Search results for "MESH: Mutation*"

showing 10 items of 21 documents

The Monod-Wyman-Changeux allosteric model accounts for the quaternary transition dynamics in wild type and a recombinant mutant human hemoglobin

2012

International audience; The acknowledged success of the Monod-Wyman-Changeux (MWC) allosteric model stems from its efficacy in accounting for the functional behavior of many complex proteins starting with hemoglobin (the paradigmatic case) and extending to channels and receptors. The kinetic aspects of the allosteric model, however, have been often neglected, with the exception of hemoglobin and a few other proteins where conformational relaxations can be triggered by a short and intense laser pulse, and monitored by time-resolved optical spectroscopy. Only recently the application of time-resolved wide-angle X-ray scattering (TR-WAXS), a direct structurally sensitive technique, unveiled th…

Models MolecularProtein ConformationcooperativityMESH: Catalytic DomainCooperativity01 natural sciencesMESH: Recombinant ProteinsHemoglobinsProtein structureMESH: Protein ConformationCatalytic Domainprotein structural dynamicsMESH: Allosteric Site0303 health sciencesMultidisciplinaryallosterybiologyMESH: KineticsChemistryBiological SciencesRecombinant Proteins[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsMESH: HemoglobinsAllosteric SiteMESH: Models MolecularAdultMESH: MutationStereochemistryKineticsAllosteric regulation010402 general chemistry03 medical and health sciencesprotein conformational changesflash photolysisallostery; cooperativity; flash photolysis; hemoglobin; protein conformational changes; protein structural dynamics; time-resolved wide angle x ray scattering; time-resolved x-ray scatteringHumans030304 developmental biologytime-resolved X-ray scattering; protein conformational changes; cooperativity; flash photolysisMESH: Humanstime-resolved X-ray scatteringWild typeActive sitetime-resolved wide angle x ray scatteringMESH: AdulthemoglobinSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)0104 chemical sciencesprotein conformational changeKineticsAllosteric enzymeMutationbiology.proteinHemoglobin
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Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants

2020

Mice lacking GAD1 show neonatal mortality, but the human phenotype associated with GAD1 disruption is poorly characterized. Neuray et al. describe six patients with biallelic GAD1 mutations, presenting with early-infantile onset epilepsy, neurodevelopmental delay, muscle weakness and non-CNS manifestations.

Male0301 basic medicineGlutamate decarboxylaseMalalties cerebralsNeurotransmissorsNeurodevelopmental delayEpilepsy0302 clinical medicineMESH: ChildAge of OnsetChildcleft palateGAD1AcademicSubjects/SCI01870Glutamate DecarboxylaseGlutamate receptorMuscle weakness//purl.org/becyt/ford/3.1 [https]NeurotransmittersMESH: InfantHypotoniamuscle weakneCleft palateMESH: EpilepsyChild PreschoolMuscle Hypotonia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]//purl.org/becyt/ford/3 [https]FemaleBrain diseasesAbnormalitiesmedicine.symptomMultiplemedicine.drugcleft palate; epilepsy; GAD1; muscle weakness; neurodevelopmental delayMESH: Glutamate Decarboxylasemedicine.medical_specialtyMESH: Abnormalities MultipleMESH: MutationMESH: Age of OnsetBiologyInhibitory postsynaptic potentialGAD1 cleft palate epilepsy muscle weakness neurodevelopmental delay.gamma-Aminobutyric acidGAD1neurodevelopmental delay03 medical and health sciencesExcitatory synapseInternal medicinemedicineHumansAbnormalities MultiplePreschoolAllelesMESH: Neurodevelopmental Disordersmuscle weaknessMESH: HumansEpilepsyMESH: Muscle HypotoniaMESH: AllelesMESH: Child PreschoolInfantmedicine.diseaseMESH: MaleEpilèpsiaEditor's Choice030104 developmental biologyEndocrinologyNeurodevelopmental DisordersMutationepilepsyAcademicSubjects/MED00310Neurology (clinical)Cleft palate; Epilepsy; GAD1; Muscle weakness; Neurodevelopmental delay; Abnormalities Multiple; Age of Onset; Alleles; Child; Child Preschool; Epilepsy; Female; Glutamate Decarboxylase; Humans; Infant; Male; Muscle Hypotonia; Mutation; Neurodevelopmental DisordersMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology030217 neurology & neurosurgeryReports
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Excess of de novo variants in genes involved in chromatin remodelling in patients with marfanoid habitus and intellectual disability.

2020

PurposeMarfanoid habitus (MH) combined with intellectual disability (ID) (MHID) is a clinically and genetically heterogeneous presentation. The combination of array CGH and targeted sequencing of genes responsible for Marfan or Lujan–Fryns syndrome explain no more than 20% of subjects.MethodsTo further decipher the genetic basis of MHID, we performed exome sequencing on a combination of trio-based (33 subjects) or single probands (31 subjects), of which 61 were sporadic.ResultsWe identified eight genes with de novo variants (DNVs) in at least two unrelated individuals (ARID1B, ATP1A1, DLG4, EHMT1, NFIX, NSD1, NUP205 and ZEB2). Using simulation models, we showed that five genes (DLG4, NFIX, …

ProbandMale[SDV]Life Sciences [q-bio]intellectual deficiencyMESH: NFI Transcription Factorschromatin remodelingMarfan SyndromeCraniofacial AbnormalitiesMESH: ChildIntellectual disabilityMESH: Craniofacial AbnormalitiesMESH: Mental Retardation X-LinkedExomeChildde novo variantsGenetics (clinical)Exome sequencingGeneticsMESH: ExomeMESH: Middle AgedbiologyMESH: Genetic Predisposition to DiseaseMiddle AgedNFIXMESH: Young AdultFemaleAdultMESH: MutationAdolescentChromatin remodelingMESH: Intellectual DisabilityMESH: Marfan SyndromeEHMT1Young AdultMESH: Whole Exome SequencingIntellectual DisabilityExome SequencingGeneticsmedicineHumansGenetic Predisposition to Diseasemarfanoid habitusGeneMESH: Neurodevelopmental DisordersMESH: AdolescentMESH: HumansGenetic heterogeneityMESH: Chromatin Assembly and DisassemblyMESH: Histone-Lysine N-MethyltransferaseMESH: AdultHistone-Lysine N-Methyltransferasemedicine.diseaseChromatin Assembly and DisassemblyMESH: MaleNFI Transcription FactorsNeurodevelopmental DisordersMutationbiology.proteinMental Retardation X-LinkedMESH: FemaleJournal of medical genetics
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Presence of calreticulin mutations in JAK2-negative polycythemia vera

2014

Abstract Calreticulin (CALR) mutations have recently been reported in JAK2- and MPL-negative Myeloproliferative Neoplasms (MPN), particularly essential thrombocythemia (ET) and primary myelofibrosis (PMF).The clinical course of sporadic CALR-mutated patients seems to be more indolent than that of JAK2-mutated patients. In contrast, no CALR mutation has been found in the 647 published cases of Polycythemia Vera (PV) patients tested. Consequently, CALR mutations were considered exclusive to JAK2 and MPL mutations. Since 98% of PV patients harbor a JAK2 mutation (mostly the V617F mutation in exon 14 and more rarely, in exon 12), the absence of CALR mutations in PV seemed logical. Here, we desc…

MaleErythrocytesMESH: Thrombocytosismedicine.disease_causeMESH: Polycythemia VeraBiochemistryMESH: Janus Kinase 2MESH: GenotypeHemoglobinsMESH: Aged 80 and overPolycythemia verahemic and lymphatic diseasesPolycythemia VeraMESH: HeterozygoteAged 80 and overThrombocytosisMESH: AgedMutation[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyJanus kinase 2biologyMESH: ErythrocytesExonsHematologyLeukemiaMESH: HemoglobinsMESH: Primary MyelofibrosisThrombocythemia EssentialHeterozygoteMESH: MutationGenotypeMESH: CalreticulinImmunologyContext (language use)medicineHumansMyelofibrosisAllelesAgedMESH: HumansEssential thrombocythemiabusiness.industryMESH: AllelesCell BiologyJanus Kinase 2medicine.diseaseMESH: MalePrimary MyelofibrosisMESH: Gene DeletionMutationImmunologybiology.proteinCancer researchMESH: Thrombocythemia EssentialCalreticulinMESH: ExonsbusinessCalreticulinGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBlood
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Higher risk of death among MEN1 patients with mutations in the JunD interacting domain: a Groupe d'etude des Tumeurs Endocrines (GTE) cohort study.

2013

International audience; Multiple endocrine neoplasia syndrome type 1 (MEN1), which is secondary to mutation of the MEN1 gene, is a rare autosomal-dominant disease that predisposes mutation carriers to endocrine tumors. Although genotype-phenotype studies have so far failed to identify any statistical correlations, some families harbor recurrent tumor patterns. The function of MENIN is unclear, but has been described through the discovery of its interacting partners. Mutations in the interacting domains of MENIN functional partners have been shown to directly alter its regulation abilities. We report on a cohort of MEN1 patients from the Groupe d'étude des Tumeurs Endocrines. Patients with a…

OncologyMaleendocrine system diseasesProto-Oncogene Proteins c-jun[SDV]Life Sciences [q-bio]Diseasemedicine.disease_causeMESH: Protein Structure Tertiary0302 clinical medicineRisk FactorsMESH: Risk FactorsMESH : FemaleGenetics (clinical)MutationGeneral MedicineMESH: Follow-Up StudiesMESH : Risk Factors3. Good health030220 oncology & carcinogenesisCohortMESH : Proto-Oncogene ProteinsFemaleMESH : MutationMESH : Protein Structure TertiaryMESH : Proto-Oncogene Proteins c-junMESH : Multiple Endocrine Neoplasia Type 1Cohort studymedicine.medical_specialtyendocrine systemMESH: MutationGenetic counselingMESH : MaleMESH: Multiple Endocrine Neoplasia Type 1030209 endocrinology & metabolismBiology03 medical and health sciencesInternal medicineProto-Oncogene ProteinsGeneticsmedicineMultiple Endocrine Neoplasia Type 1HumansMEN1FamilyMolecular BiologyMESH: FamilyMESH: HumansMESH: Proto-Oncogene Proteins c-jun[ SDV ] Life Sciences [q-bio]Proportional hazards modelMESH : HumansCancerMESH : Follow-Up Studiesmedicine.diseaseMESH: MaleProtein Structure TertiaryMESH: Proto-Oncogene ProteinsMutationCancer researchMESH : FamilyMESH: FemaleFollow-Up Studies
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Diversifying selection on MHC class I in the house sparrow (Passer domesticus).

2009

10 pages; International audience; Genes of the major histocompatibility complex (MHC) are the most polymorphic loci known in vertebrates. Two main hypotheses have been put forward to explain the maintenance of MHC diversity: pathogen-mediated selection and MHC-based mate choice. Host-parasite interactions can maintain MHC diversity via frequency-dependent selection, heterozygote advantage, and diversifying selection (spatially and/or temporally heterogeneous selection). In this study, we wished to investigate the nature of selection acting on the MHC class I across spatially structured populations of house sparrows (Passer domesticus) in France. To infer the nature of the selection, we comp…

0106 biological sciencesMESH : Gene FlowMESH: Selection (Genetics)MESH: GeographyGenes MHC Class IMESH: Genetic MarkersBalancing selectionMESH : Microsatellite Repeats[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology01 natural sciencesmicrosatellitesMESH: SparrowsMESH : Genetic MarkersMESH: AnimalsMESH: Genetic VariationMESH: Evolution MolecularGenetics0303 health scienceseducation.field_of_studyGeographybiology[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE]MESH : GeographyMESH: Genes MHC Class I[ SDE.MCG ] Environmental Sciences/Global Changes[ SDV.BID.EVO ] Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE][SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyMate choiceMESH: Stochastic ProcessesMHC class IMESH : MutationSparrowsGene FlowGenetic MarkersMESH: Mutationbalancing selection[SDE.MCG]Environmental Sciences/Global ChangesPopulationMESH : Genetic DriftMESH: Genetics Populationchemical and pharmacologic phenomenaMESH : Stochastic ProcessesMajor histocompatibility complex010603 evolutionary biologyMESH : Genes MHC Class IEvolution Molecular03 medical and health sciencesMESH : Genetic VariationMHC class IGeneticsPasser domesticusMESH : Selection (Genetics)AnimalsMESH : Evolution MolecularSelection GeneticMESH: Genetic DrifteducationAllelesMESH: Gene FlowEcology Evolution Behavior and SystematicsSelection (genetic algorithm)030304 developmental biologyLocal adaptationIsolation by distanceStochastic Processes[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologyhouse sparrowMESH: AllelesGenetic DriftGenetic Variationdiversifying selectionPasser domesticus.[ SDV.GEN.GA ] Life Sciences [q-bio]/Genetics/Animal geneticsMESH : Genetics Population[SDE.ES]Environmental Sciences/Environmental and Society[SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal geneticsGenetics PopulationEvolutionary biologyMutationbiology.proteinMESH: Microsatellite RepeatsMESH : AnimalsMESH : Sparrows[SDE.BE]Environmental Sciences/Biodiversity and EcologyMESH : Alleles[ SDE.ES ] Environmental Sciences/Environmental and SocietyMicrosatellite Repeats
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S-nitrosylation of the death receptor fas promotes fas ligand-mediated apoptosis in cancer cells.

2011

International audience; BACKGROUND & AIMS: Fas belongs to the family of tumor necrosis factor receptors which induce apoptosis. Many cancer cells express Fas but do not undergo Fas-mediated apoptosis. Nitric oxide reverses this resistance by increasing levels of Fas at the plasma membrane. We studied the mechanisms by which NO affects Fas function. METHODS: Colon and mammary cancer cell lines were incubated with the NO donor glyceryl trinitrate or lipid A; S-nitrosylation of Fas was monitored using the biotin switch assay. Fas constructs that contained mutations at cysteine residues that prevent S-nitrosylation were used to investigate the involvement of S-nitrosylation in Fas-mediated cell…

MESH: NitroglycerinMESH: Signal TransductionTime FactorsMESH: Membrane MicrodomainsApoptosisMESH : Fas Ligand ProteinCytoplasmic partMESH: Lipid AFas ligandMiceNitroglycerin0302 clinical medicineMESH : Protein TransportMESH : FemaleMESH: AnimalsFADDLipid raft0303 health sciencesTumorbiologyColon CancerMESH : Lipid AMESH : BiotinylationGastroenterologyFas receptorMESH: Antigens CD95Protein TransportLipid AMESH : Colonic NeoplasmsMESH : Nitric OxideMESH : Nitric Oxide Donors030220 oncology & carcinogenesisColonic NeoplasmsDeath-inducing signaling complexFemale[ SDV.MHEP.HEG ] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH : MutationMESH : TransfectionSignal TransductionMESH : Time FactorsMESH: Protein TransportFas Ligand ProteinMESH : Mammary Neoplasms ExperimentalMESH: MutationMESH: Cell Line TumorMESH: Mammary Neoplasms ExperimentalNitric OxideTransfectionCaspase 803 medical and health sciencesMembrane MicrodomainsCell Line TumorMESH : MiceAnimalsHumansBiotinylationNitric Oxide DonorsMESH: BiotinylationCysteinefas ReceptorMESH: MiceMESH : Protein Processing Post-Translational030304 developmental biologyMESH : Signal TransductionMESH: Colonic NeoplasmsMESH : CysteineMESH: HumansHepatologyMESH : Cell Line TumorMESH: ApoptosisMESH: TransfectionMESH : HumansMESH: Time FactorsMammary Neoplasms Experimental[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: CysteineMESH: Nitric Oxide DonorsMolecular biologySignalingMESH: Fas Ligand ProteinMESH : NitroglycerinApoptosisLocalizationMESH: Nitric OxideMESH: Protein Processing Post-TranslationalMutationbiology.proteinMESH : Membrane MicrodomainsMESH : AnimalsMESH : Antigens CD95Protein Processing Post-TranslationalMESH: FemaleMESH : Apoptosis
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Functional genomics of Lactobacillus casei establishment in the gut

2014

International audience; Although the composition of the gut microbiota and its symbiotic contribution to key host physiological functions are well established, little is known as yet about the bacterial factors that account for this symbiosis. We selected Lactobacillus casei as a model microorganism to proceed to genomewide identification of the functions required for a symbiont to establish colonization in the gut. As a result of our recent development of a transposon-mutagenesis tool that overcomes the barrier that had prevented L. casei random mutagenesis, we developed a signature-tagged mutagenesis approach combining whole-genome reverse genetics using a set of tagged transposons and in…

Transposable elementLactobacillus caseiMESH: MutationMutagenesis (molecular biology technique)MESH: RabbitsGenomicsBiologyMESH: Genome BacterialGenomedigestive system03 medical and health sciencesIleumLactic acid bacteriaAnimalsMESH: AnimalsGene030304 developmental biologyMESH: MutagenesisGenetics0303 health sciencesMultidisciplinaryMESH: Lactobacillus casei030306 microbiologyMESH: Genomicsdigestive oral and skin physiologyfood and beveragesGenomicsbiology.organism_classificationReverse geneticsCommensalismLacticaseibacillus caseiPNAS PlusMutagenesisMESH: IleumMutationMESH: Genome-Wide Association StudybacteriaRabbitsFunctional genomics[SDV.AEN]Life Sciences [q-bio]/Food and NutritionGenome BacterialGenome-Wide Association Study
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Reverse-engineering the Arabidopsis thaliana transcriptional network under changing environmental conditions

2009

46 pages, 4 tables, 6 figures, 3 additinoal files.

0106 biological sciencesMESH: Genome PlantArabidopsis thalianaGene regulatory networkArabidopsis01 natural sciencesTranscriptomeGene Expression Regulation PlantArabidopsisMESH: Gene Expression Regulation DevelopmentalCluster AnalysisGene Regulatory NetworksMESH: ArabidopsisMESH: EcosystemMESH: Models GeneticOligonucleotide Array Sequence AnalysisMESH: Gene Regulatory NetworksGenetics0303 health sciencesMESH: Stress MechanicalbiologyMESH: Genomicsfood and beveragesGene Expression Regulation DevelopmentalGenomicsPhenotypeAlgorithmsGenome PlantMESH: MutationSystems biologyGenomicsMESH: AlgorithmsComputational biologyMESH: Arabidopsis ProteinsMESH: Phenotype03 medical and health sciencesMESH: Gene Expression Profiling[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Gene Expression Regulation PlantEcosystem030304 developmental biologyModels GeneticMicroarray analysis techniquesArabidopsis ProteinsGene Expression ProfilingResearchfungiRobustness (evolution)biology.organism_classificationMESH: Cluster AnalysisGene expression profilingMutationMESH: Oligonucleotide Array Sequence AnalysisStress Mechanical010606 plant biology & botany
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Contribution of molecular analyses in diagnosing Marfan syndrome and type I fibrillinopathies: an international study of 1009 probands.

2008

International audience; BACKGROUND: The diagnosis of Marfan syndrome (MFS) is usually initially based on clinical criteria according to the number of major and minor systems affected following international nosology. The number of FBN1 mutation carriers, at risk of aortic complications who would not be properly diagnosed based only on clinical grounds, is of growing importance owing to the increased availability of molecular screening. The aim of the study was to identify patients who should be considered for FBN1 mutation screening. METHODS: Our international series included 1009 probands with a known FBN1 mutation. Patients were classified as either fulfilling or not fulfilling "clinical"…

ProbandNosologyMarfan syndromeMalePediatricsSystemic diseaseMESH : International CooperationFibrillin-1International CooperationMESH : Aged[SDV.GEN] Life Sciences [q-bio]/GeneticsMarfan SyndromeMESH : ChildMESH: ChildEpidemiologyMESH : FemaleEctopia lentisChildGenetics (clinical)AortaAortic dissectionMESH: Aged0303 health sciences030305 genetics & heredityMicrofilament ProteinsMESH: AortaMESH : AdultConnective tissue disease3. Good healthFemaleMESH : Mutationmusculoskeletal diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesMESH: MutationMESH : Microfilament ProteinsAdolescentMESH : MaleFibrillinsMESH: Marfan Syndrome03 medical and health sciencesMESH: Microfilament ProteinsMESH : AdolescentGeneticsmedicineHumans030304 developmental biologyAgedMESH: Adolescent[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH : Marfan SyndromeMESH: Humansbusiness.industryMESH : HumansMESH : AortaMESH: Adultmedicine.diseaseMESH: MaleMESH: International CooperationMutation[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessMESH: FemaleJournal of medical genetics
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