Search results for " Mutation"

showing 10 items of 1212 documents

Novel Munc13-4 mutations in children and young adult patients with haemophagocytic lymphohistiocytosis

2006

Familial haemophagocytic lymphohistiocytosis (FHL) is a genetically heterogeneous disorder characterised by constitutive defects in cellular cytotoxicity resulting in fever, hepatosplenomegaly and cytopenia, and the outcome is fatal unless treated by chemoimmunotherapy followed by haematopoietic stem‐cell transplantation. Since 1999, mutations in the perforin gene giving rise to this disease have been identified; however, these account only for 40% of cases. Lack of a genetic marker hampers the diagnosis, suitability for transplantation, selection of familial donors, identification of carriers, genetic counselling and prenatal diagnosis. Mutations in the Munc13–4 gene have recently been des…

EXPRESSIONMalePRF1AdolescentFHLBlotting WesternDNA Mutational AnalysisHepatosplenomegalyDONORSPrenatal diagnosisBiologymedicine.disease_causeLymphohistiocytosis HemophagocyticGeneticsmedicinePERFORIN GENE-MUTATIONSHumansUNC13DChildGenetics (clinical)Family HealthSPECTRUMHemophagocytic lymphohistiocytosisMutationCytopeniaMicroscopy ConfocalIDENTIFICATIONGenetic heterogeneityInfant NewbornCYTOTOXIC T-LYMPHOCYTESInfantMembrane Proteinsmedicine.diseaseBONE-MARROW-TRANSPLANTATIONTransplantationMicroscopy ElectronChild PreschoolMutationImmunologyFemalemedicine.symptomLetter to JMGT-Lymphocytes CytotoxicJournal of Medical Genetics
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Sequence variation and regulatory variation in acetylcholinesterase genes contribute to insecticide resistance in different populations of Leptinotar…

2021

Abstract Although insect herbivores are known to evolve resistance to insecticides through multiple genetic mechanisms, resistance in individual species has been assumed to follow the same mechanism. While both mutations in the target site insensitivity and increased amplification are known to contribute to insecticide resistance, little is known about the degree to which geographic populations of the same species differ at the target site in a response to insecticides. We tested structural (e.g., mutation profiles) and regulatory (e.g., the gene expression of Ldace1 and Ldace2, AChE activity) differences between two populations (Vermont, USA and Belchow, Poland) of the Colorado potato beet…

Ecologyorganophosphatetarget site mutationkoloradonkuoriainencarbamatekarbamaatitinsecticide resistancecarbamate; gene expression; insecticide resistance; organophosphate; target site mutationinsektisiditresistenssipopulaatiogenetiikkagene expressiongeeniekspressiomutaatiotQH540-549.5Research ArticlesResearch Article
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A comparative investigation of DNA adducts, DNA strand breaks and gene mutations induced by benzo[a]pyrene and (+/-)-anti-benzo[a]pyrene-7,8-diol 9,1…

1997

Abstract Genotoxic effects of benzo[ a ]pyrene (BP) and its reactive metabolites (±)- anti -benzo[ a ]pyrene-7,8-diol 9,10-oxide ((±)- anti -BPDE) were comparatively investigated in vitro with the permanent human fibroblast cell line MRC5CV1. Induced DNA adducts were measured by 32 P-postlabeling, DNA strand breakage was determined by the comet assay and the HPRT gene mutation test was used to detect cytotoxicity and mutagenicity. Treatment of MRC5CV1 cells with S9 mix-activated BP or with (±)- anti -BPDE resulted in a concentration-dependent increase in DNA adducts and strand breaks. Genotoxic effects of BP and (±)- anti- BPDE were detected by 32 P-postlabeling and the comet assay with sim…

ElectrophoresisHypoxanthine PhosphoribosyltransferaseHealth Toxicology and Mutagenesis78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideGene mutationmedicine.disease_causechemistry.chemical_compoundDNA AdductsDNA adductpolycyclic compoundsGeneticsmedicineBenzo(a)pyreneHumansGeneCells CulturedMutationChemistryMutagenicity TestsDNAFibroblastsMolecular biologyComet assayBenzo(a)pyreneBiochemistryGenetic TechniquesCell cultureMutationPhosphorus RadioisotopesDNADNA DamageMutagensMutation research
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Genetic basis of human complement C4A deficiency. Detection of a point mutation leading to nonexpression.

1993

Abstract The fourth component of the human complement system (C4) is coded for by two genes, C4A and C4B, located within the MHC. Null alleles of C4 (C4Q0) are defined by the absence of C4 protein in plasma. These null alleles are due either to large gene deletions or to nonexpression of the respective genes. In a previous study, evidence was obtained for nonexpressed defective genes at the C4A locus, and for gene conversion at the C4B locus. To further characterize the molecular basis of these non-expressed C4A genes, we selected nine pairs of PCR primers from flanking genomic intron sequences to amplify all 41 exons from individuals with a defective C4A gene. The amplified products were s…

ElectrophoresisMolecular Sequence DataLocus (genetics)BiologyPolymerase Chain ReactionAutoimmune DiseasesHumansPoint MutationGene conversionAmino Acid SequenceGeneGeneticsPolymorphism GeneticBase SequenceHaplotypeC4AGene AmplificationImmunologic Deficiency SyndromesComplement C4aSingle-strand conformation polymorphismGeneral MedicineExonsSequence Analysis DNAMolecular biologyNull alleleStop codonHaplotypesResearch Article
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A temperature-sensitive brain tumor suppressor mutation of Drosophila melanogaster: Developmental studies and molecular localization of the gene

1993

The recessive-lethal, temperature-sensitive (ts) mutation of the tumor suppressor gene lethal(3)malignant brain tumor (l(3)mbt) causes in a single step the malignant transformation of the adult optic neuroblasts and ganglion mother cells in the larval brain at the restrictive temperature of 29 degrees C. The transformed cells are differentiation-incompetent and grow autonomously in a lethal and invasive fashion in situ in the brain as well as after transplantation in vivo into wild-type adult hosts. The imaginal discs show epithelial overgrowth. At the permissive temperature of 22 degrees C development is completely normal. The ts-period of gene activity responsible for 100% brain tumor sup…

EmbryologyHot TemperatureTumor suppressor geneBiologymedicine.disease_causeMalignant transformationmedicineAnimalsGenes Tumor SuppressorGeneSuppressor mutationGeneticsMutationBrain NeoplasmsStem CellsOptic Lobe NonmammalianChromosome Mappingbiology.organism_classificationCell biologyTransplantationImaginal discDrosophila melanogasterGangliaGenes LethalDrosophila melanogasterDevelopmental BiologyMechanisms of Development
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Biological effects and photodegradation by TiO(2) of terpenes present in industrial wastewater.

2010

Abstract The aim of this work was to study the biological effects of four monoterpenes, i.e. α-pinene, β-pinene, 3-carene and d -limonene present in the wastewater of a citrus transformation factory. The study was carried out by exposing V79 Chinese hamster cells to single terpene or to the mixture of four terpenes at concentrations corresponding to those in the wastewater evaluated by head space solid phase micro extraction and gas chromatography (HS-SPME-GC) analyses. Treatments with single or combined terpenes similarly affected cell vitality, but only the combined treatments induced the 6-thioguanine resistant mutants. Moreover the photocatalytic degradation of the four terpenes was suc…

Environmental EngineeringChromatography GasSettore CHIM/10 - Chimica Degli AlimentiHealth Toxicology and MutagenesisIndustrial WasteCatalysisCell LineTerpeneIndustrial wastewater treatmentchemistry.chemical_compoundCricetulusCricetinaeEnvironmental ChemistryAnimalsWater PollutantsPhotodegradationWaste Management and DisposalEffluentSolid Phase MicroextractionTitaniumLimoneneChromatographyPhotolysisTerpenesTerpenes clonogenicassay Terpenes mutationassay TiO2 photocatalysisPollutionSettore BIO/18 - GeneticaWastewaterchemistryEnvironmental chemistryPhotocatalysisSettore CHIM/07 - Fondamenti Chimici Delle TecnologieGas chromatographyJournal of hazardous materials
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A familial disorder of altered DNA-methylation

2014

BackgroundIn a subset of imprinting disorders caused by epimutations, multiple imprinted loci are affected. Familial occurrence of multilocus imprinting disorders is rare.Purpose/objectiveWe have investigated the clinical and molecular features of a familial DNA-methylation disorder.MethodsTissues of affected individuals and blood samples of family members were investigated by conventional and molecular karyotyping. Sanger sequencing and RT-PCR of imprinting-associated genes (NLRP2, NLRP7, ZFP57, KHDC3L, DNMT1o), exome sequencing and locus-specific, array-based and genome-wide technologies to determine DNA-methylation were performed.ResultsIn three offspring of a healthy couple, we observed…

EpigenomicsMaleGeneticsSanger sequencingDNA Mutational AnalysisGenetic Diseases InbornInfant NewbornMedizinDNA MethylationBiologyPedigreesymbols.namesakeDNA methylationGeneticssymbolsHumansFemaleEpigeneticsImprinting (psychology)Genomic imprintingGeneAllelesGenetics (clinical)Exome sequencingEpigenomics
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Extensive molecular analysis of patients bearing CFTR-related disorders.

2012

Cystic fibrosis transmembrane conductance regulator (CFTR)–related disorders (CFTR-RDs) may present with pancreatic sufficiency, normal sweat test results, and better outcome. The detection rate of mutations is lower in CFTR-RD than in classic CF: mutations may be located in genes encoding proteins that interact with CFTR or support channel activity. We tested the whole CFTR coding regions in 99 CFTR-RD patients, looking for gene mutations in solute carrier (SLC) 26A and in epithelial Na channel (ENaC) in 33 patients who had unidentified mutations. CFTR analysis revealed 28 mutations, some of which are rare. Of these mutations, RT-PCR demonstrated that the novel 1525-1delG impairs exon 10 s…

Epithelial sodium channelcongenital hereditary and neonatal diseases and abnormalitiesCystic fibrosis CFTR SLC26A SCNNCystic FibrosisAnion Transport ProteinsDNA Mutational Analysismolecular analysiCystic Fibrosis Transmembrane Conductance RegulatorGene mutationPathology and Forensic Medicinecongenital bilateral absence of vasa deferentesExonGene Frequencydisseminated bronchiectasiscongenital bilateral absence of vasa deferenteHumansTrypsinmolecular analysisEpithelial Sodium ChannelsGeneCells CulturedGenetic Association StudiesGeneticsbiologydisseminated bronchiectasiEpithelial Cellsrespiratory systemrecurrent pancreatitidigestive system diseasesCystic fibrosis transmembrane conductance regulatorrespiratory tract diseasesSolute carrier familyCFTR related disordersTrypsin Inhibitor Kazal PancreaticCase-Control StudiesRNA splicingMutationbiology.proteinMolecular MedicineCFTR related disorderSLC26 familyCarrier ProteinsNa channel ENaCMinigenerecurrent pancreatitis
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The Epithelial Mesenchymal Transition Process in Wilms Tumor

2011

Background Until now, only a few mouse-transplanted human tumors or experimental Wilms tumor (WT) cell lines have been described. The aim of this study was to show the biological behavior, including histology, immunohistochemistry (IHC), and molecular biology, of a WT including the original tumor and metastasis transferred into nude mice and followed for successive generations in xenografts. Methods A WT metastasis was xenotransplanted into nude mice and the mice was monitored for 7 passages over a period of 29 months; the original neoplasm was comparatively studied. The morphology was evaluated by optical and electron microscopy. The protein expression was analyzed by immunohistochemistry …

Epithelial-Mesenchymal TransitionHistologyDNA Mutational AnalysisMice NudeCell Growth ProcessesWilms TumorBone and BonesPathology and Forensic MedicineMetastasisMicemedicineAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarrayChemistryMesenchymal stem cellNuclear ProteinsEye Diseases HereditaryWilms' tumorHistologyStriated muscle cell differentiationMicroarray Analysismedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysKidney NeoplasmsWnt ProteinsRadiusMedical Laboratory TechnologyMutationCancer researchImmunohistochemistrySignal TransductionApplied Immunohistochemistry & Molecular Morphology
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Prevalence of Angelman syndrome and Prader-Willi syndrome in Estonian children: sister syndromes not equally represented.

2006

In 2000-2004, we performed a focused search for individuals with Angelman syndrome (AS) and Prader-Willi syndrome (PWS) aiming to establish the prevalence data for the individuals born between 1984 and 2004 in Estonia. All persons with probable AS or PWS (n = 184) were studied using the DNA methylation test. Individuals with abnormal methylation were all further tested by chromosomal and FISH analysis, and if necessary for uniparental disomy and UBE3A gene mutation. Nineteen cases with abnormal methylation test result were identified. Seven of them had AS, including six (85.7%) due to 15q11-13 deletion and one paternal UPD15. Twelve subjects had PWS: 4 (33%) 15q11-13 deletions, 6 (50%) mate…

EstoniaMalePediatricsmedicine.medical_specialtyPopulationDNA Mutational AnalysisPrevalenceChromosomal translocationAngelman syndromeInternal medicineEpidemiologyHappy puppet syndromeGeneticsmedicinePrevalenceHumanseducationChildGenetics (clinical)In Situ Hybridization Fluorescenceeducation.field_of_studyMolecular Epidemiologybusiness.industryDNA Methylationmedicine.diseaseUniparental disomyChromosome BandingEndocrinologyEl NiñoFemaleAngelman SyndromebusinessPrader-Willi SyndromeAmerican journal of medical genetics. Part A
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