Search results for "Point Mutation"

showing 10 items of 199 documents

Increased risk for venous thrombosis in carriers of the prothrombin G→A20210 gene variant

1998

A mutation in the prothrombin gene (G--A20210) has been associated with higher plasma prothrombin levels and an increased tendency for venous thrombosis.To determine whether the prothrombin A20210 allele is independently associated with the occurrence of venous thrombosis.Case-control study.Two thrombosis centers in southern Italy.281 consecutive patients with venous thrombosis confirmed by objective tests and 850 controls.Medical history was collected on standardized questionnaires. The presence of prothrombin G--A2020 and factor V Leiden mutations was determined by polymerase chain reaction. The presence of anticoagulant factors and prothrombin activity was determined by tests of function…

AdultMaleHeterozygotePathologymedicine.medical_specialtyAdolescentStatistics as TopicGastroenterologyRisk FactorsSurveys and Questionnaireshemic and lymphatic diseasesInternal medicineBlood plasmaInternal MedicinemedicineFactor V LeidenHumansPoint MutationRisk factorChildVeinAllelesAgedAged 80 and overbusiness.industryVascular diseaseFactor VGeneral MedicineMiddle AgedThrombophlebitismedicine.diseaseThrombosisPulmonary embolismVenous thrombosismedicine.anatomical_structureCase-Control StudiesChild PreschoolMutationFemaleProthrombinbusinesscirculatory and respiratory physiology
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Mutation screening for the prothrombin variant G20210A by melting point analysis with the Light Cycler system: atypical results, detection of the var…

2005

In the differential diagnosis of thrombophilic disorders genotyping of prothrombin and factor V are nowadays performed as a routine analysis. In the following we describe the unusual results of the mutation screening using melting point analysis for two patients and the consecutive detection of the mutation C20209T by sequencing the corresponding gene fragments. The molecular result is discussed with special respect to the medical history, ethnic background and clinical findings of both patients.

AdultMaleHot TemperatureDNA Mutational AnalysisClinical BiochemistryBiologyNucleic Acid DenaturationThrombophiliaPolymerase Chain Reactionlaw.inventionlawmedicineHumansPoint MutationThrombophiliaMedical historyGenotypingPolymerase chain reactionGeneticsPoint mutationBiochemistry (medical)Factor VSequence Analysis DNAHematologyGeneral Medicinemedicine.diseaseMutation (genetic algorithm)biology.proteinFemaleProthrombinDifferential diagnosisClinical and Laboratory Haematology
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Molecular basis of a new type of C1q-deficiency associated with a non-functional low molecular weight (LMW) C1q: parallels and differences to other k…

1998

Analysis of an abnormal C1q molecule of individuals of a Moroccan family by ultracentrifugation in sucrose gradients revealed a low molecular weight C1q (LMW-C1q). We investigated the molecular basis of this defect by sequencing all six exons of the three C1q genes. One point mutation in the codon for Gly at position 15 (GGT) of the B chain was found resulting in an amino acid substitution to Asp (GAT). The exchange not only leads to an interruption of the collagen-like motif Gly-X-Y, but also introduces one negatively charged residue per B chain which results in two additional charges per structural subunit (A-B, C-C, A-B). The mutation which has been identified by DNA-sequencing in the C1…

AdultMaleImmunodiffusionAdolescentSequence analysisProtein subunitchemical and pharmacologic phenomenaBiologyComplement Hemolytic Activity AssayPolymerase Chain Reactionlaw.inventionExonlawHumansLupus Erythematosus SystemicPoint MutationChildGenePolymerase chain reactionPharmacologychemistry.chemical_classificationPoint mutationComplement C1qDNAExonsMolecular biologyAmino acidMolecular WeightMoroccoBiochemistrychemistryFemaleUltracentrifugeCollagenSequence AnalysisImmunopharmacology
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Recessive multiple epiphyseal dysplasia (rMED): phenotype delineation in eighteen homozygotes for DTDST mutation R279W.

2003

Multiple epiphyseal dysplasia (MED) is a generalised skeletal dysplasia that although relatively mild is associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. In the past, the disorder was subdivided into the milder Ribbing type, usually with flattened epiphyses,1 and the more severe Fairbank type with round epiphyses,2 but many cases were not classifiable as clearly either type.3 MED can be caused by mutations in at least six separate genes: COMP ,4–7 collagen IX ( COL9A1 , COL9A2 , and COL9A3 ),8–13 matrilin 3 ( MATN3 ),15 and the sulphate transporter, DTDST ( DTDST/SLC26A2 ). We have previously repor…

AdultMalePathologymedicine.medical_specialtyAdolescentAnion Transport ProteinsGenes RecessiveBiologySLC26A2ArginineOsteochondrodysplasiasShort statureMultiple epiphyseal dysplasiaGeneticsmedicineHumansChildGenetics (clinical)GeneticsAchondrogenesisSulfatesPoint mutationHomozygoteTryptophanChromosome MappingMembrane Transport ProteinsBiological TransportMiddle Agedmedicine.diseasePhenotypeGenetic defects of metabolism [UMCN 5.1]Amino Acid SubstitutionDysplasiaSulfate TransportersMutation (genetic algorithm)MutationMutation testingbiology.proteinFemalemedicine.symptomCarrier ProteinsLetter to JMGJournal of medical genetics
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The Disease-Specific Phenotype in Cardiomyocytes Derived from Induced Pluripotent Stem Cells of Two Long QT Syndrome Type 3 Patients

2013

Long QT syndromes (LQTS) are heritable diseases characterized by prolongation of the QT interval on an electrocardiogram, which often leads to syncope and sudden cardiac death. Here we report the generation of induced pluripotent stems (iPS) cells from two patients with LQTS type 3 carrying a different point mutation in a sodium channel Nav1.5 (p.V240M and p.R535Q) and functional characterization of cardiomyocytes (CM) derived from them. The iPS cells exhibited all characteristic properties of pluripotent stem cells, maintained the disease-specific mutation and readily differentiated to CM. The duration of action potentials at 50% and 90% repolarization was longer in LQTS-3 CM as compared t…

AdultMalePluripotent Stem Cellsmedicine.medical_specialtyLong QT syndromeCellular differentiationlcsh:MedicineAction PotentialsNAV1.5 Voltage-Gated Sodium ChannelQT intervalMembrane PotentialsNAV1.5 Voltage-Gated Sodium ChannelInternal medicinemedicineRepolarizationHumansPoint MutationMyocytes CardiacInduced pluripotent stem celllcsh:ScienceCells CulturedMultidisciplinarybusiness.industryPoint mutationSodium channellcsh:RCell Differentiationmedicine.diseaseLong QT SyndromeEndocrinologylcsh:QFemalebusinessResearch ArticlePLoS ONE
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Autosomal recessive hypercholesterolemia in a Sicilian kindred harboring the 432insA mutation of the ARH gene

2003

Abstract We describe a Sicilian family presenting a recessive form of hypercholesterolemia harboring a mutation of the autosomal recessive hypercholesterolemia (ARH) gene. In two of the three sibs, a 26-year-old male and a 22-year-old female, a severe hypercholesterolemia was diagnosed with very high levels of plasma cholesterol (15.9 and 12.2 mmol/l, respectively); tendon xanthomatas and xanthelasms were present and in the male proband was documented a diffuse coronary atherosclerotic disease with a rapid and fatal progression. Both the parents had normal or slightly increased levels of plasma cholesterol. All causes of secondary hypercholesterolemia were ruled out as well as an involvemen…

AdultMaleProbandHeterozygotemedicine.medical_specialtyApolipoprotein BDNA Mutational AnalysisMolecular Sequence DataGenes RecessiveARH geneCoronary AngiographyRisk AssessmentGenetic determinismHyperlipoproteinemia Type IIInternal medicinemedicineHumansPoint MutationRNA MessengerSicilyGeneAdaptor Proteins Signal TransducingHypolipidemic AgentsGeneticsBase SequencebiologySiblingsCoronary StenosisHeterozygote advantageAutosomal recessive hypercholesterolemiaPedigreeAdaptor Proteins Vesicular TransportTreatment OutcomeEndocrinologyAutosomal Recessive HypercholesterolemiaMutationLDL receptorMutation (genetic algorithm)biology.proteinFemalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineFollow-Up StudiesAtherosclerosis
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De novo mutation in a male patient with Fabry disease: a case report

2014

Abstract Background Fabry disease is an X-linked inherited metabolic condition where the deficit of the α-galactosidase A enzyme, encoded by the GLA gene, leads to glycosphingolipid storage, mainly globotriaosylceramide. To date, more than 600 mutations have been identified in human GLA gene that are responsible for FD, including missense and nonsense mutations, small and large deletions. Such mutations are usually inherited, and cases of de novo onset occur rarely. Case presentation In this article we report an interesting case of a 44-year-old male patient suffering from a severe form of Fabry disease, with negative family history. The patient showed signs such as cornea verticillata, ang…

AdultMaleProtein Foldingα-galactosidase ADe novo mutationNonsense mutationD165H mutationGlobotriaosylceramideMutation MissenseCase ReportBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundGermline mutationmedicineMissense mutationHumansPoint MutationThrombophiliaEnzyme Replacement TherapyAmino Acid SequenceChildGLA geneConserved SequenceGerm-Line MutationMedicine(all)GeneticsMutationFabry diseaseSequence Homology Amino AcidBiochemistry Genetics and Molecular Biology(all)Point mutationGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseasePedigreeStrokechemistryAmino Acid Substitutionalpha-GalactosidaseKidney Failure ChronicFemaleSymptom AssessmentSequence AlignmentBMC Research Notes
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Gly114Asp mutation of rhodopsin in autosomal dominant retinitis pigmentosa

1995

Two autosomal dominant retinitis pigmentosa families of different origin were screened for rhodopsin mutations using the method of single strand conformation polymorphism and direct sequencing. We found a CGG-CAG substitution in codon 114 of rhodopsin in both families. This change predicted the replacement of a glycine by an aspartic acid and suggested that this change is the cause of the disease in these families.

AdultMaleRhodopsincongenital hereditary and neonatal diseases and abnormalitiesAdolescentgenetic structuresMolecular Sequence DataGlycinemedicine.disease_causeAutosomal dominant retinitis pigmentosaRetinitis pigmentosaAspartic acidmedicineHumansPoint MutationAmino Acid SequenceCodonMolecular BiologyGenes DominantGeneticsAspartic AcidMutationPolymorphism GeneticBase SequencebiologyDirect sequencingSingle-strand conformation polymorphismCell BiologyMiddle Agedmedicine.diseasePedigreeRhodopsinGlycinebiology.proteinFemalesense organsRetinitis PigmentosaMolecular and Cellular Probes
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Phenotypic variability in patients with generalised resistance to thyroid hormone.

1995

Genetic linkage of generalised resistance to thyroid hormone (GRTH) to the human thyroid receptor beta 1 gene has been identified. To date 38 different mutations in several kindreds have been documented. We report on a family with GRTH displaying an adenine for guanine substitution at nucleotide 1234 resulting in a threonine for alanine substitution at codon 317 of exon 9. This mutation has been described for different phenotypes, suggesting that the heterogeneity in GRTH may be the result of multiple genetic factors.

AdultMaleThyroid Hormone Resistance SyndromeThyroid Hormonesmedicine.medical_specialtyGenetic LinkageMolecular Sequence DataThyroid Function TestsBiologymedicine.disease_causeThyroid function testsGenetic HeterogeneityExonGenetic linkageInternal medicineGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildGeneGenetics (clinical)GeneticsMutationReceptors Thyroid HormoneBase Sequencemedicine.diagnostic_testGenetic heterogeneityPoint mutationThyroidPedigreePhenotypemedicine.anatomical_structureEndocrinologyChild PreschoolFemaleResearch ArticleJournal of Medical Genetics
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Factor V Leiden and prothrombin gene G20210A mutations in Italian patients with Behcet's disease and deep vein thrombosis

2004

OBJECTIVE: To evaluate the frequency and type of vascular lesions and to study the association of factor V gene G1691A (Leiden) and prothrombin gene G20210A polymorphisms with venous thrombosis in Italian patients with Behçet's disease (BD). METHODS: Included were 118 consecutive Italian BD patients followed over a 3-year period (1997-1999) who satisfied the International Study Group criteria for BD. The control group consisted of 132 healthy Italian blood donors. All BD patients and controls were genotyped by polymerase chain reaction and allele-specific restriction enzyme techniques for factor V Leiden and prothrombin gene G20210A polymorphisms. RESULTS: Vascular lesions were observed in …

AdultMaleVenous ThrombosisFactor V Leiden mutation Prothrombin G20210A mutationAdolescentGenotypeBehcet SyndromeFactor VMiddle AgedBehc ̧et’s disease; Deep vein thrombosis; Factor V Leiden mutation Prothrombin G20210A mutationAdolescent; Adult; Behcet Syndrome; Factor V; Female; Gene Frequency; Genotype; Humans; Italy; Male; Middle Aged; Prothrombin; Risk Factors; Venous Thrombosis; Point MutationGene FrequencyItalyDeep vein thrombosiRisk FactorsFactor V Leiden mutationHumansPoint MutationFemaleProthrombinProthrombin G20210A mutationBehcet’s disease
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