Search results for "MUTATION"

showing 10 items of 2830 documents

Absence of mutation at the GAP-related domain of the neurofibromatosis type 1 gene in sporadic neurofibrosarcomas and other bone and soft tissue sarc…

1995

The NF1 gene encodes neurofibromin, a GTPase-activating protein containing a GAP-related domain (NF1-GRD) that is capable of downregulating ras by stimulating ras intrinsic GTPase activity. We tested 44 sarcomas, nine of which corresponded to sporadic neurofibrosarcomas, for mutations at the NF1-GRD by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) technique, finding no mutation in every sample tested. We suggest that inactivation of the NF1-GRD by gene mutation seems not to be an important event in the tumorigenesis of sarcomas.

congenital hereditary and neonatal diseases and abnormalitiesCancer ResearchNeurofibromatosis 1DNA Mutational AnalysisBone NeoplasmsSoft Tissue NeoplasmsGTPaseBiologyGene mutationmedicine.disease_causePolymerase Chain ReactionGeneticsmedicineHumansneoplasmsMolecular BiologyGenePolymorphism Single-Stranded ConformationalGeneticsMutationNeurofibromin 1ProteinsSarcomaSingle-strand conformation polymorphismmedicine.diseaseNeurofibromin 1eye diseasesnervous system diseasesNeurofibrosarcomaCancer researchbiology.proteinSarcomaCarcinogenesisCancer Genetics and Cytogenetics
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Functional Assessment of Variants in the TSC1 and TSC2 Genes Identified in Individuals with Tuberous Sclerosis Complex

2011

The effects of missense changes and small in-frame deletions and insertions on protein function are not easy to predict, and the identification of such variants in individuals at risk of a genetic disease can complicate genetic counselling. One option is to perform functional tests to assess whether the variants affect protein function. We have used this strategy to characterize variants identified in the TSC1 and TSC2 genes in individuals with, or suspected of having, Tuberous Sclerosis Complex (TSC). Here we present an overview of our functional studies on 45 TSC1 and 107 TSC2 variants. Using a standardized protocol we classified 16 TSC1 variants and 70 TSC2 variants as pathogenic. In add…

congenital hereditary and neonatal diseases and abnormalitiesGenetic counselingtuberous sclerosis complexBiologyTuberous Sclerosis Complex 1 Protein03 medical and health sciencesTuberous sclerosis0302 clinical medicineTuberous SclerosisGenetic variationTuberous Sclerosis Complex 2 ProteinGeneticsmedicineMissense mutationHumansunclassified variantsGeneGenetics (clinical)Cells Cultured030304 developmental biologyGenetics0303 health sciencesModels GeneticTumor Suppressor ProteinsLife SciencesGenetic Variationmedicine.diseaseTSC23. Good healthnervous system diseasesTSC1medicine.anatomical_structureTSC1TSC2030217 neurology & neurosurgeryCommon disease-common variant
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Current development of CFTR potentiators in the last decade

2020

Cystic fibrosis (CF) is a genetic disorder produced by the loss of function of CFTR, a main chloride channel involved in transepithelial salt and water transport. CFTR function can be rescued by small molecules called "potentiators" which increase gating activity of CFTR on epithelial surfaces. High throughput screening (HTS) assays allowed the identification of new chemical entities endowed with potentiator properties, further improved through medicinal chemistry optimization. In this review, the most relevant classes of CFTR potentiators developed in the last decade were explored, focusing on structure-activity relationships (SAR) of the different chemical entities, as a useful tool for t…

congenital hereditary and neonatal diseases and abnormalitiesHigh-throughput screeningGlycineComputational biologyQuinolonesVX-770Aminophenols01 natural sciencesCystic fibrosisCystic fibrosisSmall Molecule LibrariesStructure-Activity Relationship03 medical and health sciencesDrug DiscoverymedicineHumansCFTR potentiatorCFTRLoss function030304 developmental biologyPharmacology0303 health sciencesWater transportbiology010405 organic chemistryChemistryOrganic ChemistryCFTR potentiatorsBiological activityGeneral MedicineTriazolesPotentiatormedicine.diseaseCystic fibrosis transmembrane conductance regulator0104 chemical sciencesCystic fibrosiMutationChloride channelbiology.proteinCystic fibrosis transmembrane conductance regulatorEuropean Journal of Medicinal Chemistry
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Sp1 transcription factor interaction with accumulated prelamin a impairs adipose lineage differentiation in human mesenchymal stem cells: essential r…

2012

Abstract Lamin A (LMNA)-linked lipodystrophies may be either genetic (associated with LMNA mutations) or acquired (associated with the use of human immunodeficiency virus protease inhibitors [PIs]), and in both cases they share clinical features such as anomalous distribution of body fat or generalized loss of adipose tissue, metabolic alterations, and early cardiovascular complications. Both LMNA-linked lipodystrophies are characterized by the accumulation of the lamin A precursor prelamin A. The pathological mechanism by which prelamin A accumulation induces the lipodystrophy associated phenotypes remains unclear. Since the affected tissues in these disorders are of mesenchymal origin, we…

congenital hereditary and neonatal diseases and abnormalitiesLipodystrophySp1 Transcription FactorCellular differentiationAdipose tissueBiologyLMNAHumansProtein PrecursorsTranscription factorOriginal Articles and ReviewsAdipogenesisintegumentary systemSecretory VesiclesMesenchymal stem cellnutritional and metabolic diseasesNuclear ProteinsCell DifferentiationMesenchymal Stem CellsCell BiologyGeneral MedicineLamin Type ALipid MetabolismCell biologyExtracellular MatrixBiochemistryAdipose TissueGene Expression RegulationAdipogenesisDifferentiationMutationMesenchymal stem cellsTranscription factorStem cellExperimental modelsLaminDevelopmental BiologyStem cells translational medicine
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GLI3 is rarely implicated in OFD syndromes with midline abnormalities

2011

A range of phenotypes including Greig cephalopolysyndactyly and Pallister-Hall syndromes (GCPS, PHS) are caused by pathogenic mutation of the GLI3 gene. To characterize the clinical variability of GLI3 mutations, we present a subset of a cohort of 174 probands referred for GLI3 analysis. Eighty-one probands with typical GCPS or PHS were previously reported, and we report the remaining ninety-three probands here. This includes nineteen probands (twelve mutations) who fulfilled clinical criteria for GCPS or PHS, forty-eight probands (sixteen mutations) with features of GCPS or PHS but who did not meet the clinical criteria (sub-GCPS and sub-PHS), twenty-one probands (six mutations) with featu…

congenital hereditary and neonatal diseases and abnormalitiesPallister-Hall SyndromeKruppel-Like Transcription FactorsNerve Tissue ProteinsBiologyBioinformaticsArticlePolydactylyMutationGLI3Mutation (genetic algorithm)GeneticsHumansAbnormalities MultipleSyndactylyGenetics (clinical)Human Mutation
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Methionine in a protein hydrophobic core drives tight interactions required for assembly of spider silk

2019

Web spiders connect silk proteins, so-called spidroins, into fibers of extraordinary toughness. The spidroin N-terminal domain (NTD) plays a pivotal role in this process: it polymerizes spidroins through a complex mechanism of dimerization. Here we analyze sequences of spidroin NTDs and find an unusually high content of the amino acid methionine. We simultaneously mutate all methionines present in the hydrophobic core of a spidroin NTD from a nursery web spider’s dragline silk to leucine. The mutated NTD is strongly stabilized and folds at the theoretical speed limit. The structure of the mutant is preserved, yet its ability to dimerize is substantially impaired. We find that side chains of…

congenital hereditary and neonatal diseases and abnormalitiesProtein Foldinggenetic structuresProtein ConformationScienceSilkmacromolecular substancesCircular dichroismcomplex mixturesArticleMethionineddc:590ddc:570AnimalsAmino Acid Sequencelcsh:ScienceFluorescence spectroscopySequence Homology Amino AcidfungiQtechnology industry and agricultureSpidersSpectrometry FluorescenceMutationThermodynamicslcsh:QProtein MultimerizationFibroinsSolution-state NMRHydrophobic and Hydrophilic InteractionsAlgorithmsNature Communications
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Investigating REPAIRv2 as a Tool to Edit CFTR mRNA with Premature Stop Codons

2020

Cystic fibrosis (CF) is caused by mutations in the gene encoding the transmembrane conductance regulator (CFTR) protein. Some CF patients are compound heterozygous or homozygous for nonsense mutations in the CFTR gene. This implies the presence in the transcript of premature termination codons (PTCs) responsible for a truncated CFTR protein and a more severe form of the disease. Aminoglycoside and PTC124 derivatives have been used for the read-through of PTCs to restore the full-length CFTR protein. However, in a precision medicine framework, the CRISPR/dCas13b-based molecular tool &ldquo

congenital hereditary and neonatal diseases and abnormalitiesRNA editingMutantNonsense mutationSettore BIO/11 - Biologia MolecolareBiologyCRISPR/dCas13bCatalysislcsh:Chemistrycystic fibrosisInorganic ChemistryGuide RNASettore BIO/06 - Anatomia Comparata E CitologiaPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologyGeneSpectroscopyMessenger RNApremature termination codons (PTCs)Organic ChemistryGeneral Medicinerespiratory systemStop codonTransmembrane proteinrespiratory tract diseasesComputer Science ApplicationsCell biologySettore BIO/18 - Geneticalcsh:Biology (General)lcsh:QD1-999RNA editingInternational Journal of Molecular Sciences
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Genetische Hämochromatose und das HFE-Gen: von der Molekulargenetik zur klinischen Diagnostik

2000

More than 90% of patients with genetic hemochromatosis carry a characteristic mutation in the HFE-gene (C282Y). HFE modulates the iron uptake by the transferrin receptor. Duodenal crypt cells of HFE-knockout mice show low intracellular iron concentrations which lead to an upregulation of the divalent metal transporter and enhanced iron uptake by duodenal enterocytes. Heterozygosity for the C282Y mutation appears to alter the course of other liver diseases like porphyria cutanea tarda and nonalcoholic steatohepatitis.

congenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyMutationdigestive oral and skin physiologyGastroenterologynutritional and metabolic diseasesTransferrin receptorBiologymedicine.diseasemedicine.disease_causedigestive systemPathogenesisLoss of heterozygosityEndocrinologyDownregulation and upregulationInternal medicineMolecular geneticsmedicinePorphyria cutanea tardaskin and connective tissue diseasesHemochromatosisZeitschrift für Gastroenterologie
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Matthieu Lecoutre, Atlas historique du vin en France. De l’Antiquité à nos jours, préface de Jean-Robert Pitte, Paris, Éditions Autrement, 2019, 95 p.

2020

International audience

consommation[SHS.HIST] Humanities and Social Sciences/Historycrisevinmondialisationproductionmutationproduit civilisationnelvigne[SHS.HIST]Humanities and Social Sciences/HistoryComputingMilieux_MISCELLANEOUS
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A short story of 3AB-OS Cancer Stem Cells, a possible model for studying cancer stemness

2014

All tumors contain a population of Cancer Stem Cells (CSCs) responsible for the initiation, growth and development of the tumor and a challenge in cancer research is their identification and eradication. In our laboratory, by chemical treatment of the human osteosarcoma MG63 cell line, we have isolated and characterized the human OS CSC line (3AB-OS). 3AB-OS CSCs have a significant chromosomal complexity and a large number of molecular abnormalities which appear to be strongly congruent with those described in a large number of pediatric and adult osteosarcomas. 3AB-OS cells transdifferentiated in vitro into cells of all three primary germ layers and, when xenografted in athymic mice they w…

education.field_of_studyMutationPopulationCancerGeneral MedicineGerm layerBiologymedicine.disease_causemedicine.diseaseMolecular biologyIn vitroCancer stem cellCancer researchmedicineOsteosarcoma3AB-OS cancer stem cells cancer stemnesseducationGeneCancer Cell & Microenvironment
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