Search results for "MISSENSE MUTATION"

showing 10 items of 223 documents

Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3.

2014

Many neurodegenerative disorders present with sensory loss. In the group of hereditary sensory and autonomic neuropathies loss of nociception is one of the disease hallmarks. To determine underlying factors of sensory neurodegeneration we performed whole-exome sequencing in affected individuals with the disorder. In a family with sensory neuropathy with loss of pain perception and destruction of the pedal skeleton we report a missense mutation in a highly conserved amino acid residue of atlastin GTPase 3 (ATL3), an endoplasmic reticulum-shaping GTPase. The same mutation (p.Tyr192Cys) was identified in a second family with similar clinical outcome by screening a large cohort of 115 patients …

AtlastinAdultMaleIntracellular SpaceMutation MissenseSensory systemBiologymedicine.disease_causeEndoplasmic ReticulumGTP PhosphohydrolasesCohort StudiesFractures BoneYoung AdultmedicineMissense mutationHumansExomenociceptionAxonAge of OnsetHereditary Sensory and Autonomic NeuropathiesGenes DominantaxonGeneticsMutationEndoplasmic reticulumNeurodegenerationneurodegenerationmedicine.diseasePenetrancePedigreeHSANsensory neuronsmedicine.anatomical_structurePhenotypeCoughHaplotypesMutationGastroesophageal RefluxFemaleNeurology (clinical)Human medicineBone DiseasesNeuroscienceBrain : a journal of neurology
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The clinical and molecular spectrum of QRICH1 associated neurodevelopmental disorder

2022

De novo variants in QRICH1 (Glutamine-rich protein 1) has recently been reported in 11 individuals with intellectual disability. The function of QRICH1 is largely unknown but it is likely to play a key role in the unfolded response of endoplasmic reticulum (ER) stress through transcriptional control of proteostasis. In this study, we present 27 additional individuals and delineate the clinical and molecular spectrum of the individuals (n=38) with QRICH1 variants. The main clinical features were mild to moderate developmental delay/intellectual disability (71%), non-specific facial dysmorphism (92%) and hypotonia (39%). Additional findings included poor weight gain (29%), short stature (29%)…

Autism Spectrum Disorder[SDV]Life Sciences [q-bio]DwarfismBiologyBioinformaticsWeight GainShort stature03 medical and health sciences0302 clinical medicineNeurodevelopmental disorderNeuroimagingSeizuresvariable expressivityIntellectual disabilityGeneticsmedicineMissense mutationHumansQRICH1hypotoniaGenetics (clinical)030304 developmental biology0303 health sciencesmedicine.diseaseQRICH1Hypotoniashort statureScoliosisvariantAutism spectrum disorderNeurodevelopmental Disordersintellectual disabilityMuscle Hypotoniamedicine.symptom030217 neurology & neurosurgery
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Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer

2013

The insulin/insulin-like growth factor pathway is involved in breast and colorectal cancer (CRC) development. In the present study, we analyzed the coding region and short intron-exon borders of the insulin receptor substrate 1 and 2 (IRS‑1 and IRS‑2) genes in 12 cell lines derived from breast cancer (BC), 14 cell lines derived from CRC and 33 primary CRCs. The nucleotide variants identified in BC were 3 in IRS‑1, 1 of which (p.Arg267Cys) was novel and with a pathogenic potential as predicted by in silico analysis and 6 in IRS‑2. Twenty‑one variants in IRS‑1 and 18 in IRS‑2 were identified in the CRC samples. These included 11 novel IRS‑1 variants detected exclusively in CRCs, which include…

Cancer ResearchInsulin Receptor Substrate ProteinsSettore MED/06 - Oncologia MedicaIn silicoMutation MissenseBreast NeoplasmsColorectal NeoplasmBiologymedicine.disease_causeFrameshift mutationBreast cancerBreast cancerMCF-7 CellCell Line TumormedicineHumansMissense mutationFrameshift MutationInsulin Receptor Substrate ProteinSequence DeletionGeneticsMutationCaco-2 CellPolymorphism GeneticCancerGenetic VariationInsulin receptor substrate 1ArticlesGeneral MedicineInsulin receptor substrate 2HCT116 Cellsmedicine.diseaseColorectal cancerIRS1Mutagenesis InsertionalCell Transformation NeoplasticHT29 CellOncologyHCT116 CellBreast cancer; Colorectal cancer; Insulin receptor substrate 1; Insulin receptor substrate 2; Breast Neoplasms; Caco-2 Cells; Cell Line Tumor; Cell Transformation Neoplastic; Colorectal Neoplasms; Female; Frameshift Mutation; Genetic Variation; HCT116 Cells; HT29 Cells; Humans; Insulin Receptor Substrate Proteins; MCF-7 Cells; Mutagenesis Insertional; Mutation Missense; Polymorphism Genetic; Sequence Deletion; Signal Transduction; Cancer Research; OncologyInsulin Receptor Substrate ProteinsMCF-7 CellsFemaleCaco-2 CellsColorectal NeoplasmsHT29 CellsBreast NeoplasmHumanSignal Transduction
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Novel form of X-linked nonsyndromic hearing loss with cochlear malformation caused by a mutation in the type IV collagen gene COL4A6

2013

Hereditary hearing loss is the most common human sensorineural disorder. Genetic causes are highly heterogeneous, with mutations detected in >40 genes associated with nonsyndromic hearing loss, to date. Whereas autosomal recessive and autosomal dominant inheritance is prevalent, X-linked forms of nonsyndromic hearing impairment are extremely rare. Here, we present a Hungarian three-generation family with X-linked nonsyndromic congenital hearing loss and the underlying genetic defect. Next-generation sequencing and subsequent segregation analysis detected a missense mutation (c.1771G>A, p.Gly591Ser) in the type IV collagen gene COL4A6 in all affected family members. Bioinformatic analysis an…

Collagen Type IVMaleHearing lossDNA Mutational AnalysisMolecular Sequence DataMutation MissenseGene ExpressionDeafnessBiologyCongenital hearing lossmedicine.disease_causeArticleType IV collagenotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansMissense mutationGenetic Predisposition to DiseaseAmino Acid SequenceAlport syndromeGeneCells CulturedGenetic Association StudiesZebrafishGenetics (clinical)GeneticsMutationGenetic Diseases X-LinkedMiddle Agedmedicine.diseaseCochleaPedigreeMice Inbred C57BLChild PreschoolFemaleRNA Splice SitesOtic vesiclemedicine.symptomEuropean Journal of Human Genetics
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Mutation Analysis of Core Binding Factor A1 in Patients with Cleidocranial Dysplasia

1999

SummaryCleidocranial dysplasia (CCD) is a dominantly inherited disorder characterized by patent fontanelles, wide cranial sutures, hypoplasia of clavicles, short stature, supernumerary teeth, and other skeletal anomalies. We recently demonstrated that mutations in the transcription factor CBFA1, on chromosome 6p21, are associated with CCD. We have now analyzed the CBFA1 gene in 42 unrelated patients with CCD. In 18 patients, mutations were detected in the coding region of the CBFA1 gene, including 8 frameshift, 2 nonsense, and 9 missense mutations, as well as 2 novel polymorphisms. A cluster of missense mutations at arginine 225 (R225) identifies this residue as crucial for CBFA1 function. …

Core binding factorRecombinant Fusion ProteinsDNA Mutational AnalysisGreen Fluorescent ProteinsMolecular Sequence DataMutation MissenseHuman malformation syndromeCore Binding Factor Alpha 1 SubunitBiologyTransfectionmedicine.disease_causeBone and BonesCleidocranial dysplasiaCell LineFrameshift mutationCBFA1GeneticsmedicineHumansMissense mutationGenetics(clinical)SupernumeraryFrameshift MutationGenetics (clinical)Sequence DeletionGeneticsMutationPolymorphism GeneticCleidocranial DysplasiaCore Binding FactorsArticlesmedicine.diseaseOsteochondrodysplasiaNeoplasm ProteinsRadiographyNuclear localizationLuminescent ProteinsPhenotypeMicroscopy FluorescenceMutation testingTranscription factorHaploinsufficiencyToothTranscription FactorsThe American Journal of Human Genetics
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Engineering of a bacterial tyrosinase for improved catalytic efficiency towards D-tyrosine using random and site directed mutagenesis approaches

2013

The tyrosinase gene from Ralstonia solanacearum (GenBank NP518458) was subjected to random mutagenesis resulting in tyrosinase variants (RVC10 and RV145) with up to 3.2-fold improvement in kcat, 5.2-fold lower Km and 16-fold improvement in catalytic efficiency for D-tyrosine. Based on RVC10 and RV145 mutated sequences, single mutation variants were generated with all variants showing increased kcat for D-tyrosine compared to the wild type (WT). All single mutation variants based on RV145 had a higher kcat and Km value compared to the RV145 and thus the combination of four mutations in RV145 was antagonistic for turnover, but synergistic for affinity of the enzyme for D-tyrosine. Single muta…

DNA BacterialProtein ConformationSequence analysisTyrosinasehomology modelingMolecular Sequence DataMutation Missenserandom mutagenesisBioengineeringtyrosinaseProtein Engineering010402 general chemistry01 natural sciencesApplied Microbiology and Biotechnologyenzyme catalysis03 medical and health sciencessite specific mutagenesisMissense mutationSite-directed mutagenesisHistidine030304 developmental biology0303 health sciencesRalstonia solanacearumbiologyMonophenol MonooxygenaseWild typeActive siteSequence Analysis DNAbiology.organism_classificationMolecular biologyRecombinant Proteins0104 chemical sciencesKineticsMutagenesisRalstonia solanacearumbiology.proteinTyrosineD-tyrosineMutant ProteinsBiotechnology
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Congenital secretory diarrhoea caused by activating germline mutations in GUCY2C

2016

Objective Congenital sodium diarrhoea (CSD) refers to a form of secretory diarrhoea with intrauterine onset and high faecal losses of sodium without congenital malformations. The molecular basis for CSD remains unknown. We clinically characterised a cohort of infants with CSD and set out to identify disease-causing mutations by genome-wide genetic testing. Design We performed whole-exome sequencing and chromosomal microarray analyses in 4 unrelated patients, followed by confirmatory Sanger sequencing of the likely disease-causing mutations in patients and in their family members, followed by functional studies. Results We identified novel de novo missense mutations in GUCY2C, the gene encod…

DiarrheaMale0301 basic medicinemedicine.medical_specialtyReceptors PeptideColonGuanylinGuanosine MonophosphateMutation MissenseReceptors EnterotoxinGUANYLATE CYCLASEBiologyCHRONIC DIARRHOEAPathogenesis03 medical and health scienceschemistry.chemical_compoundsymbols.namesakeGermline mutationInternal medicineBACTERIAL ENTEROTOXINSmedicineHumansMissense mutationAbnormalities MultipleGenetic Predisposition to Disease1506Intestinal MucosaCyclic guanosine monophosphateSanger sequencingPAEDIATRIC DIARRHOEASodiumGastroenterologyInfantMolecular Reproduction Development & Genetics (formed by the merger of DBGL and CRBME)Molecular biologyIntestines030104 developmental biologyEndocrinologyIntestinal AbsorptionReceptors Guanylate Cyclase-CoupledchemistryINTESTINAL ION TRANSPORTsymbolsFemaleMetabolism Inborn ErrorsIntracellularUroguanylinGut
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Localization of non-specific X-linked mental retardation gene (MRX73) to Xp22.2.

2001

Clinical and molecular studies are reported on a family (MRX73) of five males with non-specific X-linked mental retardation (XLMR). A total of 33 microsatellite and RFLP markers was typed. The gene for this XLMR condition was been linked to DXS1195, with a lod score of 2.36 at theta = 0. The haplotype and multipoint linkage analyses suggest localization of the MRX73 locus to an interval of 2 cM defined by markers DXS8019 and DXS365, in Xp22.2. This interval contains the gene of Coffin-Lowry syndrome (RSK2), where a missense mutation has been associated with a form of non-specific mental retardation. Therefore, a search for RSK2 mutations was performed in the MRX73 family, but no causal muta…

Family HealthMaleGeneticscongenital hereditary and neonatal diseases and abnormalitiesCoffin–Lowry syndromeX ChromosomeGenetic LinkageHaplotypeChromosome MappingLocus (genetics)Biologymedicine.diseasePedigreeGenetic linkageIntellectual DisabilitymedicineHumansMissense mutationMicrosatelliteFemaleLod ScoreRestriction fragment length polymorphismGenetics (clinical)X chromosomeMicrosatellite Repeats
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The FBN2 gene: new mutations, locus-specific database (Universal Mutation Database FBN2), and genotype-phenotype correlations.

2009

International audience; Congenital contractural arachnodactyly (CCA) is an extremely rare disease, due to mutations in the FBN2 gene encoding fibrillin-2. Another member of the fibrillin family, the FBN1 gene, is involved in a broad phenotypic continuum of connective-tissue disorders including Marfan syndrome. Identifying not only what is in common but also what differentiates these two proteins should enable us to better comprehend their respective functions and better understand the multitude of diseases in which these two genes are involved. In 1995 we created a locus-specific database (LSDB) for FBN1 mutations with the Universal Mutation Database (UMD) tool. To facilitate comparison of …

Fibrillin-2MESH : Polymorphism GeneticFibrillin-1DNA Mutational AnalysisMESH : Genotype[SDV.GEN] Life Sciences [q-bio]/Geneticscomputer.software_genreMESH: Genotype0302 clinical medicineGenotypeDatabases GeneticMissense mutationCongenital contractural arachnodactylyMESH: DNA Mutational AnalysisGenetics (clinical)MESH: Databases GeneticRegulation of gene expressionGenetics0303 health sciencesDatabaseMESH : Gene Expression RegulationMicrofilament ProteinsPhenotypeMESH: Gene Expression RegulationBeals-Hecht syndrome3. Good healthINCMESH : PhenotypePhenotypeMESH : MutationFibrillinmusculoskeletal diseasesMESH: MutationGenotypeMESH : Microfilament Proteinsdatabase OFFICIAL JOURNAL wwwhgvsorg & 2008 WILEY-LISSLocus (genetics)fibrillinMESH : DNA Mutational AnalysisBiologyFibrillinsMESH: PhenotypeMESH: Sequence Homology Nucleic Acidcongenital contractural arachnodactyly03 medical and health sciencesMESH: Microfilament ProteinsSequence Homology Nucleic AcidMESH: Polymorphism GeneticGeneticsmedicineHumansMESH : Sequence Homology Nucleic AcidFBN2CCAMESH : Databases GeneticGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsPolymorphism GeneticMESH: HumansMESH : Humansmedicine.diseaseGene Expression RegulationMutation[ SDV.GEN ] Life Sciences [q-bio]/Geneticscomputer030217 neurology & neurosurgery
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Non-syndromic Mitral Valve Dysplasia Mutation Changes the Force Resilience and Interaction of Human Filamin A

2018

International audience; Filamin A (FLNa), expressed in endocardial endothelia during fetal valve morphogenesis, is key in cardiac development. Missense mutations in FLNa cause non-syndromic mitral valve dysplasia (FLNA-MVD). Here, we aimed to reveal the currently unknown underlying molecular mechanism behind FLNA-MVD caused by the FLNa P637Q mutation. The solved crystal structure of the FLNa3-5 P637Q revealed that this mutation causes only minor structural changes close to mutation site. These changes were observed to significantly affect FLNa's ability to transmit cellular force and to interact with its binding partner. The performed steered molecular dynamics simulations showed that signi…

Filamins[SDV]Life Sciences [q-bio]Protein Tyrosine Phosphatase Non-Receptor Type 12Heart Valve DiseasesMutation MissenseMorphogenesisProtein tyrosine phosphataseMolecular Dynamics SimulationBiologyFilaminta3111ArticleFLNA-MVD03 medical and health sciencessteered molecular dynamics simulationsStructural Biologymechanical forcesmedicineHumansMitral valve prolapseMissense mutationFLNAmolekyylidynamiikkasydäntauditCell adhesionMolecular Biology030304 developmental biologyX-ray crystallography0303 health sciencesBinding Sites030302 biochemistry & molecular biologyta1182filamiinitprotein tyrosine phosphatase 12medicine.disease3. Good healthCell biologyFilamin AMutation (genetic algorithm)cardiovascular systemMitral Valveproteiinitmitral valve prolapseröntgenkristallografiaProtein Binding
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