Search results for "Point mutation"

showing 10 items of 199 documents

Mutant K-ras2 in serum

2003

Mutant tumour derived DNA has been detected in the sera of colorectal cancer patients. We investigated if mutant serum KRAS2 was detectable preoperatively in a large group of patients with colorectal neoplasia. A prospective study of 94 patients who underwent putative curative resection for colorectal carcinoma (CRC) was performed to ascertain if serum mutant KRAS2 could be used postoperatively as a disease marker.Preoperative sera from 78 patients were analysed (group A). Sera from 94 patients were obtained three monthly for up to three years during the postoperative period (group B). Codon 12 and 13 KRAS2 mutations were analysed in matched tumour and serum samples.In the preoperative grou…

MaleLetterColorectal cancervirusesMutantDNA Mutational AnalysisBioinformaticsProto-Oncogene Proteins p21(ras)03 medical and health sciencesCollaborative group0302 clinical medicineProto-Oncogene ProteinsMedicineHumansRas2neoplasmsGene030304 developmental biologyAged0303 health sciencesbusiness.industryPoint mutationGastroenterologyDNA NeoplasmMiddle Agedmedicine.diseasePrognosis3. Good healthProto-Oncogene Proteins p21(ras)Molecular analysisCarcinoembryonic AntigenEpidemiologic Studies030220 oncology & carcinogenesisCancer researchras ProteinsFemaleNeoplasm Recurrence LocalbusinessColorectal NeoplasmsBiomarkers
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20 ans après: a second mutation in MAOA identified by targeted high-throughput sequencing in a family with altered behavior and cognition

2013

Intellectual disability (ID) is characterized by an extraordinary genetic heterogeneity, with >250 genes that have been implicated in monogenic forms of ID. Because this complexity precluded systematic testing for mutations and because clinical features are often non-specific, for some of these genes only few cases or families have been unambiguously documented. It is the case of the X-linked gene encoding monoamine oxidase A (MAOA), for which only one nonsense mutation has been identified in Brunner syndrome, characterized in a single family by mild non-dysmorphic ID and impulsive, violent and aggressive behaviors. We have performed targeted high-throughput sequencing of 220 genes, includi…

MaleModels MolecularBrunner syndromeNonsense mutationMutation MissenseArticleIntellectual DisabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmino Acid SequenceMonoamine OxidaseGenetics (clinical)GeneticsFamily HealthbiologyBase SequenceGenetic heterogeneityPoint mutationHigh-Throughput Nucleotide Sequencingmedicine.diseasePedigreeProtein Structure TertiaryAutism spectrum disorderAttention Deficit and Disruptive Behavior DisordersChild Development Disorders Pervasivebiology.proteinAutismFemaleMonoamine oxidase A
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Construction of hevein (Hev b 6.02) with reduced allergenicity for immunotherapy of latex allergy by comutation of six amino acid residues on the con…

2004

Abstract Recently we have established that IgE Abs bind to conformational epitopes in the N- and C-terminal regions of the major natural rubber latex allergen, hevein (Hev b 6.02). To identify the critical amino acid residues that interact with IgE, the hevein sequence was scanned by using site-specific mutations. Twenty-nine hevein mutants were designed and produced by a baculovirus expression system in insect cells and tested by IgE inhibition-ELISA using sera from 26 latex allergic patients. Six potential IgE-interacting residues of hevein (Arg5, Lys10, Glu29, Tyr30, His35, and Gln38) were identified and characterized further in detail. Based on these six residues, two triple mutants (HΔ…

MaleModels MolecularProtein ConformationMutantImmunoglobulin Emedicine.disease_causeEpitopelaw.inventionEpitopes0302 clinical medicineProtein structureAllergenlawImmunology and AllergyCombinatorial Chemistry TechniquesChild0303 health sciencesbiologyChemistryMiddle AgedRecombinant Proteins3. Good healthBiochemistryLatex allergyRecombinant DNAFemalePlant LectinsProtein BindingAdultAdolescentImmunologyMutagenesis (molecular biology technique)Binding Competitive03 medical and health sciencesLatex HypersensitivitymedicineHumansPoint Mutation030304 developmental biologyAgedAllergensImmunoglobulin Emedicine.disease030228 respiratory systemAmino Acid SubstitutionDesensitization Immunologicbiology.proteinMutagenesis Site-DirectedBinding Sites AntibodyAntimicrobial Cationic PeptidesJournal of immunology (Baltimore, Md. : 1950)
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Mild mutations in the pan neural gene prospero affect male-specific behaviour in Drosophila melanogaster

2004

0376-6357 (Print) Journal Article Research Support, Non-U.S. Gov't; The fruitfly Drosophila melanogaster is one of the most appropriate model organisms to study the genetics of behaviour. Here, we focus on prospero (pros), a key gene for the development of the nervous system which specifies multiple aspects from the early formation of the embryonic central nervous system to the formation of larval and adult sensory organs. We studied the effects on locomotion, courtship and mating behaviour of three mild pros mutations. These newly isolated pros mutations were induced after the incomplete excision of a transposable genomic element that, before excision, caused a lethal phenotype during larv…

MaleMutantPoint Mutation/*geneticsSexual Behavior AnimalBehavioral NeuroscienceAnimal/*physiologyDrosophila ProteinsGeneticsBehavior AnimalbiologyReproductionHomozygoteNuclear ProteinsGeneral MedicinePhenotypeNerve Tissue Proteins/*geneticshumanitiesDNA Transposable Elements/geneticsDrosophila melanogasterLocomotion/physiologyFemaleDrosophila melanogasterLocomotionHeterozygoteFertility/physiologySexual BehavioreducationNerve Tissue ProteinsTranscription Factors/*geneticsAnimal/physiologyDrosophilidaeNuclear Proteins/*geneticsPoint MutationAnimalsAlleleGeneDrosophilaReproduction/physiologyAllelesBehaviorfungiDrosophila Proteins/*geneticsHeterozygote advantageRepressor Proteins/*geneticsbiology.organism_classificationRepressor ProteinsFertilityDNA Transposable ElementsAnimal Science and ZoologyTranscription Factors
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Actin-related myopathy without any missense mutation in the ACTA1 gene.

2004

Actinopathies are defined by missense mutations in the ACTA1 gene coding for sarcomeric actin, of which some 70 families have, so far, been identified. Often, but not always, muscle fibers carry large patches of actin filaments. Many such patients also have nemaline myopathy, qualifying actinopathies as a subgroup of nemaline myopathies. This article concerns a then newborn, now 21/2-year-old boy, the first and single child of nonconsanguineous parents, who was born floppy, requiring immediate postnatal assisted ventilation. A quadriceps muscle biopsy revealed large patches of thin myofilaments reacting at light and electron microscopic levels with antibodies against actin but only a few s…

MaleMyofilamentBiopsyDNA Mutational AnalysisMutation MissenseGene mutationBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineNemaline myopathyMuscular Diseases030225 pediatricsmedicineMissense mutationHumansPoint MutationMyopathyMuscle SkeletalActinMutationInfantmedicine.diseaseMolecular biologyCongenital myopathyActinsPediatrics Perinatology and Child HealthNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryJournal of child neurology
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Toll-like receptor 4 defective mice carrying point or null mutations do not show increased susceptibility toCandida albicansin a model of hematogenou…

2006

We have studied the role of TLR4 in murine defenses against Candida albicans in two TLR4-defective mouse strains: C3H/HeJ mice which have defective TLR4 signaling, and TLR4-/- knockout mice. Both TLR4-defective mice strains experimentally infected with virulent C. albicans cells showed no significant difference in survival as compared with their respective controls. Recruitment of neutrophils to the peritoneal cavity of i.p. infected mice was not affected in TLR4-/-animals, but significantly enhanced in C3H/HeJ mice, compared with their control mice. In vitro production of TNF-alpha by macrophages from both types of TLR4-defective mice, in response to yeasts and hyphae of C. albicans, was n…

MaleNeutrophilsBiologyMicrobiologyInterferon-gammaMicePeritoneal cavityCandida albicansSplenocytemedicineAnimalsPoint MutationGenetic Predisposition to DiseaseCandida albicansMice KnockoutMice Inbred C3HToll-like receptorTumor Necrosis Factor-alphaCandidiasisGeneral MedicineTh1 CellsFlow Cytometrybiology.organism_classificationInterleukin-12Corpus albicansMice Inbred C57BLToll-Like Receptor 4Infectious Diseasesmedicine.anatomical_structureKnockout mouseMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Tumor necrosis factor alphaMedical Mycology
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Recurrent missense variant in the nuclear export signal of FMR1 associated with FXS-like phenotype including intellectual disability, ASD, facial abn…

2021

Fragile X syndrome (FXS; MIM 300624) is an X-linked genetic disorder characterized by physical abnormalities associated with intellectual disability and a wide spectrum of neurological and psychiatric impairments. FXS occurs more frequently in males, 1 in 5000 males and 1 in 8000 females accounting for 1-2% of overall intellectual disability (ID). In more than 99% of patients, FXS results from expansions of a CGG triplet repeat (>200 in male) of the FMR1 gene. In the last years an increasing number, albeit still limited, of FXS subjects carrying FMR1 mutations including deletions, splicing errors, missense, and nonsense variants was reported. Nevertheless, the studies concerning the func…

MaleNuclear Export SignalsSettore M-PSI/02 - Psicobiologia E Psicologia FisiologicaAutism Spectrum DisorderMutation MissenseGeneral MedicineFMR1 point mutationSettore MED/39 - Neuropsichiatria InfantileFragile X Mental Retardation ProteinPhenotypeSettore MED/38 - Pediatria Generale E SpecialisticaIntellectual DisabilityAutism spectrum disorders ASDSettore M-PSI/08 - Psicologia ClinicaGeneticsHumansIntellectual disability IDFemaleNuclear export signal NES.Genetics (clinical)Fragile X syndrome
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Kirsten ras mutations in patients with colorectal cancer: the 'RASCAL II' study

2001

Researchers worldwide with information about the Kirsten ras (Ki-ras) tumour genotype and outcome of patients with colorectal cancer were invited to provide that data in a schematized format for inclusion in a collaborative database called RASCAL (The Kirsten ras in-colorectal-cancer collaborative group). Our results from 2721 such patients have been presented previously and for the first time in any common cancer, showed conclusively that different gene mutations have different impacts on outcome, even when the mutations occur at the same site on the genome. To explore the effect of Ki-ras mutations at different stages of colorectal cancer, more patients were recruited to the database, whi…

MaleOncologyCancer ResearchPathologyMultivariate analysisDatabases FactualSettore MED/06 - Oncologia MedicaColorectal cancerGene mutationmedicine.disease_cause0302 clinical medicineGenotypeColorectal cancer Ki-ras mutationRegistriesAged 80 and over0303 health sciencesMutationValineMiddle Aged3. Good healthKRAS Mutation Analysismedicine.anatomical_structureOncologyPresented by the Kirsten ras in-colorectal-cancer collaborative group030220 oncology & carcinogenesisFemaleColorectal NeoplasmsAdultmedicine.medical_specialtyAdolescentGenotypeoverall survivalMutation MissenseRectumcolorectal cancerDisease-Free Survival03 medical and health sciencesInternal medicinemedicineHumansPoint MutationK-rasCodoncolorectal cancer; K-ras; prognosis; overall survivalAgedNeoplasm StagingProportional Hazards Models030304 developmental biologybusiness.industryCancermedicine.diseaseSurvival AnalysisGenes rasMultivariate Analysisprognosisbusiness
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A new mitochondrial point mutation in the transfer RNALys gene associated with progressive external ophthalmoplegia with impaired respiratory regulat…

2011

Abstract We report a novel heteroplasmic point mutation G8299A in the gene for mitochondrial tRNA Lys in a patient with progressive external ophthalmoplegia complicated by recurrent respiratory insufficiency. Biochemical analysis of respiratory chain complexes in muscle homogenate showed a combined complex I and IV deficiency. The transition does not represent a known neutral polymorphism and affects a position in the tRNA acceptor stem which is conserved in primates, leading to a destabilization of this functionally important domain. In vitro analysis of an essential maturation step of the tRNA transcript indicates the probable pathogenicity of this mutation. We hypothesize that there is a…

MaleOphthalmoplegia Chronic Progressive ExternalRNA MitochondrialMitochondrial diseaseMolecular Sequence DataRespiratory chainBiologymedicine.disease_causeSecondary PreventionmedicineHumansPoint MutationGeneticsMutationBase SequenceTransition (genetics)Point mutationExternal ophthalmoplegiaMiddle Agedmedicine.diseaseHeteroplasmyNeurologyRespiratory failureRNARNA Transfer LysNeurology (clinical)Respiratory InsufficiencyJournal of the Neurological Sciences
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A European family with histidine 58 transthyretin mutation in familial amyloid polyneuropathy

1997

1. IntroductionMore than 50 mutations of the transthyretin (TTR) [1]molecule resulting in different clinical forms of amyloidosisincluding familial amyloid polyneuropathy (FAP) havebeen reported to date. Within this FAP spectrum severaltransthyretin mutations are more frequent, others are rare.One mutation, the codon 58 histidine for leucine has pre-viously been recorded only in American subjects (Mary-land/German type), originally reported in a large kinship[2,3] and in another family from Ohio [4]. In the originaldescription of the Maryland/German type of amyloidosis[2], it was stated that the early immigrants in this pedigreewere from the Rhine river area, "nearly all of them from thelef…

MalePathologymedicine.medical_specialtyAtaxiaAmyloid Neuropathiesmedicine.disease_causeAtrophyLeucineGermanymedicineHumansPoint MutationPrealbuminHistidineCodonGenetics (clinical)Genes DominantMutationDysesthesiabiologybusiness.industryPoint mutationAmyloidosisMiddle Agedmedicine.diseaseUnited StatesTransthyretinNeurologyPediatrics Perinatology and Child Healthbiology.proteinNeurology (clinical)medicine.symptomRestriction fragment length polymorphismbusinessNeuromuscular Disorders
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