Search results for "missense"

showing 10 items of 303 documents

Two distinct phenotypes, hemiplegic migraine and episodic Ataxia type 2, caused by a novel common CACNA1A variant

2020

Abstract Background To investigate the genetic and environmental factors responsible for phenotype variability in a family carrying a novel CACNA1A missense mutation. Mutations in the CACNA1A gene were identified as responsible for at least three autosomal dominant disorders: FHM1 (Familial Hemiplegic Migraine), EA2 (Episodic Ataxia type 2), and SCA6 (Spinocerebellar Ataxia type 6). Overlapping clinical features within individuals of some families sharing the same CACNA1A mutation are not infrequent. Conversely, reports with distinct phenotypes within the same family associated with a common CACNA1A mutation are very rare. Case presentation A clinical, molecular, neuroradiological, neuropsy…

MaleProbandmedicine.medical_specialtyNeurologyMigraine with AuraFamilial hemiplegic migraine type 1Mutation MissenseneuropsychologyCase Reportmedicine.disease_causeNystagmus Pathologiclcsh:RC346-42903 medical and health sciences0302 clinical medicinemedicineHumansSpinocerebellar ataxia type 6Missense mutationFamilyChildFamilial hemiplegic migrainelcsh:Neurology. Diseases of the nervous system030304 developmental biologyEpisodic ataxiaGenetics0303 health sciencesMutationbusiness.industryCACNA1A geneEpisodic ataxia type2Cognitive affective syndromeGeneral Medicinemedicine.diseasePhenotypePhenotypeAtaxiaCalcium ChannelsNeurology (clinical)businessCognitive affective syndrome neuropsychology.030217 neurology & neurosurgeryBMC Neurology
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Natural and engineered carboxy-terminal variants: decreased secretion and gain-of-function result in asymptomatic coagulation factor VII deficiency.

2012

We report 2 asymptomatic homozygotes for the nonsense p.R462X mutation affecting the carboxy-terminus of coagulation factor VII (FVII, 466 aminoacids). FVII levels of 3-5% and 2.7 ± 0.4% were found in prothrombin time-based and activated factor X (FXa) generation assays with human thromboplastins. Noticeably, FVII antigen levels were barely detectable (0.7 ± 0.2%) which suggested a gain-of-function effect. This effect was more pronounced with bovine thromboplastin (4.8 ± 0.9%) and disappeared with rabbit thromboplastin (0.7 ± 0.2%). This suggests that the mutation influences tissue factor/FVII interactions. Whereas the recombinant rFVII-462X variant confirmed an increase in specific activit…

MaleProteasesHeterozygoteFactor VII DeficiencyEnzyme-Linked Immunosorbent AssayFVIIBiologymedicine.disease_causeThromboplastinTissue factorchemistry.chemical_compoundCarboxy-terminalhemic and lymphatic diseasesmedicineFACTOR VII DEFICIENCY MOLECULAR VARIANTSThromboplastinMissense mutationAnimalsHumanscardiovascular diseasesChildBlood CoagulationProthrombin timeMutationmedicine.diagnostic_testFactor VIIHomozygoteHematologyFactor VIIMiddle AgedMolecular biologyAsymptomatic; Carboxy-terminal; FVII; Mutation;AsymptomaticchemistryCoagulationCodon NonsenseMutationMutagenesis Site-DirectedProthrombin TimeCattleFemaleRabbitsOriginal Articles and Brief Reports
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New Hyperekplexia Mutations Provide Insight into Glycine Receptor Assembly, Trafficking, and Activation Mechanisms*

2013

Hyperekplexia is a syndrome of readily provoked startle responses, alongside episodic and generalized hypertonia, that presents within the first month of life. Inhibitory glycine receptors are pentameric ligand-gated ion channels with a definitive and clinically well stratified linkage to hyperekplexia. Most hyperekplexia cases are caused by mutations in the α1 subunit of the human glycine receptor (hGlyR) gene (GLRA1). Here we analyzed 68 new unrelated hyperekplexia probands for GLRA1 mutations and identified 19 mutations, of which 9 were novel. Electrophysiological analysis demonstrated that the dominant mutations p.Q226E, p.V280M, and p.R414H induced spontaneous channel activity, indicat…

MaleProtein subunitMutation MissenseBiologyBiochemistryProtein Structure SecondaryReceptors GlycinemedicineHumansHyperekplexiaReceptorMolecular BiologyGlycine receptorIon channelGeneticsWild typeMolecular Bases of DiseaseCell BiologyMuscle RigidityProtein Structure TertiaryAmino Acid SubstitutionGene Expression RegulationFemalemedicine.symptomIon channel linked receptorsCys-loop receptors
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Prevalence of ANGPTL3 and APOB gene mutations in subjects with combined hypolipidemia.

2012

Objective— Mutations of the ANGPTL3 gene have been associated with a novel form of primary hypobetalipoproteinemia, the combined hypolipidemia (cHLP), characterized by low total cholesterol and low HDL-cholesterol levels. The aim of this work is to define the role of ANGPTL3 gene as determinant of the combined hypolipidemia phenotype in 2 large cohorts of 913 among American and Italian subjects with primary hypobetalipoproteinemia (total cholesterol <5th percentile). Methods and Results— The combined hypolipidemia cut-offs were chosen according to total cholesterol and HDL-cholesterol levels reported in the ANGPTL3 kindred described to date: total cholesterol levels, <2nd percentile …

MaleSettore MED/09 - Medicina InternaApolipoprotein BGene mutationCompound heterozygositymedicine.disease_causeSeverity of Illness IndexHypobetalipoproteinemiaschemistry.chemical_compoundGene Frequency80 and overPrevalenceMissense mutationgeneticsepidemiology; genetics; hypobetalipoproteinemia; lipoproteins; Adolescent; Adult; Aged; Aged 80 and over; Amino Acid Sequence; Angiopoietins; Apolipoproteins B; Biomarkers; Cholesterol; Cholesterol HDL; Female; Gene Frequency; Genetic Predisposition to Disease; Heterozygote; Homozygote; Humans; Hypobetalipoproteinemias; Italy; Male; Middle Aged; Missouri; Molecular Sequence Data; Phenotype; Prevalence; Severity of Illness Index; Young Adult; Codon Nonsense; Mutation Missense; Cardiology and Cardiovascular MedicineAged 80 and overMutationHomozygotehypobetalipoproteinemiaMiddle AgedCholesterolPhenotypeItalyCodon NonsenseepidemiologyFemaleCardiology and Cardiovascular MedicineHumanAdultmedicine.medical_specialtyHeterozygoteHDLAdolescentMolecular Sequence DataMutation MissenseSocio-culturaleAngiopoietinepidemiology; lipoproteins; genetics; hypobetalipoproteinemiaBiologyYoung AdultInternal medicinemedicineHumansGenetic Predisposition to DiseaseAmino Acid SequenceCodonAllele frequencyAgedAngiopoietin-Like Protein 3Apolipoproteins BMissouriCholesterolCholesterol HDLmedicine.diseaselipoproteinsEndocrinologyAngiopoietin-like ProteinsNonsensechemistryBiological MarkerMutationbiology.proteinHypobetalipoproteinemiaMissenseAngiopoietinsBiomarkersArteriosclerosis, thrombosis, and vascular biology
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A new mutation in EDA gene in X-linked hypohidrotic ectodermal dysplasia associated with keratoconus

2012

Hypohidrotic ectodermal dysplasia (HED) was first described in 1848 by Thurnam. HED belongs to ectodermal dysplasias (EDs), which are developmental impairments of ectodermal-derived tissues. X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of the EDs and consists in abnormal development of teeth, hair, and eccrine sweat glands. XLHED is determined by mutations in the ED1 gene, which is responsible for the coding of ectodysplasin-A(EDA-A), a protein that regulates ectodermal appendage formation. In the present study we found both in our proband and in the mother the same missense mutation in exon 9 (c.957 CA), which resulted in an aminoacid change at position 319 (S…

MaleSettore MED/38 - Pediatria Generale E SpecialisticaEctodermal Dysplasia 1 AnhidroticMutationHumansInfantEctodysplasinsKeratoconusEctodermal dysplasia –mutation missense keratoconus
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Mutation analysis of the SPG4 gene in Italian patients with pure and complicated forms of spastic paraplegia

2010

Mutations in the SPG4 gene are the most common causes of hereditary spastic paraplegia (HSP) accounting for up to 40% of autosomal dominant (AD) forms and 12-18% of sporadic cases. The phenotype associated with HSP due to mutations in the SPG4 gene tends to be pure. There is increasing evidence, however, of patients with complicated forms of spastic paraplegia in which SPG4 mutations were identified. A cohort of 38 unrelated Italian patients with spastic paraplegia, of which 24 had a clear dominant inheritance and 14 were apparently sporadic, were screened for mutations in the SPG4 gene.We identified 11 different mutations, six of which were novel (p.Glu143GlyfsX8, p.Tyr415X, p.Asp548Asn, c…

MaleSpastinDNA Mutational AnalysisHereditary spastic paraplegiaEXON DELETIONSGene mutationmedicine.disease_causeSpastinFAMILIESCohort StudiesExonGenotypeSpasticMutation frequencyChild3' Untranslated RegionsChromatography High Pressure LiquidAdenosine TriphosphatasesGeneticsMutationHereditary spastic paraplegia SPG4Reverse Transcriptase Polymerase Chain ReactionMutation analysiExonsMiddle AgedMLPAPhenotypeMutation analysisItalyNeurologySettore MED/26 - NeurologiaFemaleAdultAdolescentGenotypeHereditary spastic paraplegia3 ' UTR3′ UTRMutation MissenseFREQUENTSPG4CLASSIFICATIONYoung AdultmedicineHumansAgedParaplegiaSPECTRUMbusiness.industrymedicine.diseaseNeurology (clinical)businessCOLLECTIONEXPRESSION ANALYSISGene Deletion
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Mutations in the PDS Gene in German Families with Pendred’s Syndrome: V138F Is a Founder Mutation

2003

Pendred's syndrome, an autosomal-recessive condition characterized by congenital sensorineural hearing loss and goiter, is caused by mutations in the PDS gene. Located on chromosome 7q22-q31, it encodes a chloride-iodide transporter expressed in the thyroid, inner ear, and kidney. We investigated the PDS gene of six affected individuals from four unrelated families with Pendred's syndrome by direct sequencing. PDS mutations were identified in homozygous or compound heterozygous state in all six cases. A homozygous missense mutation leading to the amino acid substitution S133T was detected in a family of Turkish origin. The mutations found in the other affected individuals, who originate fro…

MaleThreoninemedicine.medical_specialtyAdolescentTurkeyHearing Loss SensorineuralEndocrinology Diabetes and MetabolismClinical BiochemistryMutation MissenseBiologyCompound heterozygositymedicine.disease_causeBiochemistryGenetic determinismEndocrinologyHypothyroidismGermanyInternal medicineSerinemedicineHumansMissense mutationAlleleChildPendred syndromeGeneticsMutationBase SequenceBiochemistry (medical)HaplotypeInfant NewbornMembrane Transport Proteinsfood and beveragesSyndromemedicine.diseaseFounder EffectPedigreeEndocrinologyAmino Acid SubstitutionHaplotypesSulfate TransportersChild PreschoolMicrosatelliteFemaleCarrier ProteinsThe Journal of Clinical Endocrinology & Metabolism
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Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III

2006

International audience; Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema. Three forms of HAE have been described. The classic forms, HAE types I and II, occur as a consequence of mutations in the C1-inhibitor gene. In contrast to HAE types I and II, HAE type III has been observed exclusively in women, where it appears to be correlated with conditions of high estrogen levels--for example, pregnancy or the use of oral contraceptives. A recent report proposed two missense mutations (c.1032C-->A and c.1032C-->G) in F12, the gene encoding human coagulation factor XII (FXII, or Hageman factor…

MaleTime FactorsKinins030204 cardiovascular system & hematologyMESH: Founder Effect[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityLinkage Disequilibrium0302 clinical medicineMissense mutationHereditary Angioedema Type IIIGenetics(clinical)MESH: Models GeneticGenetics (clinical)MESH: Heterozygote0303 health sciencesFactor XII[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyFounder EffectMarkov ChainsPedigree3. Good healthMESH: Linkage DisequilibriumFactor XIIHereditary angioedemaFemalemedicine.symptomMESH: Factor XIIHeterozygotemedicine.medical_specialtyMESH: MutationMESH: PedigreeMESH: Bayes TheoremCoagulation Factor XIIBiology03 medical and health sciencesMESH: Markov ChainsReportInternal medicinemedicineGeneticsHumansMESH: AngioedemaAngioedema030304 developmental biologyMESH: HumansModels GeneticAngioedemaHaplotypeMESH: Time FactorsBayes TheoremHeterozygote advantageMESH: Haplotypesmedicine.diseaseMESH: KininsMESH: MaleEndocrinologyHaplotypesMutationImmunologyMESH: Microsatellite RepeatsMESH: FemaleMicrosatellite RepeatsThe American Journal of Human Genetics
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Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
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Novel missense mutation in the ATP1A2 gene associated with atypical sporapedic hemiplegic migraine

2019

Hemiplegic migraine (HM) is a rare subtype of migraine with aura in which attacks include transient motor weakness or hemiparesis that can last several days. HM is linked to mutations in three different genes, CACNA1A, ATP1A2 and SCN1A, which encode for ion transporters. The clinical spectrum includes atypical symptoms such as impaired consciousness, epileptic seizures, permanent cerebellar ataxia or mental retardation. We describe a novel mutation found in the ATP1A2 gene in a patient with late-onset HM. His attacks were characterised by motor weakness associated with altered mental status, diplopia and ataxia. He also showed up MRI abnormalities and incomplete response to prophylactic the…

MaleWeaknessPediatricsmedicine.medical_specialtyAtaxiaNeurologyMigraine with AuraMutation MissenseNeuroimagingneuro geneticsDiagnosis Differential03 medical and health sciences0302 clinical medicineRare DiseaseATP1A2medicineHumansMissense mutationgenetic screening / counselling030212 general & internal medicineMigraineAgedNeurologic ExaminationGenetic counsellingCerebellar ataxiabusiness.industryHeadacheGeneral MedicineMagnetic Resonance ImagingMigraine with auraPedigreeHemiparesisNeurologySettore MED/26 - NeurologiaSodium-Potassium-Exchanging ATPasemedicine.symptombusinessheadache (including migraines)030217 neurology & neurosurgery
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