Search results for "Exon"

showing 10 items of 437 documents

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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Patients’ experiences of continued treatment with extended-release naltrexone: a Norwegian qualitative study

2022

Abstract Background The opioid antagonist extended-release naltrexone (XR-NTX) in the treatment of opioid use disorder (OUD) is effective in terms of safety, abstinence from opioid use and retention in treatment. However, it is unclear how patients experience and adjust to losing the possibility of achieving an opioid effect. This qualitative study is the first to explore how people with opioid dependence experience XR-NTX treatment, focusing on the process of treatment over time. Methods Using a purposive sampling strategy, semi-structured interviews were undertaken with 19 persons with opioid use disorder (15 men, four women, 22–55 years of age) participating in a clinical trial of XR-NTX…

AdultMaleNarcotic AntagonistsGeneral MedicineMiddle AgedOpioid-Related DisordersInjections IntramuscularNaltrexoneAnalgesics OpioidYoung AdultVDP::Medisinske Fag: 700::Helsefag: 800Delayed-Action PreparationsHumansFemale
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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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Atypical Pleomorphic Extraosseous Ewing Tumor/Peripheral Primitive Neuroectodermal Tumor with Unusual Phenotypic/Genotypic Profile

2002

A pleomorphic undifferentiated tumor primarily located in the retroperitoneum with a phenotype compatible with an extraosseous Ewing tumor/peripheral primitive neuroectodermal tumor (ET/pPNET) pattern and unusual molecular features is described. Immunohistochemically, HBA-71 (CD99/mic2) and several neural markers were intensively expressed together with scattered cells expressing carcinoembryonic antigen (CEA). Short-term culture showed biphasic neuroblastic and epithelioid cell populations, with the latter expressing germ cell markers (CEA, alpha-fetoprotein, and the beta-subunit of chorionic gonadotrophin). Conventional cytogenetics displayed several chromosomic rearrangements, especially…

AdultMalePathologymedicine.medical_specialtyOncogene Proteins FusionChromosomes Human Pair 22CD99Soft Tissue NeoplasmsChromosomal translocationSarcoma EwingBiologyTranslocation GeneticPathology and Forensic MedicineExonFatal OutcomeCarcinoembryonic antigenBiomarkers TumorTumor Cells CulturedmedicineHumansNeuroectodermal Tumors PrimitiveRetroperitoneal NeoplasmsMolecular BiologyGene Rearrangementmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionPeripheral Primitive Neuroectodermal TumorChromosomes Human Pair 11Neoplasms Second PrimaryDNA NeoplasmCell BiologyGenes p53Chromosome Bandingmedicine.anatomical_structureKaryotypingMutationbiology.proteinEpithelioid cellGerm cellFluorescence in situ hybridizationDiagnostic Molecular Pathology
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Polymorphism of the Complement C8A and -B Genes in Two Families with C8β Deficiency and Neisserial Infections

1994

Serum samples from members of two Italian families with complement C8 beta deficiency were studied by SDS-PAGE under nonreducing conditions and by IEF. The proband of family I had suffered from two episodes of purulent meningitis and two of her uncles had suffered from only one episode, while the proband of family II had suffered from three different episodes. In contrast to previous findings, where C8 beta deficiency was cosegregating with C8A (alpha-gamma) allotype A, the proband of family II had the C8A allotype B. In addition, in one of her sons a novel variant of the C8 beta chain was detected. Studies at the DNA level in family I, using a recently described PCR system, demonstrate the…

AdultMaleProbandTaqINeisseriaceae InfectionsBlotting WesternImmunologyBiologyPolymerase Chain ReactionPathology and Forensic MedicineExonchemistry.chemical_compoundHumansImmunology and AllergyAlleleComplement ActivationGeneGeneticsPolymorphism GeneticComplement C8Stop codonAllotypePedigreeRestriction sitechemistryElectrophoresis Polyacrylamide GelFemaleIsoelectric FocusingNeisseriaClinical Immunology and Immunopathology
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A new germline mutation in BRCA1 gene in a sicilian family with ovarian cancer

2005

A group of 103 sicilian patients with hereditary and familiar breast and/or ovarian cancer were screened for Breast Cancer 1 gene (BRCA1) mutations by direct sequencing PCR products spanning the coding region and partial intronic regions of the BRCA1 gene. In this study, we report a new germline mutation in BRCA1 gene, not previously reported in the BIC database, in a woman with ovarian cancer at 46 years old. Mother's proband has been diagnosed the same histotype of ovarian cancer at 42 age. The mutational analyses that shown a 4843delC frameshift mutation in exon 16 of BRCA1 gene was extended to other family members including the proband's brother and her two sons. Direct automatic sequen…

AdultMaleProbandcongenital hereditary and neonatal diseases and abnormalitiesCancer Researchendocrine system diseasesGenetic counselingCystadenocarcinomaGenes BRCA1BiologyFrameshift mutationExonGermline mutationBreast cancermedicineHumansGenetic Predisposition to DiseaseFrameshift MutationSicilyGerm-Line MutationOvarian NeoplasmsBRCA1 Direct automatic sequencing Germline mutation Ovarian cancerGeneticsMiddle Agedmedicine.diseasePedigreeOncologyMutation (genetic algorithm)Cancer researchFemaleOvarian cancerBreast Cancer Research and Treatment
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Novel LMF1 nonsense mutation in a patient with severe hypertriglyceridemia

2009

Context: Lipase maturation factor 1 (LMF1) gene is a novel candidate gene in severe hypertriglyceridemia. Lmf1 is involved in the maturation of lipoprotein lipase (LPL) and hepatic lipase in endoplasmic reticulum. To date only one patient with severe hypertriglyceridemia and related disorders was found to be homozygous for a nonsense mutation in LMF1 gene (Y439X).Objective: The objective of the study was to investigate LMF1 gene in hypertriglyceridemic patients in whom mutations in LPL, APOC2, and APOA5 genes had been excluded.Results: The resequencing of LMF1 gene led to the discovery of a novel homozygous nonsense mutation in one patient with severe hypertriglyceridemia and recurrent epis…

AdultMaleProbandmedicine.medical_specialtyCandidate geneEndocrinology Diabetes and MetabolismMolecular Sequence DataClinical BiochemistryNonsense mutationContext (language use)macromolecular substances030204 cardiovascular system & hematologyBiologyBiochemistry03 medical and health sciencesExon0302 clinical medicineEndocrinologyInternal medicinemedicineHumansTriglyceridesHypolipidemic Agents030304 developmental biologyHypertriglyceridemia0303 health sciencesLipoprotein lipaseBase Sequencedigestive oral and skin physiologyBiochemistry (medical)Hypertriglyceridemianutritional and metabolic diseasesGenetic VariationLMF1 gene; nonsense mutation; hypertriglyceridemiaLMF1 hypertriglyceridemiamedicine.disease3. Good healthLipoprotein LipaseEndocrinologyCodon NonsenseOriginal Articlelipids (amino acids peptides and proteins)Hepatic lipaseGemfibrozil
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Variable phenotypic expression of chylomicron retention disease in a kindred carrying a mutation of the Sara2 gene

2010

Chylomicron retention disease is a recessive inherited disorder characterized by fat malabsorption and steatorrhea and is associated with failure to thrive in infancy. We describe a kindred carrying a mutation of Sara2 gene causing a chylomicron retention phenotype. The proband was a 5-month-old baby, born of consanguineous, apparently healthy parents from Morocco, with failure to thrive. There was a large quantity of fats in feces and malabsorption of fat-soluble vitamins. Intestinal biopsies showed a diffused enterocyte vacuolization with large cytosolic lipid droplets. Chylomicron retention disease or Anderson disease was hypothesized, and the Sara2 gene was analyzed by direct sequencing…

AdultMaleProbandmedicine.medical_specialtychylomicron retention disease phenotypic expression Sara2Settore MED/09 - Medicina InternaMalabsorptionEndocrinology Diabetes and MetabolismBiologySettore MED/42 - Igiene Generale E ApplicataExonEndocrinologyMalabsorption SyndromesInternal medicineChylomicronsmedicineHumansAlleleMonomeric GTP-Binding ProteinsGeneticsHaplotypeInfantmedicine.diseaseSteatorrheaPedigreeFat malabsorptionPhenotypeEndocrinologyChild PreschoolMutationFailure to thriveFabry DiseaseFemalemedicine.symptomChylomicron retention diseaseMetabolism
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