Search results for "Exons"

showing 10 items of 197 documents

Two novel mutations at exon 8 of the Sequestosome 1 (SQSTM1) gene in an Italian series of patients affected by Paget's disease of bone (PDB).

2003

PDB is genetically heterogeneous. Mutations of the sequestosome1 gene have been reported in sporadic and familial forms of Paget's in patients of French Canadian and British descent. Mutational analyses in different ethnic groups are needed to accurately investigate hereditary diseases. We describe two novel mutations of sequestosome1 in 62 Italian sporadic patients, confirming the role of the encoded protein in this disorder. Introduction: Paget's disease of bone (PDB) is a relatively common disease of bone metabolism reported to affect up to 3% of whites over 55 years of age. The disorder is genetically heterogeneous, and at present, there is scientific evidence that at least eight differ…

AdultMaleEndocrinology Diabetes and MetabolismPopulationExonSequestosome 1GenotypeSequestosome-1 ProteinmedicineHumansOrthopedics and Sports MedicineeducationAdaptor Proteins Signal TransducingAgedDNA PrimersGeneticsAged 80 and overeducation.field_of_studyBase SequenceGenetic heterogeneitybusiness.industryProteinsExonsMiddle Agedmedicine.diseaseOsteitis DeformansPenetrancePaget's disease of boneHereditary DiseasesMutationFemalebusinessJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
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A novel mutation in the coagulation factor 12 gene in subjects with hereditary angioedema and normal C1-inhibitor.

2011

In hereditary angioedema with normal C1-inhibitor two different missense mutations of codon p.Thr328* in the coagulation factor 12 gene have been reported in some families. In this study a novel factor 12 gene mutation, the deletion of 72 base pairs (bp) (c.971_1018+24del72*), was identified in a family of Turkish origin, in two sisters with recurrent skin swellings and abdominal pain attacks and in their symptom-free father. This deletion caused a loss of 48 bp of exon 9 (coding amino acids 324* to 340*) in addition to 24 bp of intron 9, including the authentic donor splice site of exon 9. The large deletion of 72 bp was located in the same F12 gene region as the missense mutations p.Thr32…

AdultMaleFactor XII DeficiencyTurkeyImmunologyDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeC1-inhibitorExonImmunology and AllergyMedicineMissense mutationHumansHereditary Angioedema Type IIISequence DeletionGeneticsMutationAngioedemabiologybusiness.industryAngioedemas HereditaryExonsmedicine.diseaseMolecular biologyIntronsPedigreeHereditary angioedemaFactor XIIMutationbiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinClinical immunology (Orlando, Fla.)
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Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis.

2010

Hajdu-Cheney syndrome is a rare autosomal dominant skeletal disorder with facial anomalies, osteoporosis and acro-osteolysis. We sequenced the exomes of six unrelated individuals with this syndrome and identified heterozygous nonsense and frameshift mutations in NOTCH2 in five of them. All mutations cluster to the last coding exon of the gene, suggesting that the mutant mRNA products escape nonsense-mediated decay and that the resulting truncated NOTCH2 proteins act in a gain-of-function manner.

AdultMaleHeterozygoteHajdu–Cheney syndromeAdolescentmedia_common.quotation_subjectNonsenseMolecular Sequence DataBiologymedicine.disease_causeHajdu-Cheney SyndromeFrameshift mutationExonYoung AdultRare DiseasesSkeletal disorderGeneticsmedicineHumansAmino Acid SequenceReceptor Notch2Frameshift MutationGeneExome sequencingmedia_commonGeneticsMutationBase SequenceDNAExonsMiddle Agedmedicine.diseasePedigreeCodon NonsenseChild PreschoolMutationFemaleSignal TransductionNature genetics
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Characterization of non-expressed C4 genes in a case of complete C4 deficiency: identification of a novel point mutation leading to a premature stop …

1998

The genetic basis of complete C4 deficiency in a patient with SLE was investigated. Previous studies have demonstrated that this patient has two different major histocompatibility complex (MHC) haplotypes that each contain a major deletion and a non-expressed C4 gene. In the present study, non-expression of the C4 genes was explained by the finding of two distinct C4 gene mutations. A previously described two base pair insertion in exon 29 of the C4 gene was detected in the paternal MHC haplotype [HLA-A2, B40, SC00, DR6]. The maternal haplotype [HLA-A30, B18, F1C00, DR3] carried a C4 gene with a one base pair deletion in exon 20 generating a premature stop codon. This mutation was neither f…

AdultMaleHeterozygoteImmunologyGene mutationBiologymedicine.disease_causePolymerase Chain ReactionCell LineMajor Histocompatibility ComplexExonmedicineImmunology and AllergyHumansLupus Erythematosus SystemicPoint MutationGenePolymorphism Single-Stranded ConformationalGeneticsMutationPoint mutationHaplotypeC4AComplement C4General MedicineExonsSequence Analysis DNAMolecular biologyIsotypePedigreeHaplotypesCodon TerminatorFemalePolymorphism Restriction Fragment LengthHuman immunology
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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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Association of attentional network function with exon 5 variations of the CHRNA4 gene

2007

Mutational analyses in xenopus oocyte and mice models indicate that the positive effect of nicotine on attention may be modulated by genetic variations within exon 5 of the alpha4 subunit of the nicotinergic acetylcholine receptor gene CHRNA4. The potential relevance of exon 5 is further emphasized by two recent family-based association studies of nicotine dependence because subgroups of nicotine-dependent subjects are thought to 'self-medicate' attentional deficits with nicotine. We investigated a synonymous single nucleotide polymorphisms (SNP): rs1044396, which has recently been associated with nicotine-dependence, plus two adjacent synonymous SNPs rs1044394 and rs1044393 in exon 5 of n …

AdultMaleNicotineXenopusPosterior parietal cortexSingle-nucleotide polymorphismReceptors NicotinicBiologyModels BiologicalWhite PeopleMiceExonParietal LobeGeneticsmedicineAnimalsHumansAttentionMolecular BiologyOddball paradigmGenetics (clinical)Genetic associationGeneticsSupplementary motor areamedicine.diagnostic_testParietal lobeExonsTobacco Use DisorderGeneral MedicineMagnetic Resonance ImagingRadiographymedicine.anatomical_structureAttention Deficit Disorder with HyperactivityFemaleFunctional magnetic resonance imagingHuman Molecular Genetics
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Sporadic ALS is not associated with VAPB gene mutations in Southern Italy

2006

Abstract Mutations in the Cu/Zn superoxide dismutase (Sod1) gene have been reported to cause adult-onset autosomal dominant Amyotrophic Lateral Sclerosis (FALS). In sporadic cases (SALS) de novo mutations in the Sod1 gene have occasionally been observed. The recent finding of a mutation in the VAMP/synaptobrevin-associated membrane protein B (VAPB) gene as the cause of amyotrophic lateral sclerosis (ALS8), prompted us to investigate the entire coding region of this gene in SALS patients. One hundred twenty-five unrelated patients with adult-onset ALS and 150 healthy sex-age-matched subjects with the same genetic background were analyzed. Genetic analysis for all exons of the VAPB gene by DH…

AdultMaleSOD1Vesicular Transport ProteinsGlutamic AcidBiologyGene mutationmedicine.disease_causeGenetic analysisGeneral Biochemistry Genetics and Molecular BiologyPharmacology Toxicology and Pharmaceutics(all)03 medical and health sciencesExon0302 clinical medicineGene FrequencymedicineHumansCoding regionGeneral Pharmacology Toxicology and PharmaceuticsGeneAged030304 developmental biologyMedicine(all)Aged 80 and overGeneticsAspartic Acid0303 health sciencesMutationBase SequenceBiochemistry Genetics and Molecular Biology(all)Brief ReportAmyotrophic Lateral SclerosisGenetic VariationExonsGeneral MedicineMiddle AgedVAPBMolecular biologyIntrons3. Good healthAmino Acid SubstitutionItalyCase-Control StudiesMutationFemale030217 neurology & neurosurgeryJournal of Negative Results in BioMedicine
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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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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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Congenital goitrous primary hypothyroidism in two German families caused by novel thyroid peroxidase (TPO) gene mutations.

2013

Congenital hypothyroidism occurs with a prevalence of approximately 1:3 500. Defects in thyroid hormone synthesis which lead to goitrous hypothyroidism account for 10-15% of these cases. Several genetic defects have been characterized and mutations in the thyroid peroxidase (TPO) gene are the most common cause for dyshormonogenesis.So far, more than 80 mutations in the TPO gene have been described, resulting in a variable decrease in TPO bioactivity. Clinically TPO defects manifest with congenital primary goitrous hypothyroidism.We here present 2 children with congenital primary hypothyroidism, who were identified to have compound heterozygous TPO mutations. They both shared the same novel …

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismMutation MissenseGene mutationmedicine.disease_causeCompound heterozygosityAutoantigensIodide Peroxidasefluids and secretionsEndocrinologyThyroid dyshormonogenesisThyroid peroxidaseInternal medicineGermanyIron-Binding ProteinsInternal MedicinemedicineCongenital HypothyroidismMissense mutationHumansFamilyMutationbiologybusiness.industryGoiterPrimary hypothyroidismInfant Newbornfood and beveragesGeneral MedicineExonsmedicine.diseaseCongenital hypothyroidismEndocrinologyembryonic structuresbiology.proteinFemalebusinessExperimental and clinical endocrinologydiabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
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