Search results for "translational readthrough inducing drugs"

showing 3 items of 3 documents

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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Strategies against nonsense: oxadiazoles as translational readthrough-inducing drugs (TRIDs)

2019

This review focuses on the use of oxadiazoles as translational readthrough-inducing drugs (TRIDs) to rescue the functional full-length protein expression in mendelian genetic diseases caused by nonsense mutations. These mutations in specific genes generate premature termination codons (PTCs) responsible for the translation of truncated proteins. After a brief introduction on nonsense mutations and their pathological effects, the features of various classes of TRIDs will be described discussing differences or similarities in their mechanisms of action. Strategies to correct the PTCs will be presented, particularly focusing on a new class of Ataluren-like oxadiazole derivatives in comparison …

0301 basic medicinemedia_common.quotation_subjectNonsenseNonsense mutationRegulatorSettore BIO/11 - Biologia MolecolareReviewComputational biologyBiologyOxadiazoleCatalysiscystic fibrosislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicineAtalurenTranslational readthrough inducing drugsPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyGeneSpectroscopymedia_commonNonsense mutationOrganic ChemistryTranslational readthroughoxadiazolesPremature termination codonTranslation (biology)General MedicineSettore CHIM/06 - Chimica OrganicaSmall moleculeSettore CHIM/08 - Chimica FarmaceuticaTransmembrane proteinComputer Science ApplicationsSettore BIO/18 - Genetica030104 developmental biologyPharmaceutical Preparationslcsh:Biology (General)lcsh:QD1-999Codon NonsenseProtein Biosynthesis030220 oncology & carcinogenesisCystic fibrosi
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Nonsense codons suppression. An acute toxicity study of three optimized TRIDs in murine model, safety and tolerability evaluation.

2022

Stop mutations cause 11% of the genetic diseases, due to the introduction of a premature termination codon (PTC) in the mRNA, followed by the production of a truncated protein. A promising therapeutic approach is the suppression therapy by Translational Readthrough Inducing Drugs (TRIDs), restoring the expression of the protein. Recently, three new TRIDs (NV848, NV914, NV930) have been proposed, and validated by several in vitro assays, for the rescue of the CFTR protein, involved in Cystic Fibrosis disease. In this work, an acute toxicological study for the three TRIDs was conducted in vivo on mice, according to the OECD No.420 guidelines. Animals were divided into groups and treated with …

PharmacologyNonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorGeneral MedicineOxadiazoleMiceDisease Models AnimalPremature termination codon (PTC)Pharmaceutical PreparationsCodon NonsenseProtein BiosynthesisAnimalsToxicity studyTranslational readthrough inducing drugs(TRIDs)Biomedicinepharmacotherapy = Biomedecinepharmacotherapie
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