Search results for "MUTATION"

showing 10 items of 2830 documents

Multiple identification of a particular type of hereditary C1q deficiency in the Turkish population: review of the cases and additional genetic and f…

1997

Complete selective deficiencies of the complement component C1q are rare genetic disorders that are associated with recurrent infections and a high prevalence of lupus erythematosus-like symptoms. All C1q deficiencies studied at the genetic level revealed single-base mutations leading to termination codons, frameshifts or amino acid exchanges and these were thought to be responsible for the defects as no other aberrations were found. One particular mutation, leading to a stop codon in the C1qA gene, was first identified in members of a Gypsy family from the Slovak Republic. The same mutation has been found in all cases of C1q deficiency from Turkey that have been investigated. Here we prese…

MaleHeterozygoteSlovakiaTurkish populationRomaTurkeyGenetic counselingMolecular Sequence DataPopulationBiologyPolymerase Chain ReactionGenetic analysisGeneticsHumansPoint MutationAmino Acid SequenceeducationGeneGenetics (clinical)Geneticseducation.field_of_studyBase SequenceComplement C1qImmunologic Deficiency SyndromesHuman geneticsStop codonPedigreeChild PreschoolMutation (genetic algorithm)Codon TerminatorFemalePolymorphism Restriction Fragment LengthHuman Genetics
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Compound heterozygosity in the SPG4 gene causes hereditary spastic paraplegia

2008

The SPG4 gene is frequently mutated in autosomal dominant form of hereditary spastic paraplegia (HSP). We report that the compound heterozygous sequence variants S44L, a known polymorphism, and c.1687G>A, a novel mutation in SPG4 cause a severe form of HSP in a patient. The family members carrying solely c.1687G>A mutation are asymptomatic for HSP. The reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed that the c.1687G>A mutation is a splice site mutation and causes skipping of the exon 15 of spastin. Furthermore, quantification of RT-PCR products by sequencing and quantification of allele-specific expression by pyrosequencing assay revealed that c.1687G>A is a leaky…

MaleHeterozygoteSpastinHereditary spastic paraplegiaDNA Mutational AnalysisMolecular Sequence DataMutantIntracellular SpaceBiologyCompound heterozygositySpastinPolymorphism Single NucleotideWhite PeopleLoss of heterozygosity03 medical and health sciencesExon0302 clinical medicineGermanyGeneticsmedicineHumansRNA MessengerAllelesGenetics (clinical)030304 developmental biologyAdenosine TriphosphatasesRegulation of gene expressionGenetics0303 health sciencesSplice site mutationBase SequenceSpastic Paraplegia HereditaryComputational BiologyExonsmedicine.diseasePedigreeProtein TransportAmino Acid SubstitutionGene Expression RegulationMutationFemaleRNA Splice Sites030217 neurology & neurosurgeryHeLa CellsClinical Genetics
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Association between the HFE mutations and unsuccessful ageing: a study in Alzheimer's disease patients from Northern Italy

2003

Mutations in the class I-like Major Histocompatibility Complex gene HFE are associated with hereditary hemochromatosis (HH), a disorder caused by excessive iron uptake. Three common mutations have been found: C282Y, H63D, and S65C. Moreover, several studies have suggested that HFE mutations may be involved in several age-related chronic diseases such as Alzheimer's disease (AD) and coronary heart disease, but apparently paradoxically also with longevity. In particular, in AD, patients carrying the H63D allele have been suggested to have a mean age at onset of 72 vs. 77 years for those who were homozygous for the wild-type allele. Thus, it seems that H63D mutations may anticipate sporadic AD…

MaleHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAgingDiseasemedicine.disease_causeDegenerative diseaseGene FrequencyAlzheimer DiseaseGenotypeHumansPoint MutationMedicineAlleleHemochromatosis ProteinHemochromatosisAgedGeneticsMutationbusiness.industryHistocompatibility Antigens Class IHomozygoteMembrane Proteinsnutritional and metabolic diseasesMiddle Agedmedicine.diseaseItalyHereditary hemochromatosisFemaleAlzheimer's diseasebusinessDevelopmental BiologyMechanisms of Ageing and Development
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A Single Copy of the Recently Identified Dual Oxidase Maturation Factor (DUOXA) 1 Gene Produces Only Mild Transient Hypothyroidism in a Patient with …

2011

Dual oxidases (DUOX1 and DUOX2) play a crucial role in the generation of hydrogen peroxide required in the oxidation of iodide and the synthesis of thyroid hormone. Heterodimerization with specific maturation factors (DUOXA1 and DUOXA2) is essential for the maturation and function of the DUOX enzyme complexes. Biallelic loss-of-function mutations of DUOX2 result in congenital hypothyroidism (CH), whereas a single reported case of homozygous DUOXA2 mutation (Y246X) has been associated with mild CH.We now report an infant with transient CH due to a complex genetic alteration of the DUOX/DUOXA system.Our patient was born to euthyroid nonconsanguineous parents and presented with an elevated TSH…

MaleHeterozygoteendocrine system diseasesEndocrinology Diabetes and MetabolismBlotting WesternGenetic VectorsClinical BiochemistryGene DosageMutation MissenseThyrotropinBiologyTransfectionmedicine.disease_causePolymorphism Single NucleotideBiochemistryGene dosageEndocrinologyHypothyroidismPolymorphism (computer science)medicineHumansMissense mutationAlleleGeneAllelesCells CulturedOligonucleotide Array Sequence AnalysisGeneticsMutationfungiBiochemistry (medical)Infant NewbornMembrane ProteinsNADPH OxidasesNucleic Acid Hybridizationfood and beveragesHeterozygote advantageJCEM Online: Brief ReportsDNADual OxidasesMolecular biologyMembrane proteinGene DeletionThe Journal of Clinical Endocrinology & Metabolism
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Goitrous Congenital Hypothyroidism and Hearing Impairment Associated with Mutations in the TPO and SLC26A4/PDS Genes

2006

Abstract Context: Pendred syndrome (PS) and thyroid peroxidase (TPO) deficiency are autosomal-recessive disorders that result in thyroid dyshormonogenesis. They share congenital hypothyroidism, goiter, and an iodide organification defect as common features. Whereas the hallmark of PS is sensorineural deafness, other forms of congenital hypothyroidism may also lead to hearing impairment. Therefore, a definite diagnosis may be difficult and require molecular genetic analyses. Case Report: The propositus presented at birth with primary hypothyroidism and goiter. He also had congenital bilateral moderate hearing loss, and PS was suspected. Methods: We sequenced the SLC26A4/PDS and TPO genes in …

MaleHeterozygoteendocrine systemmedicine.medical_specialtyGenotypeHearing lossEndocrinology Diabetes and MetabolismClinical BiochemistryMutation MissenseTransfectionIodide PeroxidaseBiochemistryEndocrinologyThyroid dyshormonogenesisThyroid peroxidaseInternal medicineCongenital Hypothyroidismotorhinolaryngologic diseasesHumansMedicineMissense mutationHearing LossPendred syndromebiologyGoiterbusiness.industryBiochemistry (medical)Infant NewbornPrimary hypothyroidismMembrane Transport ProteinsPendrinmedicine.diseasePedigreeCongenital hypothyroidismEndocrinologySulfate Transportersbiology.proteinmedicine.symptombusinessThe Journal of Clinical Endocrinology & Metabolism
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Novel slow-skeletal myosin (MYH7) mutation in the original myosin storage myopathy kindred

2006

Abstract Myosin storage myopathy (OMIM 608358), a congenital myopathy characterised by subsarcolemmal, hyaline-like accumulations of myosin in Type I muscle fibres, was first described by Cancilla and Colleagues in 1971 [Neurology 1971;21:579–585] in two siblings as ‘familial myopathy with probable lysis of myofibrils in type I muscle fibres'. Two mutations in the slow skeletal myosin heavy chain gene ( MYH7 ) have recently been associated with the disease in other families. We have identified a novel heterozygous Leu1793Pro mutation in MYH7 in DNA from paraffin sections of one of the original siblings. This historical molecular analysis confirms the original cases had myosin storage myopat…

MaleHeterozygotemacromolecular substancesMyosinsBiologymedicine.disease_causeMuscular DiseasesMyofibrilsMyosinmedicineHumansMyopathyGeneGenetics (clinical)GeneticsMutationMyosin Heavy ChainsMyosin storage myopathyDNAExonsmedicine.diseaseMolecular biologyCongenital myopathyMuscle Fibers Slow-TwitchNeurologyChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleMYH7Neurology (clinical)medicine.symptomMyofibrilCardiac MyosinsNeuromuscular Disorders
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Delineation of a new chromosome 20q11.2 duplication syndrome including the ASXL1 gene.

2013

We report on three males with de novo overlapping 7.5, 9.8, and 10 Mb duplication of chromosome 20q11.2. Together with another patient previously published in the literature with overlapping 20q11 microduplication, we show that such patients display common clinical features including metopic ridging/trigonocephaly, developmental delay, epicanthal folds, and short hands. The duplication comprised the ASXL1 gene, in which de novo heterozygous nonsense or truncating mutations have recently been reported in patients with Borhing-Opitz syndrome. Because of craniofacial features in common with Borhing-Opitz syndrome, in particular metopic ridging/trigonocephaly, we suggest that duplication of ASX…

MaleHeterozygotemedia_common.quotation_subjectDevelopmental DisabilitiesNonsenseChromosomes Human Pair 20TrigonocephalyTrisomyBiologymedicine.disease_causeCraniosynostosesPregnancyIntellectual DisabilityGene duplicationGeneticsmedicineHumansCraniofacialChildGenetics (clinical)media_commonGeneticsMutationMosaicismChromosomeInfantHeterozygote advantageSyndromemedicine.diseasePhenotypeRepressor ProteinsChild PreschoolMutationFemaleHand Deformities CongenitalAmerican journal of medical genetics. Part A
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H-ficolin (ficolin-3) concentrations and FCN3 gene polymorphism in neonates

2011

Serum H-ficolin (ficolin-3) concentrations (n=613) and FCN3 genotypes (n=529) from a large group of neonates are presented. Both pre-term deliveries and low birthweight (independently of gestational age) were significantly associated with low H-ficolin concentrations but not with heterozygosity for the FCN3 1637delC frameshift mutation. The presence of the variant allele, however, apparently influenced the protein level. No association of FCN3 gene heterozygosity or relative functional H-ficolin insufficiency (determined as serum level ≤8.6 μg/ml) with perinatal infections was found. One premature newborn, with confirmed infection caused by Streptococcus agalactiae, was H-ficolin-deficient …

MaleHeterozygotemedicine.medical_specialtyGenotypeImmunologyGestational AgeBiologymedicine.disease_causeMannose-Binding LectinStreptococcus agalactiaeFrameshift mutationLoss of heterozygosityPolymorphism (computer science)LectinsStreptococcal InfectionsInternal medicineGenotypemedicineHumansImmunology and AllergyFrameshift MutationAllelesGlycoproteinsMannan-binding lectinPolymorphism GeneticHomozygoteInfant NewbornHematologyInfant Low Birth WeightEndocrinologyStreptococcus agalactiaeMannose-Binding Protein-Associated Serine ProteasesImmunologyPremature BirthFemaleGene polymorphismFicolinImmunobiology
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Regional distribution of the leucine-rich glioma inactivated (LGI) gene family transcripts in the adult mouse brain

2009

25 p., figuras y bibliografía

MaleHippocampusSubstantia nigraNerve Tissue ProteinsHippocampal formationGene mutationBiologyReticular formationMiceC57BL/6J micemedicineGene familyAnimalsMolecular BiologyThalamic reticular nucleusBrain MappingGeneral NeuroscienceDentate gyrusIntracellular Signaling Peptides and ProteinsBrainProteinsMice Inbred C57BLmedicine.anatomical_structureLGI2LGI1Neurology (clinical)LGI4LGI3NeuroscienceIn situ hybridizationDevelopmental Biology
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Prothrombotic gene variants as risk factors of acute myocardial infarction in young women

2012

Abstract Background Acute myocardial infarction (AMI) in young women represent an extreme phenotype associated with a higher mortality compared with similarly aged men. Prothrombotic gene variants could play a role as risk factors for AMI at young age. Methods We studied Factor V Leiden, FII G20210A, MTHFR C677T and beta-fibrinogen -455G>A variants by real-time PCR in 955 young AMI (362 females) and in 698 AMI (245 females) patients. The data were compared to those obtained in 909 unrelated subjects (458 females) from the general population of the same geographical area (southern Italy). Results In young AMI females, the allelic frequency of either FV Leiden and of FII G20210A was signif…

MaleHomocysteineMyocardial Infarctionlcsh:Medicinegene variantsprothrombotic gene variantsAMIchemistry.chemical_compoundGene FrequencyRisk FactorsgenderMyocardial infarctionMedicine(all)GeneticsYoung AMI Gender AMI Gene variants Mutations Prothrombotic variants Genetic predispositioneducation.field_of_studyprothrombotic variantsbiologyHomozygoteFactor VGeneral MedicineFemaleProthrombinyoung AMIAdultmedicine.medical_specialtyPopulationyoung AMI gender AMI gene variants mutations prothrombotic variants genetic predisposition.Polymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyInternal medicinemedicineFactor V LeidenGenetic predispositionHumansGenetic Predisposition to Diseasecardiovascular diseaseseducationAllele frequencyAgedBiochemistry Genetics and Molecular Biology(all)business.industryResearchlcsh:RFactor VThrombosismutationsmedicine.diseasechemistryMethylenetetrahydrofolate reductasebiology.proteinbusinessgenetic predispositionJournal of Translational Medicine
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