Search results for "missense mutation"

showing 10 items of 223 documents

Analysis of the LRP10 gene in patients with Parkinson's disease and dementia with Lewy bodies from Southern Italy

2020

Recently, the LRP10 gene has been associated with Parkinson's disease (PD), Parkinson's disease with dementia (PDD), and dementia with Lewy bodies (DLB). The aim of the present study was to evaluate the presence of mutations of the LRP10 gene in patients with PD or DLB from Southern Italy. Sequencing analysis revealed only 2 missense and 3 synonymous variants in patients and control subjects and a rare variant p.L622F in a PD case. These results suggest that LRP10 mutations are not a frequent cause of PD and DLB in Southern Italy.

Lewy Body Diseasemedicine.medical_specialtyNeurologyParkinson's diseaseLRP10 . Parkinson’s disease . Dementia with Lewy bodiesDermatologyDiseasebehavioral disciplines and activities03 medical and health sciences0302 clinical medicineAlzheimer DiseaseInternal medicineDementia with Lewy bodies; LRP10; Parkinson's disease.mental disordersmedicineDementiaMissense mutationHumans030212 general & internal medicineNeuroradiologyDementia with Lewy bodiesbusiness.industryParkinson DiseaseGeneral Medicinemedicine.diseasenervous system diseasesPsychiatry and Mental healthItalyMutationSettore MED/26 - NeurologiaNeurology (clinical)Neurosurgerybusiness030217 neurology & neurosurgery
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Mutation profile of the MYO7A gene in Spanish patients with Usher syndrome type I.

2006

Usher syndrome type I is the most severe form of Usher syndrome. It is an autosomal recessive disorder characterized by profound congenital sensorineural deafness, retinitis pigmentosa, and vestibular abnormalities. Mutations in the myosin VIIA gene (MYO7A) are responsible for Usher syndrome type 1B (USH1B). This gene is thought to bear greatest responsibility for USH1 and, depending on the study, has been reported to account for between 24% and 59% of USH1 cases. In this report a mutation screening of the MYO7A gene was carried out in a series of 48 unrelated USH1 families using single strand conformation polymorphism analysis (SSCP) and direct sequencing of those fragments showed an abnor…

MYO7AUsher syndromeDNA Mutational AnalysisBiologyMyosinsFrameshift mutationRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseGeneGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsPolymorphism GeneticModels GeneticDyneinsSingle-strand conformation polymorphismmedicine.diseaseeye diseasesStop codonGene Expression RegulationSpainMyosin VIIaMutationUsher SyndromesHuman mutation
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TBL1XR1 mutations in Pierpont syndrome are not restricted to the recurrent p.Tyr446Cys mutation

2018

IF 2.264; International audience; Pierpont syndrome is a rare and sporadic syndrome, including developmental delay, facial characteristics, and abnormal extremities. Recently, a recurrent de novo TBL1XR1 variant (c.1337A > G; p.Tyr446Cys) has been identified in eight patients by whole‐exome sequencing. A dominant‐negative effect of this mutation is strongly suspected, since patients with TBL1XR1 deletion and other variants predicting loss of function do not share the same phenotype. We report two patients with typical Pierpont‐like syndrome features. Exome sequencing allowed identifying a de novo heterozygous missense TBL1XR1 variant in both patients, different from those already reported: …

Male0301 basic medicineAdolescentGenotypeReceptors Cytoplasmic and NuclearBiology03 medical and health sciences0302 clinical medicinePIERPONT SYNDROMEGeneticsHumansTBL1XR1Missense mutationAbnormalities MultipleRecurrent mutationGenetic TestingAllelesGenetics (clinical)Exome sequencingLoss functionUltrasonographyGeneticsComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsBrainFaciesNuclear ProteinsSyndromeMagnetic Resonance ImagingPhenotype3. Good healthRepressor ProteinsPhenotype030104 developmental biologyAmino Acid Substitution030220 oncology & carcinogenesisMutationMutation (genetic algorithm)Pierpont syndromeAmerican Journal of Medical Genetics Part A
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De Novo Mutations in SLC25A24 Cause a Disorder Characterized by Early Aging, Bone Dysplasia, Characteristic Face, and Early Demise

2017

International audience; A series of simplex cases have been reported under various diagnoses sharing early aging, especially evident in congenitally decreased subcutaneous fat tissue and sparse hair, bone dysplasia of the skull and fingers, a distinctive facial gestalt, and prenatal and postnatal growth retardation. For historical reasons, we suggest naming the entity Fontaine syndrome. Exome sequencing of four unrelated affected individuals showed that all carried the de novo missense variant c.649C>T (p.Arg217Cys) or c.650G>A (p.Arg217His) in SLC25A24, a solute carrier 25 family member coding for calcium-binding mitochondrial carrier protein (SCaMC-1, also known as SLC25A24). SLC25A24 all…

Male0301 basic medicineAgingMitochondrionPetty syndromeAntiportersATP-Mg/Pi carriersAdenosine TriphosphateCytosol0302 clinical medicineAdenine nucleotideMissense mutation[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)Exome sequencingMembrane Potential MitochondrialGeneticsProgeriaATP synthaseSCaMC-1SyndromeMitochondria3. Good healthFemalemedicine.medical_specialtylipodystrophyMolecular Dynamics SimulationBiologyPhosphatesMitochondrial Proteins03 medical and health sciencesReportInternal medicineGeneticsmedicineHumansFetal DeathBone Diseases DevelopmentalAdenineSLC25A24Calcium-Binding ProteinsagingInfant NewbornInfantprogeriaFibroblastsmedicine.diseaseMitochondrial carrierSolute carrier familyOxygenprogeroid disorder030104 developmental biologyEndocrinology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationbiology.protein030217 neurology & neurosurgery
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Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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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
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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
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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
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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
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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
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