Search results for "Exons"

showing 10 items of 197 documents

Recurrent Granular Dystrophy of the Cornea

2006

Purpose: To describe a case of severe corneal granular dystrophy with clinicopathologic and molecular genetic findings. Methods: The DNAs of a 53-year-old male patient suffering from corneal granular dystrophy and nonaffected family members was analyzed by molecular genetic methods. Clinical features, and histopathologic and immunohistochemical findings from the penetrating keratoplasty specimen, are described. Results: Histopathologic and molecular genetic findings confirmed the diagnosis. A new genetic polymorphism is described. Histopathologic evidence supports the assumption of the epithelial origin of the described dystrophy. Conclusions: A severe course of corneal granular dystrophy c…

MalePathologymedicine.medical_specialtymedicine.medical_treatmentDNA Mutational AnalysisBiologyPolymerase Chain ReactionPhototherapeutic keratectomyRecurrenceTransforming Growth Factor betaCorneamedicineHumansMutational statusMolecular BiologyCorneal Dystrophies HereditaryExtracellular Matrix ProteinsPolymorphism GeneticUnusual caseDystrophyExonsMiddle AgedOphthalmologymedicine.anatomical_structureMutationImmunohistochemistrySevere courseNovel mutationKeratoplasty PenetratingCornea
researchProduct

A methodological strategy for PAH genotyping in populations with a marked molecular heterogeneity of hyperphenylalaninemia.

2001

Abstract The elucidation of the molecular basis of hyperphenylalaninemia in various world populations (PKU Consortium Database: http://www.mcgill.ca/pahdb/) has revealed a remarkable molecular heterogeneity at the locus encoding for phenylalanine hydroxylase. As a consequence, genotyping of HPA patients has prompted the establishment of an impressive number of mutation detection protocols. In spite of the large variety of methods proposed so far, no comprehensive strategy has been yet developed for the detection of PAH gene mutations. Therefore, new approaches, combining the advantages of individual methods are required, especially in populations with a high number of PAH gene mutations. In…

MalePhenylalanine hydroxylaseGenotypeDNA Mutational AnalysisLocus (genetics)Gene mutationMolecular heterogeneityPolymerase Chain ReactionHyperphenylalaninemiaPhenylketonuriasmedicineHumansMutation detectionGenetic TestingMolecular BiologyGenotypingSicilyReverse dot blotGeneticsbiologyGenetic VariationNucleic Acid HybridizationPhenylalanine HydroxylaseCell BiologyExonsmedicine.diseasePedigreeHaplotypesMutationbiology.proteinFemaleOligonucleotide ProbesMolecular and cellular probes
researchProduct

Sequence variation in couch potato and its effects on life-history traits in a northern malt fly, Drosophila montana

2011

Abstract Couch potato ( cpo ) has previously been connected to reproductive diapause in several insect species including Drosophila melanogaster , where it has been suggested to provide a link between the insulin signalling pathway and the hormonal control of diapause. In the first part of the study we sequenced nearly 3.6 kb of this gene in a northern Drosophila species ( Drosophila montana ) with a robust photoperiodically determined diapause and found several types of polymorphisms along the sequenced area. We also found variation among five Drosophila virilis group species in the length of the 5th exon of cpo and in the site of the stop codon at the end of this exon. The second part of …

MalePhysiologyAmino Acid MotifsMolecular Sequence DataPopulationDiapauseExonSpecies SpecificityAnimalsDrosophila ProteinsAmino Acid SequenceeducationGeneConserved SequenceSequence DeletionGeneticseducation.field_of_studyPolymorphism GeneticSequence Homology Amino AcidbiologyWild typeNuclear ProteinsExonsSequence Analysis DNAbiology.organism_classificationIntronsStop codonDrosophila virilisPhenotypeInsect ScienceDrosophilaFemaleDrosophila melanogasterSequence AlignmentJournal of Insect Physiology
researchProduct

TP53 in gastric cancer: mutations in the l3 loop and LSH motif DNA-binding domains of TP53 predict poor outcome.

2004

The aim of this study was to clarify whether specific p53 mutations may have biological relevance in terms of disease relapse or death in gastric carcinomas (GC). Resected specimens from a consecutive series of 62 patients with GC undergoing potentially curative surgery were prospectively studied. The mutational status of exons 5-8 of the p53 gene was investigated in 62 cases using the PCR-SSCP and sequencing. Presence of microsatellite instability (MSI) was evaluated in 56 cases by analyzing loci highly sensitive of MSI. Twenty mutations of p53 were detected in 17 of the 62 cases analyzed (27%). Ten mutations (50%) occurred in highly conserved domains. According to the p53 specific functio…

MalePhysiologyClinical BiochemistryBiologyBioinformaticsExonchemistry.chemical_compoundAge DistributionStomach NeoplasmsmedicineHumansCancer mutationsTP53Prospective StudiesProspective cohort studyGeneSurvival analysisPolymorphism Single-Stranded ConformationalAgedNeoplasm StagingCarcinomaMicrosatellite instabilityCell BiologyDNA-binding domainDNA NeoplasmExonsMiddle Agedmedicine.diseaseGenes p53PrognosisSurvival AnalysisProtein Structure TertiarychemistryItalyMutationCancer researchFemaleDNAFollow-Up StudiesMicrosatellite RepeatsJournal of cellular physiology
researchProduct

Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
researchProduct

Linking C5 deficiency to an exonic splicing enhancer mutation

2005

Abstract As an important component of the innate immune system, complement provides the initial response to prevent infections by pathogenic microorganisms. Patients with dysfunction of C5 display a propensity for severe recurrent infections. In this study, we present a patient with C5 deficiency demonstrated by immunochemical and functional analyses. Direct sequencing of all C5 exons displayed no mutation of obvious functional significance, except for an A to G transition in exon 10 predicting an exchange from lysine to arginine. This sequence alteration was present in only one allele of family members with a reduced serum C5 concentration and in both alleles of the patient with almost com…

MaleSequence analysisDNA Mutational AnalysisImmunologyExonic splicing enhancerBiologymedicine.disease_causeExonmedicineHumansImmunology and AllergyGeneFamily HealthGeneticsMutationSplice site mutationComplement C5ExonsSequence Analysis DNAC5 DeficiencyMolecular biologyAlternative SplicingPhenotypeChild PreschoolMutationRNA splicingThe Journal of Immunology
researchProduct

p53 mutations in L3-loop zinc-binding domain, DNA-ploidy, and S phase fraction are independent prognostic indicators in colorectal cancer: A prospect…

2002

p53 gene alterations are among the most common events observed in colorectal cancer,and are accompanied frequently by DNA aneuploidy and high proliferative activity. The prognostic significance of such mutations remains controversial. We prospectively evaluated the prognostic significance of p53 mutations, DNA-ploidy, and S phase fraction (SPF) in a consecutive series of 160 colorectal cancer patients (median follow-up 71 months). Tumor DNA was screened for p53 mutations by PCR/single-strand conformational polymorphism/sequencing. DNA-ploidy and SPF were assessed by DNA flow cytometry. p53 mutations were detected in 68 of 160 (42.5%) cases. In 56% (38 of 68) of these, p53 mutations were fou…

MaleSettore MED/06 - Oncologia Medicaprotein p53S PhaseBiomarkers TumorHumansProspective StudiesCodonAgedPloidiesPolymorphism GeneticDNA NeoplasmExonsDNAMiddle AgedGenes p53PrognosisSurvival AnalysisProtein Structure TertiaryItalyMultivariate AnalysisMutationFemaleCarrier ProteinsColorectal NeoplasmsFollow-Up Studies
researchProduct

Identification of a novel mutation in the alpha-galactosidase A gene in patients with Fabry disease.

2012

Abstract Objectives Mutation analysis of the alpha-galactosidase A (GLA) gene is a valuable tool for the diagnosis of affected families. In our work, we analyze about one thousand samples per year from patients suspected of having Fabry disease (FD). Design and methods We carried out high resolution melting analysis (HRM) and DNA sequencing of all the exons of the GLA gene. We also assayed the alpha-galactosidase A activity in patients' blood. Results In some members of one family, we identified a new mutation in the GLA gene, c.614delC. This is a deletion of a single nucleotide, a cytosine, in exon 4 of the gene which causes a frameshift mutation. Conclusions Patients with the c.614delC mu…

MaleSettore MED/09 - Medicina InternaClinical BiochemistryDNA Mutational AnalysisHigh Resolution MeltFrameshift mutationExonmedicineHumansFrameshift MutationGeneSequence DeletionGeneticsFamily HealthAlpha-galactosidasebiologyBase Sequencealpha-galactosidase A geneGeneral MedicineExonsmedicine.diseaseMolecular biologyFabry diseasealpha-GalactosidaseMutation (genetic algorithm)Mutation testingbiology.proteinFabry DiseaseFemalemutationClinical biochemistry
researchProduct

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
researchProduct

Molecular, genetic, and functional analysis of homozygous C8 beta-chain deficiency in two siblings.

1998

Abstract C8 deficiency is associated with an increased susceptibility to neisserial infections. We present a case of an 11 year old boy who suffered from infection with Neisseria meningitidis . Medical history of the patient and his family ( n = 5) did not indicate any previous immunodeficiency symptoms. Results from the analysis of phagocyte and lymphocyte functions were within the normal range. No hemolytic activities of the classical (CH50) and the alternative (APH50) pathways of complement were measurable, and SC5b-9 protein complexes could not be detected in the patient's plasma. Further analysis by highly sensitive ELISA and functional assays revealed a complete deficiency of C8. Upon…

MaleT-LymphocytesComplement Membrane Attack ComplexBiologyMeningitis Meningococcalmedicine.disease_causeAsymptomaticGenetic analysisComplement Hemolytic Activity AssayExonmedicineHumansMedical historyChildGeneImmunodeficiencyAllelesPharmacologyGeneticsBosnia and HerzegovinaMutationPhagocytesNeisseria meningitidisHomozygoteDNAExonsmedicine.diseaseComplement C8ImmunologyFemalemedicine.symptomImmunopharmacology
researchProduct