Search results for "mutational analysis"

showing 10 items of 245 documents

Mutational screening of the USH2A gene in Spanish USH patients reveals 23 novel pathogenic mutations

2011

Abstract Background Usher Syndrome type II (USH2) is an autosomal recessive disorder, characterized by moderate to severe hearing impairment and retinitis pigmentosa (RP). Among the three genes implicated, mutations in the USH2A gene account for 74-90% of the USH2 cases. Methods To identify the genetic cause of the disease and determine the frequency of USH2A mutations in a cohort of 88 unrelated USH Spanish patients, we carried out a mutation screening of the 72 coding exons of this gene by direct sequencing. Moreover, we performed functional minigene studies for those changes that were predicted to affect splicing. Results As a result, a total of 144 DNA sequence variants were identified.…

AdultMaleSequence VariantsAdolescentGenotypegenetic structuresUsher syndromeDNA Mutational AnalysisMutation Missenselcsh:MedicineBiologymedicine.disease_causeExonYoung AdultUSH2ARetinitis pigmentosaGenotypemedicineotorhinolaryngologic diseasesHumansGenetics(clinical)Pharmacology (medical)<it>USH2A</it>GeneAllele frequencyGenetics (clinical)GeneticsMedicine(all)MutationExtracellular Matrix ProteinsResearchlcsh:RGeneral MedicineExonsMiddle Agedmedicine.diseaseeye diseasesPhenotypeSpainMutationFemalesense organsUsher SyndromeUsher SyndromesMutationsMinigeneOrphanet Journal of Rare Diseases
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Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

2014

SASH1 (SAM and SH3 domain-containing protein 1) is a tumor suppressor gene involved in the tumorigenesis of a spectrum of solid cancers. Heterozygous SASH1 variants are known to cause autosomal-dominant dyschromatosis. Homozygosity mapping and whole-exome sequencing were performed in a consanguineous Moroccan family with two affected siblings presenting an unclassified phenotype associating an abnormal pigmentation pattern (hypo- and hyperpigmented macules of the trunk and face and areas of reticular hypo- and hyperpigmentation of the extremities), alopecia, palmoplantar keratoderma, ungueal dystrophy and recurrent spinocellular carcinoma. We identified a homozygous variant in SASH1 (c.1849…

AdultMaleSkin NeoplasmsDNA Mutational AnalysisMutation MissenseGenes RecessiveConsanguinityBiologyArticleConsanguinityKeratoderma PalmoplantarGeneticsmedicineHumansExomeGenetic Predisposition to DiseaseGenetics (clinical)Pigmentation disorderSkinFamily HealthGeneticsSiblingsTumor Suppressor ProteinsHomozygoteGenodermatosisSequence Analysis DNAFibroblastsmedicine.diseaseDisease gene identificationHyperpigmentationPedigreePalmoplantar keratodermaFemaleSkin cancermedicine.symptomSkin CarcinomaPigmentation DisordersEuropean Journal of Human Genetics
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Autosomal dominant hereditary spastic paraplegia: report of a large italian family with R581X spastin mutation

2007

We describe a large kindred with a typical pure form of autosomal dominant hereditary spastic paraplegia (ADHSP). On the basis of maximum LOD score of 1.94 at theta (max)=0 with marker D2S367, we obtained suggestive evidence for linkage of ADHSP to SPG4 locus. Denaturing high-performance liquid chromatography (DHPLC) and direct sequence analysis allowed us to identify a nonsense mutation (1741* C > T) in exon 17 of the Spastin gene. This transition, carried by all the affected family members and two apparently healthy individuals, lead to truncation of the last 36 amino acids in the C-terminus of the protein. These results confirm the existence of mutation in the SPG4 gene with a reduced pe…

AdultMaleSpastinGenotypeSequence analysisHereditary spastic paraplegiaDNA Mutational AnalysisNonsense mutationLocus (genetics)DermatologyBiologyArginineSpastinExonHereditary spastic paraplegia Spastin Neurological diseasemedicineHumansGeneAgedAdenosine TriphosphatasesFamily HealthGeneticsSpastic Paraplegia HereditaryGeneral MedicineMiddle Agedmedicine.diseaseMolecular biologyPenetrancePsychiatry and Mental healthItalyMutationFemaleNeurology (clinical)Lod ScoreNeurological Sciences
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A novel constitutional mutation affecting splicing of retinoblastoma tumor suppressor gene intron 23 causes partial loss of pRB activity.

2005

Hereditary predisposition to retinoblastoma is caused by germ line mutations in the RB1 gene. Genetic counseling of affected individuals and accurate risk prediction for their families requires identification of the disease causing mutation. Furthermore, the nature of a mutation can determine genetic penetrance, disease presentation and prognosis. We describe, and functionally characterize here, a novel mutant allele of RB1 present in the germ line of a patient with sporadic bilateral retinoblastoma. The mutation generates an operational splice acceptor site resulting in a predicted protein product with loss of 81 amino acids from its carboxy terminus. We demonstrate that the aberrantly spl…

AdultMaleTumor suppressor geneRNA SplicingRetinal NeoplasmsDNA Mutational AnalysisRetinoblastoma ProteinGeneticsmedicineMissense mutationHumansDisease-causing MutationExpressivity (genetics)Genes RetinoblastomaGenetics (clinical)GeneticsbiologyRetinoblastomaRetinoblastoma proteinRetinoblastomamedicine.diseasePenetranceeye diseasesIntronsPedigreeMutation (genetic algorithm)Mutationbiology.proteinHuman mutation
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Genotypic and phenotypic spectrum in tricho-rhino-phalangeal syndrome types I and III

2000

Tricho-rhino-phalangeal syndrome (TRPS) is characterized by craniofacial and skeletal abnormalities. Three subtypes have been described: TRPS I, caused by mutations in the TRPS1 gene on chromosome 8; TRPS II, a microdeletion syndrome affecting the TRPS1 and EXT1 genes; and TRPS III, a form with severe brachydactyly, due to short metacarpals, and severe short stature, but without exostoses. To investigate whether TRPS III is caused by TRPS1 mutations and to establish a genotype-phenotype correlation in TRPS, we performed extensive mutation analysis and evaluated the height and degree of brachydactyly in patients with TRPS I or TRPS III. We found 35 different mutations in 44 of 51 unrelated p…

AdultMaleanimal structuresAdolescentGenotypeDNA Mutational AnalysisMolecular Sequence DataLimb Deformities CongenitalBiologyOsteochondrodysplasiasPolymorphism Single NucleotideShort statureLanger–Giedion syndromeGeneticsmedicineHumansMissense mutationTricho–rhino–phalangeal syndromeGenetics(clinical)Amino Acid SequenceChildGenetics (clinical)GeneticsAnthropometryBase SequenceBrachydactylyInfantZinc FingersExonsSyndromeArticlesMiddle AgedMicrodeletion syndromemedicine.diseasePenetranceBody HeightPedigreeDNA-Binding ProteinsRadiographyPhenotypeChild PreschoolMutationTrichorhinophalangeal Syndrome Type IErythroid-Specific DNA-Binding FactorsFemalemedicine.symptomChromosomes Human Pair 8Transcription Factors
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Ten novel mutations found in Aniridia.

1998

Aniridia (AN) is a sight-threatening congenital ocular disorder characterized by iris hypoplasia, corneal pannus, foveal and optic nerve hypoplasia, cataract formation, and glaucoma. In two-thirds of the patients, AN is inherited in an autosomal dominant fashion with almost complete penetrance but variable expression. The remaining cases are sporadic. Aniridia has been shown to be associated with mutations in the PAX6 gene, located on chromosome 11p13, telomeric to the Wilms' tumor predisposition gene (WT1). This paper describes 14 mutations in the PAX6 gene in patients with AN. Among these 14 mutations, 10 have been unpublished until now. They result most probably in haploinsufficiency and…

AdultMalegenetic structuresAdolescentPAX6 Transcription FactorDNA Mutational AnalysisMolecular Sequence DataBiologyPolymerase Chain ReactionVariable ExpressionGeneticsmedicineHumansPaired Box Transcription FactorsAmino Acid SequenceChildEye ProteinsGeneAniridiaGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsHomeodomain ProteinsOptic nerve hypoplasiaInfantMiddle Agedmedicine.diseasePenetranceeye diseasesDNA-Binding ProteinsRepressor ProteinsAniridiaChild PreschoolMutationHomeoboxFemalesense organsPAX6HaploinsufficiencyTranscription FactorsHuman mutation
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Influence of CYP3A5 and ABCB1 gene polymorphisms and other factors on tacrolimus dosing in Caucasian liver and kidney transplant patients

2011

Tacrolimus is a substrate of cytochrome P4503A (CYP3A) enzymes as well as of the drug transporter ABCB1. We have investigated the possible influence of CYP3A5 and ABCB1 single nucleotide polymorphisms (SNPs) and other factors (e.g. albumin, hematocrit and steroids) on tacrolimus blood levels achieved in a population of Caucasian liver (n=51) and kidney (n=50) transplant recipients. At 1, 3 and 6 months after transplantation, tacrolimus doses (mg/kg/day) and trough blood levels (C0) were recorded and the weight-adjusted tacrolimus dosage (mg/kg/day) was calculated. Polymerase chain reaction followed by restriction fragment length polymorphism analysis was used for genotyping CYP3A5*1 and *3 …

AdultMalemedicine.medical_specialtyATP Binding Cassette Transporter Subfamily BGenotypemedicine.medical_treatmentDNA Mutational AnalysisPopulationSingle-nucleotide polymorphismLiver transplantationBiologyKidneyPolymorphism Single NucleotideGastroenterologyBiomarkers PharmacologicalTacrolimusWhite PeopleGene FrequencyInternal medicineGeneticsmedicineCytochrome P-450 CYP3AHumansDrug Dosage CalculationsATP Binding Cassette Transporter Subfamily B Member 1educationAllele frequencyAllelesKidney transplantationAgededucation.field_of_studyKidney metabolismGeneral MedicineMiddle Agedmedicine.diseaseKidney TransplantationTacrolimusLiver TransplantationTransplantationsurgical procedures operativeItalyLiverImmunologySettore BIO/14 - FarmacologiaPharmacogenetics CYP3A5 ABCB1 TacrolimusTransplant patientsFemaleImmunosuppressive AgentsPolymorphism Restriction Fragment LengthInternational Journal of Molecular Medicine
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Gender specific associations of the Trp64Arg mutation in the beta3-adrenergic receptor gene with obesity-related phenotypes in a Mediterranean popula…

2001

Abstract. Corella D, Guillen M, Portoles O, Sorli JV, Alonso V, Folch J, Saiz C (School of Medicine, University of Valencia, Valencia, Spain). Gender specific associations of the Trp64Arg mutation in the β3-adrenergic receptor gene with obesity-related phenotypes in a Mediterranean population: interaction with a common lipoprotein lipase gene variation. J Intern Med 2001; 250: 348–360. Objective. To investigate the association between the Trp64Arg β3-adrenergic receptor (ADRB3) mutation and obesity-related phenotypes in a Mediterranean Spanish population considering the effect of other genetic and environmental factors. Design and subject. Cross-sectional study in 1063 (476 men and 587 wome…

AdultMalemedicine.medical_specialtyAdolescentDNA Mutational AnalysisPopulationBiologyArginineGenetic determinismBody Mass IndexSex FactorsPolymorphism (computer science)Internal medicineGenotypeInternal MedicinemedicineHumansGenetic Predisposition to DiseaseObesityAlleleeducationAllelesAgedLipoprotein lipaseeducation.field_of_studyGenetic Carrier ScreeningBody WeightTryptophanGenetic VariationMiddle Agedmedicine.diseaseObesityLipoprotein LipasePhenotypeEndocrinologySpainReceptors Adrenergic beta-3FemaleBody mass indexJournal of Internal Medicine
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Analysis of the gastrin-releasing peptide receptor gene in Italian patients with autism spectrum disorders

2008

The gastrin-releasing peptide receptor (GRPR) was implicated for the first time in the pathogenesis of Autism spectrum disorders (ASD) by Ishikawa-Brush et al. [Ishikawa-Brush et al. (1997): Hum Mol Genet 6: 1241-1250]. Since this original observation, only one association study [Marui et al. (2004): Brain Dev 26: 5-7] has further investigated, though unsuccessfully, the involvement of the GRPR gene in ASD. With the aim of contributing further information to this topic we have sequenced the entire coding region and the intron/exon junctions of the GRPR gene in 149 Italian autistic patients. The results of this study led to the identification of four novel point mutations, two of which, that…

AdultMalemedicine.medical_specialtyBALB 3T3 CellsAdolescentDNA Mutational AnalysisPopulationRett syndromeBiologyMiceCellular and Molecular NeuroscienceExonSettore BIO/13 - Biologia ApplicataInternal medicineGastrin-releasing peptideChlorocebus aethiopsmedicineGastrin-releasing peptide receptorAnimalsHumansPoint MutationAutistic DisorderChildautism gastrin-releasing peptide receptor signal transductionG-protein-coupled receptor association studyeducationGeneGenetics (clinical)AgedGeneticseducation.field_of_studyPoint mutationMiddle Agedmedicine.diseasePedigreeReceptors BombesinDevelopmental disorderPsychiatry and Mental healthEndocrinologyItalyCase-Control StudiesCOS CellsFemaleAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Franceschetti Hereditary Recurrent Corneal Erosion

2011

To describe new affected individuals of Franceschetti's original pedigree of hereditary recurrent erosion and to classify a unique entity called Franceschetti corneal dystrophy.Observational case series.Slit-lamp examination of 10 affected individuals was conducted. Biomicroscopic examinations were supplemented by peripheral corneal biopsy in 1 affected patient with corneal haze. Tissue was processed for light and electron microscopy and immunohistochemistry was performed. DNA analysis was carried out in 12 affected and 3 nonaffected family members.All affected individuals suffered from severe ocular pain in the first decade of life, attributable to recurrent corneal erosions. Six adult pat…

AdultMalemedicine.medical_specialtyBiopsyDNA Mutational AnalysisDermatan SulfateCorneal dystrophyCorneal OpacityCorneal erosionAntigens NeoplasmRecurrenceTransforming Growth Factor betaOphthalmologymedicineEye PainHumansChildAgedAged 80 and overCorneal Dystrophies HereditaryExtracellular Matrix Proteinsbusiness.industryCadherinsmedicine.diseaseImmunohistochemistryPedigreeRecurrent corneal erosionOphthalmologyClaudinsFemaleDecorinbusinessCell Adhesion MoleculesChondroitinBiomarkersAmerican Journal of Ophthalmology
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