerOncology030220 oncology & carcinogenesisMale breast cancermedicineskin and connective tissue diseasesExome sequencingCancer
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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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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Caffeine boosts Ataluren's readthrough activity

2019

Abstract The readthrough of nonsense mutations by small molecules like Ataluren is considered a novel therapeutic approach to overcome the gene defect in several genetic diseases as cystic fibrosis (CF). This pharmacological approach suppresses translation termination at premature termination codons (PTCs readthrough) thus restoring the expression of a functional protein. However, readthrough might be limited by the nonsense-mediated mRNA decay (NMD), a cell process that reduces the amount/level of PTCs containing mRNAs. Here we investigate the combined action of Ataluren and caffeine to enhance the readthrough of PTCs. IB3.1 CF cells with a nonsense mutation were treated with caffeine to a…

0301 basic medicineMolecular biologymedia_common.quotation_subjectCellNonsenseNonsense mutationMRNA DecaySettore BIO/11 - Biologia MolecolareBiochemistryCystic fibrosisArticleCystic fibrosisCFTR gene03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCaffeinemedicinelcsh:Social sciences (General)Settore BIO/06 - Anatomia Comparata E Citologialcsh:Science (General)media_commonMessenger RNAMultidisciplinaryNonsense mutationNonsense mutationsPTC readthroughAtaluren/PTC124Settore CHIM/06 - Chimica Organicamedicine.diseaseCell biologyAtalurenSettore BIO/18 - Genetica030104 developmental biologymedicine.anatomical_structurechemistryCystic fibrosilcsh:H1-99Caffeine030217 neurology & neurosurgerylcsh:Q1-390Heliyon
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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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Next‐generation sequencing reveals the mutational landscape of clinically diagnosed Usher syndrome: copy number variations, phenocopies, a predominan…

2017

Background Combined retinal degeneration and sensorineural hearing impairment is mostly due to autosomal recessive Usher syndrome (USH1: congenital deafness, early retinitis pigmentosa (RP); USH2: progressive hearing impairment, RP). Methods Sanger sequencing and NGS of 112 genes (Usher syndrome, nonsyndromic deafness, overlapping conditions), MLPA, and array-CGH were conducted in 138 patients clinically diagnosed with Usher syndrome. Results A molecular diagnosis was achieved in 97% of both USH1 and USH2 patients, with biallelic mutations in 97% (USH1) and 90% (USH2), respectively. Quantitative readout reliably detected CNVs (confirmed by MLPA or array-CGH), qualifying targeted NGS as one …

0301 basic medicineUsher syndromeNonsense mutationnext‐generation sequencingBiologyGene mutationBioinformatics03 medical and health sciencessymbols.namesakeRetinitis pigmentosaGeneticsmedicineotorhinolaryngologic diseasesMultiplex ligation-dependent probe amplificationNonsyndromic deafnessMolecular BiologyGenetics (clinical)Sanger sequencingGeneticsHeimler syndromeCopy number variationPoint mutationOriginal Articlesmedicine.diseaseeye diseases030104 developmental biologysymbolsphenocopiestranslational read‐throughOriginal ArticleUsher syndromeMolecular Genetics & Genomic Medicine
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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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