Search results for "missense"

showing 10 items of 303 documents

A novel mutation of WDR62 gene associated with severe phenotype including infantile spasm, microcephaly, and intellectual disability

2017

Abstract The autosomal recessive form of primary microcephaly (MCPH) is a rare disorder characterized by head circumference of at least 3 standard deviation below the mean. The MCPH exhibits genetic heterogeneity with thirteen loci (MCPH1-MCPH13) identified, and associated with variable degree of intellectual disability. It has been reported that WDR62 is the second causative gene of autosomal recessive microcephaly (MCPH2) playing a significant role in spindle formation and the proliferation of neuronal progenitor cells. We report a clinical feature, electroclinical findings, and clinical course of a patient with a severe phenotype of MCPH2 including microcephaly, refractory infantile spas…

Male0301 basic medicineMicrocephalyAdolescentMutation MissenseIntellectual disabilityCell Cycle ProteinsNerve Tissue ProteinsGenetic analysisReceptors G-Protein-CoupledConsanguinity03 medical and health sciences0302 clinical medicineDevelopmental NeuroscienceSettore M-PSI/08 - Psicologia ClinicaIntellectual disabilityHumansMedicineMissense mutationGeneWDR62GeneticsMCPHEpilepsybusiness.industryGenetic heterogeneityInfantGeneral MedicineInfantile Spasmmedicine.diseaseSettore MED/39 - Neuropsichiatria InfantilePedigreePhenotype030104 developmental biologyGPR56MutationPediatrics Perinatology and Child HealthMicrocephalyInfantile spasmNeurology (clinical)businessSpasms Infantile030217 neurology & neurosurgeryBrain and Development
researchProduct

A Recurrent De Novo PACS2 Heterozygous Missense Variant Causes Neonatal-Onset Developmental Epileptic Encephalopathy, Facial Dysmorphism, and Cerebel…

2018

International audience; Developmental and epileptic encephalopathies (DEEs) represent a large clinical and genetic heterogeneous group of neurodevelopmental diseases. The identification of pathogenic genetic variants in DEEs remains crucial for deciphering this complex group and for accurately caring for affected individuals (clinical diagnosis, genetic counseling, impacting medical, precision therapy, clinical trials, etc.). Whole-exome sequencing and intensive data sharing identified a recurrent de novo PACS2 heterozygous missense variant in 14 unrelated individuals. Their phenotype was characterized by epilepsy, global developmental delay with or without autism, common cerebellar dysgene…

Male0301 basic medicinePathologyPACS-2Vesicular Transport ProteinsPHENOTYPEBioinformaticsDISEASESensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Epilepsy0302 clinical medicineMissense mutationGlobal developmental delayAge of OnsetChildGenetics (clinical)Epileptic encephalopathyAPOPTOSIS3. Good healthcerebellar dysgenesisMutation Missense/geneticsintellectual disabilityChild PreschoolEpilepsy GeneralizedFemalePACS2CLINICAL EPILEPSYmedicine.medical_specialtyHeterozygoteGeneralized/geneticsPROTEINSGenetic counselingMutation MissenseMissense/geneticsNeonatal onsetBiologyDIAGNOSISVesicular Transport Proteins/geneticsFacial dysmorphism03 medical and health sciencesDysgenesisAll institutes and research themes of the Radboud University Medical CenterCerebellar DiseasesReportMENDELIAN DISORDERSGeneticsmedicineHumansGeneralized epilepsyPreschoolNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cerebellar Diseases/geneticsbusiness.industryMUTATIONSInfant NewbornCorrectionInfantFaciesNewbornmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationepilepsyAutismbusinessEpilepsy Generalized/genetics030217 neurology & neurosurgery
researchProduct

First report of X-linked hypohidrotic ectodermal dysplasia with a hemizygous c.1142G > C in the EDA gene: variant of uncertain significance or new pa…

2021

AbstractBackgroundHypohidrotic Ectodermal Dysplasia (HED) is a genetic disorder which affects structures of ectodermal origin. X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of disease. XLHED is characterized by hypotrichosis, hypohydrosis and hypodontia. The cardinal features of classic HED become obvious during childhood.Identification of a hemizygous EDA pathogenic variant in an affected male confirms the diagnosis.Case presentationWe report on a male newborn with the main clinical characteristics of the X-linked HED including hypotrichosis, hypodontia and hypohidrosis. Gene panel sequencing identified a new hemizygous missense variant of uncertain significanc…

Male0301 basic medicineProbandMutation MissenseVariants of uncertain significance (VUS)Case ReportX-linked.030105 genetics & heredityPediatricsRJ1-57003 medical and health sciencesEDA geneHumansMedicineMissense mutationHypohidrotic ectodermal dysplasiaX chromosomeHemizygoteGeneticsX-linkedChromosomes Human XEctodermal Dysplasia 1 Anhidroticbusiness.industryInfant NewbornGenetic disorderGeneral MedicineEctodysplasinsmedicine.diseaseHypoidrotic ectodermal dysplasiaHypodontia030104 developmental biologyHypotrichosisEctodysplasin AbusinessItalian Journal of Pediatrics
researchProduct

Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
researchProduct

Exome sequencing of a family with lone, autosomal dominant atrial flutter identifies a rare variation in ABCB4 significantly enriched in cases

2015

Background Lone atrial flutter (AFL) and atrial fibrillation (AF) are common and sometimes consequential cardiac conduction disorders with a strong heritability, as underlined by recent genome-wide association studies that identified genetic modifiers. Follow-up family-based genetic analysis also identified Mendelian transmission of disease alleles. Three affected members were exome-sequenced for the identification of potential causative mutations, which were subsequently validated by direct sequencing in the other 3 affected members. Taqman assay was then used to confirm the role of any mutation in an independent population of sporadic lone AFL/AF cases. Results The family cluster analysis…

MaleATP Binding Cassette Transporter Subfamily BDNA Mutational AnalysisPopulationMutation MissenseSNPGenome-wide association studySingle-nucleotide polymorphismAtrial flutterBiologyBioinformaticsPolymorphism Single NucleotideDNA Mutational AnalysiExome-sequencingGeneticCardiac conductionGeneticsHumansGenetics(clinical)ExomeAlleleeducationExomeATP-binding cassette B4 (ABCB4)Genetics (clinical)Exome sequencingAgedGenetic associationAged 80 and overGeneticseducation.field_of_studyP-GlycoproteinAtrial fibrillationPedigreeFemaleHumanGenome-Wide Association StudyResearch ArticleSNPs
researchProduct

FUS MUTATIONS IN SPORADIC AMYOTROPHIC LATERAL SCLEROSIS: CLINICAL AND GENETIC ANALYSIS

2012

Fused in sarcoma (FUS) or translocation in liposarcoma (TLS), a DNA/RNA-binding protein, causes a dominant autosomal inherited form of amyotrophic lateral sclerosis (ALS), ALS 6. Its main role in neurodegeneration is highlighted by the presence of cytoplasmic accumulation of its mutant protein form in ALS patients. To further define the frequency and spectrum of FUS gene mutations, we have performed a molecular screening of a cohort of 327 Italian patients from Southern Italy with sporadic ALS (SALS). We identified 4 patients carrying 3 different missense mutations and several polymorphisms. Two different substitutions occurring in the same amino acidic position have been observed in 2 pati…

MaleAgingPopulationDNA Mutational AnalysisBiologyGene mutationmedicine.disease_causeGenetic analysisFUS geneMutant proteinALS; FUS gene; mutation; sporadicmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmyotrophic lateral sclerosiseducationAgedGeneticsAged 80 and overNeurologic ExaminationMutationeducation.field_of_studyGeneral NeuroscienceNeurodegenerationAmyotrophic Lateral SclerosisExonsMiddle AgedALS; FUS gene; Mutation; Sporadicmedicine.diseaseMagnetic Resonance ImagingSettore BIO/18 - GeneticasporadicMutationRNA-Binding Protein FUSFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSGeriatrics and GerontologyDevelopmental Biology
researchProduct

Genome-wide Analyses Identify KIF5A as a Novel ALS Gene

2018

© 2018 Elsevier Inc.

MaleAls geneGenome-wide association studyFAMILIAL ALSALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS0302 clinical medicine80 and overPsychologyGWASKIF5AAetiologycargoAged 80 and over0303 health sciencesFrench ALS ConsortiumKinesinKINESIN HEAVY-CHAINCognitive Sciencesaxonal transportHumanHereditary spastic paraplegiaNeuroscience(all)Single-nucleotide polymorphismTARGETED DISRUPTIONArticle03 medical and health sciencesGeneticsHumansAmino Acid SequenceLoss functionAgedHEXANUCLEOTIDE REPEATNeuroscience (all)MUTATIONSAmyotrophic Lateral Sclerosis3112 Neurosciences1702 Cognitive Sciencemedicine.diseaseITALSGEN ConsortiumAnswer ALS Foundation030104 developmental biologyALS Sequencing ConsortiumHuman medicine1109 Neurosciences030217 neurology & neurosurgery0301 basic medicineALS; GWAS; KIF5A; WES; WGS; axonal transport; cargo[SDV]Life Sciences [q-bio]KinesinsNeurodegenerativeGenetic analysisGenomeAMYOTROPHIC-LATERAL-SCLEROSIS3124 Neurology and psychiatryCohort StudiesPathogenesisLoss of Function MutationMissense mutation2.1 Biological and endogenous factorsAmyotrophic lateral sclerosisNYGC ALS ConsortiumGeneticsGeneral NeuroscienceALS axonal transport cargo GWAS KIF5A WES WGSMiddle AgedPhenotypeSettore MED/26 - NEUROLOGIANeurologicalProject MinE ALS Sequencing ConsortiumKinesinWESFemaleAdultBiologyGENOTYPE IMPUTATIONALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Amyotrophic Lateral Sclerosis; Cohort Studies; Female; Genome-Wide Association Study; Humans; Kinesin; Loss of Function Mutation; Male; Middle Aged; Young AdultNOYoung AdultRare DiseasesmedicineSLAGEN ConsortiumGene030304 developmental biologyClinical Research in ALS and Related Disorders for Therapeutic Development (CReATe) ConsortiumNeurology & NeurosurgeryHuman GenomeNeurosciencesAXONAL-TRANSPORTBrain DisordersALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS;Family memberDNA-DAMAGEMOTOR-NEURONS3111 BiomedicineCohort StudieALSGenomic Translation for ALS Care (GTAC) ConsortiumWGSAmyotrophic Lateral SclerosiGenome-Wide Association StudyALS; axonal transport; cargo; GWAS; KIF5A; WES; WGS; Neuroscience (all)
researchProduct

De novo loss-of-function KCNMA1 variants are associated with a new multiple malformation syndrome and a broad spectrum of developmental and neurologi…

2019

Abstract KCNMA1 encodes the large-conductance Ca2+- and voltage-activated K+ (BK) potassium channel α-subunit, and pathogenic gain-of-function variants in this gene have been associated with a dominant form of generalized epilepsy and paroxysmal dyskinesia. Here, we genetically and functionally characterize eight novel loss-of-function (LoF) variants of KCNMA1. Genome or exome sequencing and the participation in the international Matchmaker Exchange effort allowed for the identification of novel KCNMA1 variants. Patch clamping was used to assess functionality of mutant BK channels. The KCNMA1 variants p.(Ser351Tyr), p.(Gly356Arg), p.(Gly375Arg), p.(Asn449fs) and p.(Ile663Val) abolished the …

MaleAtaxiaGenotypeDevelopmental DisabilitiesMutation MissenseBiology03 medical and health sciences0302 clinical medicineNeurodevelopmental disorderProtein DomainsLoss of Function MutationGeneticsmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to DiseaseProtein Interaction Domains and MotifsAlleleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMolecular BiologyAllelesGenetic Association StudiesGenetics (clinical)Loss functionExome sequencing030304 developmental biologyGenetics0303 health sciencesInfant NewbornGeneral MedicineParoxysmal dyskinesiamedicine.diseaseElectrophysiological PhenomenaPedigreePhenotypeAmino Acid SubstitutionSpeech delayFemaleGeneral Articlemedicine.symptom030217 neurology & neurosurgeryHuman Molecular Genetics
researchProduct

Comparison between thrombotic risk scores in essential thrombocythemia and survival implications.

2019

The conventional thrombotic risk stratification in essential thrombocythemia (ET) distinguishes patients in two risk groups based on previous thrombosis and age (< or >60). The IPSET-thrombosis takes into account four risk factors: age greater than 60 years and the presence of CV risk factors, thrombosis history and JAK2 V617F presence. The revised IPSET-thrombosis uses three adverse variables to delineate four risk categories: age greater than 60, thrombosis history, and JAK2 V617F presence. We compared different risk models in the estimation of thrombotic risk in 191 patients with ET and the role of specific driver mutations affecting overall survival, according to thrombotic risk. …

MaleCancer ResearchEssential Thrombocythemia Myeloproliferative Thrombosis Thrombotic risk SurvivalKaplan-Meier EstimateSeverity of Illness IndexSettore MED/15 - Malattie Del SanguePrognostic score0302 clinical medicineRisk groupsRecurrenceRisk FactorsMutational statusThrombophiliaAged 80 and overIncidenceAge FactorsHematologyGeneral MedicineMiddle AgedPrognosisThrombosisOncology030220 oncology & carcinogenesisFemaleJAK2 V617FReceptors ThrombopoietinThrombocythemia EssentialAdultPoor prognosismedicine.medical_specialtyAdolescentMutation MissenseModels BiologicalRisk Assessment03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAgedRetrospective StudiesThrombotic riskbusiness.industryEssential thrombocythemiaThrombosisJanus Kinase 2medicine.diseasebusinessCalreticulin030215 immunologyFollow-Up StudiesHematological oncologyREFERENCES
researchProduct

Loss of function mutation in the palmitoyl-transferase HHAT leads to syndromic 46,XY disorder of sex development by impeding Hedgehog protein palmito…

2014

The Hedgehog (Hh) family of secreted proteins act as morphogens to control embryonic patterning and development in a variety of organ systems. Post-translational covalent attachment of cholesterol and palmitate to Hh proteins are critical for multimerization and long range signaling potency. However, the biological impact of lipid modifications on Hh ligand distribution and signal reception in humans remains unclear. In the present study, we report a unique case of autosomal recessive syndromic 46,XY Disorder of Sex Development (DSD) with testicular dysgenesis and chondrodysplasia resulting from a homozygous G287V missense mutation in the hedgehog acyl-transferase (HHAT) gene. This mutation…

MaleCancer Research[SDV]Life Sciences [q-bio]medicine.disease_causeCell Fate DeterminationMiceTestisMorphogenesisMissense mutationddc:576.5Genetics (clinical)MutationHomozygoteCell DifferentiationHedgehog signaling pathwayPedigreeCell biologyFemaleSignal transductionSignal TransductionResearch Articlemedicine.medical_specialtylcsh:QH426-470LipoylationMolecular Sequence DataMutation MissenseBiologyPalmitoylationHHATInternal medicineGeneticsmedicineAnimalsHumansHedgehog ProteinsAmino Acid SequenceMolecular BiologyHedgehogEcology Evolution Behavior and SystematicsDisorder of Sex Development 46XY[ SDV ] Life Sciences [q-bio]Sequence Homology Amino AcidBiology and Life SciencesSex Determinationlcsh:GeneticsEndocrinology46 XY Disorders of Sex Development/*genetics; Acyltransferases/chemistry/*genetics/metabolism; Amino Acid Sequence; Animals; Female; Hedgehog Proteins/*metabolism; Homozygote; Humans; Lipoylation/*genetics; Male; Mice; Molecular Sequence Data; *Mutation Missense; Pedigree; Sequence Homology Amino Acid; Signal Transduction/*genetics; Testis/embryologyLipid modificationAcyltransferasesDevelopmental Biology
researchProduct