Search results for "Missense mutation"

showing 10 items of 223 documents

IQSEC2-related encephalopathy in males and females: a comparative study including 37 novel patients.

2019

Variants in IQSEC2, escaping X inactivation, cause X-linked intellectual disability with frequent epilepsy in males and females. We aimed to investigate sex-specific differences.

0301 basic medicineMaleGénétique clinique[SDV]Life Sciences [q-bio]MedizinPhysiology030105 genetics & hereditySeizures/epidemiologyEpilepsyBrain Diseases/epidemiologyX-linked inheritanceIntellectual disabilityGuanine Nucleotide Exchange FactorsProtein IsoformsMissense mutationGenetics(clinical)10. No inequalityNon-U.S. Gov'tGenetics (clinical)X-linked recessive inheritanceComputingMilieux_MISCELLANEOUSBrain DiseasesSex CharacteristicsResearch Support Non-U.S. Gov'tBrainSciences bio-médicales et agricoles3. Good healthPedigreePhenotypeintellectual disabilityFemaleBrain/growth & developmentSex characteristicsGénétique moléculaireGuanine Nucleotide Exchange Factors/geneticsEncephalopathyResearch SupportX-inactivationArticle03 medical and health sciencesSeizuresProtein Isoforms/geneticsmedicineJournal ArticleIQSEC2HumansIntellectual Disability/epidemiology[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryInfant NewbornisoformsCorrectionInfantmedicine.diseaseNewbornHuman genetics030104 developmental biologyMutationepilepsyHuman medicinebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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De Novo and Inherited Pathogenic Variants in KDM3B Cause Intellectual Disability, Short Stature, and Facial Dysmorphism

2019

Contains fulltext : 202646.pdf (Publisher’s version ) (Open Access) By using exome sequencing and a gene matching approach, we identified de novo and inherited pathogenic variants in KDM3B in 14 unrelated individuals and three affected parents with varying degrees of intellectual disability (ID) or developmental delay (DD) and short stature. The individuals share additional phenotypic features that include feeding difficulties in infancy, joint hypermobility, and characteristic facial features such as a wide mouth, a pointed chin, long ears, and a low columella. Notably, two individuals developed cancer, acute myeloid leukemia and Hodgkin lymphoma, in childhood. KDM3B encodes for a histone …

0301 basic medicineMaleJumonji Domain-Containing Histone DemethylasesDevelopmental DisabilitiesWEAVER SYNDROMEPROTEINHaploinsufficiencyCraniofacial AbnormalitiesHistones0302 clinical medicineIntellectual disabilityTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Missense mutationDEMETHYLASE KDM3BExomeChildGenetics (clinical)Exome sequencingGeneticsRUBINSTEIN-TAYBI SYNDROMEMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Phenotype030220 oncology & carcinogenesisFemalemedicine.symptomHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Joint hypermobilityGENETICSJMJD1CMutation MissenseDwarfismBiologyShort statureKdm3b ; Cancer Predisposition ; Developmental Delay ; Facial Recognition ; Intellectual Disability ; Leukemia ; Lymphoma ; Short Stature03 medical and health sciencesReportIntellectual DisabilitymedicineHumansMYELOID-LEUKEMIAGenetic Association StudiesGerm-Line MutationWeaver syndromeNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Rubinstein–Taybi syndromeMUTATIONSDELETIONGenetic Variationmedicine.diseaseBody HeightMusculoskeletal AbnormalitiesINDIVIDUALS030104 developmental biologyFaceNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]American Journal of Human Genetics
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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Pathogenic DDX3X Mutations Impair RNA Metabolism and Neurogenesis during Fetal Cortical Development.

2020

Summary De novo germline mutations in the RNA helicase DDX3X account for 1%–3% of unexplained intellectual disability (ID) cases in females and are associated with autism, brain malformations, and epilepsy. Yet, the developmental and molecular mechanisms by which DDX3X mutations impair brain function are unknown. Here, we use human and mouse genetics and cell biological and biochemical approaches to elucidate mechanisms by which pathogenic DDX3X variants disrupt brain development. We report the largest clinical cohort to date with DDX3X mutations (n = 107), demonstrating a striking correlation between recurrent dominant missense mutations, polymicrogyria, and the most severe clinical outcom…

0301 basic medicineMaleNeurogenesisMutation MissenseBiologyPathogenesisDEAD-box RNA Helicases03 medical and health sciencesMice0302 clinical medicineGermline mutationStress granuleCell Line TumorPolymicrogyriamedicineMissense mutationAnimalsHumansCells CulturedGeneticsCerebral CortexGeneral NeuroscienceNeurogenesismedicine.diseaseRNA Helicase AMice Inbred C57BL030104 developmental biologyNeurodevelopmental DisordersRNAFemaleDDX3X030217 neurology & neurosurgeryNeuron
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Autosomal recessive variations of TBX6 , from congenital scoliosis to spondylocostal dysostosis

2017

International audience; Proximal 16p11.2 microdeletions are recurrent microdeletions with an overall prevalence of 0.03%. In patients with segmentation defects of the vertebra (SDV), a burden of this microdeletion was observed with TBX6 as a candidate gene for SDV. In a published cohort of patients with congenital scoliosis (CS), TBX6 haploinsufficiency was compound heterozygous with a common haplotype. Besides, a single three-generation family with spondylocostal dysostosis (SCD) was reported with a heterozygous stop-loss of TBX6. These observations questioned both on the inheritance mode and on the variable expressivity associated with TBX6-associated SDV. Based on a national recruitment …

0301 basic medicineMalePediatricsmedicine.medical_specialtyCandidate geneGenotypeScoliosis030105 genetics & heredityCompound heterozygosity03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineInheritance ModeMissense mutationHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildGenetics (clinical)GeneticsHernia Diaphragmaticbusiness.industryHaplotypeInfantmedicine.diseaseSpondylocostal dysostosisSpine3. Good healthPedigree030104 developmental biologyHaplotypesScoliosisChild PreschoolMutationFemalebusinessHaploinsufficiencyT-Box Domain Proteins[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Staphylococcal cassette chromosome mec typing and mecA sequencing in methicillin-resistant staphylococci from Algeria: a highly diversified element w…

2016

Genetic mechanisms of methicillin resistance are still relevant in staphylococci. The aims of this study are to assess the possible exchanges of staphylococcal cassette chromosome mec (SCCmec) among isolates of methicillin-resistant staphylococci (MRS) and to check for known or new mutations in mecA DNA. A total of 35 MRS non-repetitive isolates were recovered, including 20 Staphylococcus haemolyticus, 7 Staphylococcus aureus, 4 Staphylococcus sciuri, 2 Staphylococcus saprophyticus and 1 isolate each of Staphylococcus xylosus and Staphylococcus lentus. Only 16 of the 35 strains were assigned to known SCCmec types: 7 SCCmec VII, 6 SCCmec IV and 3 SCCmec III, with possible horizontal transfer…

0301 basic medicineMicrobiology (medical)Methicillin-Resistant Staphylococcus aureusSettore MED/07 - Microbiologia E Microbiologia ClinicaStaphylococcus030106 microbiologyMicrobial Sensitivity TestsBiologymedicine.disease_causebeta-LactamsMicrobiologyBacterial geneticsMicrobiology03 medical and health sciencesBacterial ProteinsmedicineMissense mutationHumansPenicillin-Binding ProteinsTypingmecAGeneticsMutationSCCmecChromosomeGeneral Medicinerespiratory systembiochemical phenomena metabolism and nutritionChromosomes BacterialStaphylococcal Infectionsbacterial infections and mycosesStaphylococcus aureusStaphylococcus aureus; Methicillin Resistance; mecAAlgeriaHorizontal gene transferMutationStaphylococcus aureuMethicillin ResistanceJournal of medical microbiology
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Functional analysis of TLK2 variants and their proximal interactomes implicates impaired kinase activity and chromatin maintenance defects in their p…

2020

IntroductionThe Tousled-like kinases 1 and 2 (TLK1 and TLK2) are involved in many fundamental processes, including DNA replication, cell cycle checkpoint recovery and chromatin remodelling. Mutations in TLK2 were recently associated with ‘Mental Retardation Autosomal Dominant 57’ (MRD57, MIM# 618050), a neurodevelopmental disorder characterised by a highly variable phenotype, including mild-to-moderate intellectual disability, behavioural abnormalities, facial dysmorphisms, microcephaly, epilepsy and skeletal anomalies.MethodsWe re-evaluate whole exome sequencing and array-CGH data from a large cohort of patients affected by neurodevelopmental disorders. Using spatial proteomics (BioID) and…

0301 basic medicineNeurobiologia del desenvolupamentMicrocephalymissenseMolecular biologyBiologymedicine.disease_causemedicalloss of function mutation03 medical and health sciencesmutation.0302 clinical medicineNeurodevelopmental disordermedicineChromatin maintenanceMissense mutationmolecular biologygeneticsDevelopmental neurobiologyKinase activitygenetic research; genetics; loss of function mutation; medical; missense; molecular biology; mutationGenetics (clinical)Exome sequencingBiologia molecularGeneticsMutationgenetic researchmedicine.diseaseChromatin030104 developmental biologymutationgenetic030217 neurology & neurosurgery
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Hereditary Leiomyomatosis and Renal Cell Cancer Syndrome in Spain: Clinical and Genetic Characterization

2020

Simple Summary Hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome is a very rare hereditary disorder characterized by cutaneous leiomyomas (CLMs), uterine leiomyomas (ULMs), renal cysts (RCys) and renal cell cancer (RCC), with no data on its prevalence worldwide. No genotype-phenotype associations have been described. The aim of our study was to describe the genotypic and phenotypic features of the largest series of patients with HLRCC from Spain reported to date. Of 27 FH germline pathogenic variants, 12 were not previously reported in databases. Patients with missense pathogenic variants showed higher frequencies of CLMs, ULMs and RCys, than those with loss-of-function varia…

0301 basic medicineOncologyCancer ResearchCancer cellsmedicine.disease_causeurologic and male genital diseases:Male Urogenital Diseases::Urogenital Neoplasms::Urologic Neoplasms::Kidney Neoplasms::Male Urogenital Diseases::Carcinoma Renal Cell [DISEASES]<i>FH</i> gene0302 clinical medicineMalalties hereditàriesMissense mutationFH geneFH gene hereditary leiomyomatosis leiomyomas missense pathogenic variants renal cell cancerRenal cell cancerMutationKidney diseasesHereditary leiomyomatosis:Otros calificadores::Otros calificadores::/genética [Otros calificadores]:enfermedades urogenitales masculinas::neoplasias urogenitales::neoplasias urológicas::neoplasias renales::enfermedades urogenitales masculinas::carcinoma de células renales [ENFERMEDADES]leiomyomasmissense pathogenic variants renal cell cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRare diseases:Geographic Locations::Europe::Spain [GEOGRAPHICALS]Oncology030220 oncology & carcinogenesisCohortCèl·lules cancerosesMalalties raresRenal Cell CancersGenetic disordersmedicine.medical_specialtyMissense pathogenic variantsBiología Celularlcsh:RC254-282Article03 medical and health sciencesLeiomyomasInternal medicine:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineRonyons - Malalties - Espanya:localizaciones geográficas::Europa (continente)::España [DENOMINACIONES GEOGRÁFICAS]business.industry:neoplasias::neoplasias por tipo histológico::neoplasias de tejido conjuntivo y de tejidos blandos::neoplasias de tejido muscular::leiomioma::leiomiomatosis [ENFERMEDADES]Retrospective cohort studymedicine.diseaseGenética030104 developmental biologyFumaraseClinical diagnosisHereditary leiomyomatosis and renal cell cancer syndromeMalalties del ronyó:Neoplasms::Neoplasms by Histologic Type::Neoplasms Connective and Soft Tissue::Neoplasms Muscle Tissue::Leiomyoma::Leiomyomatosis [DISEASES]hereditary leiomyomatosisbusiness
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