Search results for " Mutation"

showing 10 items of 1212 documents

Ehlers-Danlos syndrome type VII: phenotype and genotype

1994

A patient suffering from a severe form of Ehlers-Danlos syndrome is presented (EDS type VII). The presence of bilateral congenital hip dislocation, generalized joint hypermobility and a soft hyperelastic skin with abnormal scarring suggested a specific collagen type I defect. SDS-PAGE analysis of collagens secreted into the medium of fibroblast cultures showed a retarded migration of more than half of the alpha 2(I) chains. CNBr peptide mapping of the HPLC-purified altered chain localized the mutant locus to the N-terminal region of the protein. cDNA analysis of the corresponding gene COL1A2 revealed, in addition to the expected collagen sequence, a transcript missing the entire exon 6. Thi…

MaleGeneticsSplice site mutationBase SequenceGenotypeChemistryMolecular Sequence DataMutantIntronLocus (genetics)ExonsDermatologyGeneral Medicinemedicine.diseaseCollagen type I alpha 1ExonPhenotypeEhlers–Danlos syndromeChild PreschoolMutationmedicineHumansEhlers-Danlos SyndromeCollagenGeneArchives of Dermatological Research
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Attenuation of disease phenotype through alternative translation initiation in low-penetrance retinoblastoma

2006

Hereditary predisposition to retinoblastoma (RB) is caused by germline mutations in the retinoblastoma 1 (RB1) gene and transmits as an autosomal dominant trait. In the majority of cases disease develops in greater than 90% of carriers. However, reduced penetrance with a large portion of disease-free carrier is seen in some families. Unambiguous identification of the predisposing mutation in these families is important for accurate risk prediction in relatives and their genetic counseling but also provides conceptual information regarding the relationship between the RB1 genotype and the disease phenotype. In this study we report a novel mutation detected in 10 individuals of an extended fa…

MaleGenotypeDNA Mutational AnalysisGreen Fluorescent ProteinsMolecular Sequence DataPenetranceBiologyRetinoblastoma ProteinFrameshift mutationExonGermline mutationGeneticsmedicineHumansGenetic Predisposition to DiseaseAmino Acid SequenceRNA MessengerChildFrameshift MutationPeptide Chain Initiation TranslationalGenetics (clinical)GeneticsRetinoblastomaRetinoblastomaInfantAutosomal dominant traitExonsmedicine.diseasePenetranceAlternative SplicingPhenotypeCodon NonsenseHereditary RetinoblastomaMutation (genetic algorithm)FemaleHuman Mutation
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PAH gene mutations in the Sicilian population: association with minihaplotypes and expression analysis.

2001

Abstract The molecular basis of PAH deficiency in the Sicilian population is characterized by a marked heterogeneity, with 44 mutations at a single locus identified by a "gene-scanning" approach and accounting for a detection rate of 91%. The remaining 9% of PAH alleles does not bear mutations in any of the 13 exons and 24 exon/intron junctions. Three mutations IVS10nt-11 G > A, R261Q, and A300S accounted for 30.5%, whereas the remaining mutations were found at relative frequencies of less than 5% and 20 mutations were observed once only. Five mutations have been detected only in Sicilians so far. By studying the association of mutations with intragenic STR-VNTR haplotypes ("minihaplotypes"…

MaleGenotypeEndocrinology Diabetes and MetabolismRecombinant Fusion ProteinsPopulationDNA Mutational AnalysisBiologyGene mutationBiochemistryIdentity by descentGene Expression Regulation EnzymologicEndocrinologyHyperphenylalaninemiaPhenylketonuriasGenotypeGeneticsmedicineAnimalsHumansRNA MessengerAlleleeducationChildMolecular BiologySicilyAllelesGeneticseducation.field_of_studyPolymorphism GeneticHaplotypePhenylalanine HydroxylaseDNAmedicine.diseaseBlotting NorthernPhenotypePhenotypeHaplotypesCOS CellsMutationFemaleMolecular genetics and metabolism
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A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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No pol mutation is associated independently with the lack of immune recovery in patients infected with HIV and failing antiretroviral therapy

2011

An investigation was undertaken to determine whether specific pol mutations hinder long-term immune recovery regardless of virological response. In total, 826 patients with >50 HIV RNA copies/ml, who underwent genotypic resistance testing between 1 January 2000 and 31 December 2003 after >3 years of antiretroviral treatment, and were followed up for >3 years after genotypic resistance testing, were analyzed retrospectively. The outcome of the study was the lack of immune recovery after >3 years of follow-up, defined as a slope by linear regression 50 copies/ml divided by the number of HIV RNA measurements during follow-up. Logistic regression was used for univariable and multivariable analy…

MaleHIV InfectionsDrug resistanceLogistic regressionResistance to nucleoside reverse transcriptase inhibitorCD4+ T-lymphocyteRetrospective StudieImmunopathologyAntiretroviral Therapy Highly ActiveResistance to non-nucleoside reverse transcriptase inhibitorgeneticsResistance to protease inhibitorHIV Infectionresistance to nucleoside reverse transcriptase inhibitorsViralSidaresistance to protease inhibitorsbiologyReverse-transcriptase inhibitorViral LoadGenes poldrug therapy/immunology/virologyReverse Transcriptase InhibitorInfectious DiseasesTreatment Outcomeresistance to non-nucleoside reverse transcriptase inhibitorsReverse Transcriptase InhibitorsFemaleViral loadmedicine.drugHumanpolAnti-HIV AgentsAntiretroviral TherapyViremiaInfectious DiseaseSettore MED/17 - MALATTIE INFETTIVEpharmacology/therapeutic useAcquired immunodeficiency syndrome (AIDS)VirologyDrug Resistance ViralmedicineHumansHighly ActiveRetrospective StudiesAnti-HIV Agents; pharmacology/therapeutic use Antiretroviral Therapy; Highly Active CD4 Lymphocyte Count Drug Resistance; Viral; genetics Female Genes; pol HIV Infections; drug therapy/immunology/virology HIV-1; drug effects/enzymology/genetics Humans Male Mutation Retrospective Studies Reverse Transcriptase Inhibitors; therapeutic use Treatment Outcome Viral Loaddrug resistanceAnti-HIV Agentbiology.organism_classificationmedicine.diseaseVirologyCD4 Lymphocyte CountGenesdrug effects/enzymology/geneticstherapeutic useMutationCD4+ T-lymphocytesHIV-1
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A novel mutation of gene CBFA1/RUNX2 in cleidocranial dysplasia.

2007

Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal dysplasia characterised by abnormal clavicles, patent sutures and fontanelles, supernumerary teeth, short stature, and a variety of other skeletal changes. The disease gene is CBFA1/RUNX2, which is mapped to chromosome 6p21. Inactivation of the CBFA1/RUNX2 gene by mutations is involved in the skeletal defects that occur in patients with CCD. CBFA1/RUNX2 controls the differentiation of precursor cells into osteoblasts and is essential for membranous as well as endochondral bone formation. In this study of a 14-yr-old boy with typical CCD phenotype, the authors found a novel CBFA1/RUNX2 gene mutation. All of the amplified segment…

MaleHeterozygoteAdolescentDNA Mutational AnalysisCore Binding Factor Alpha 1 SubunitPolymerase Chain ReactionPedigreeAdolescent Chromosomes Human Pair 6 Cleidocranial Dysplasia/genetics* Cleidocranial Dysplasia/pathology Codon Nonsense/genetics* Core Binding Factor Alpha 1 Subunit/genetics* DNA Mutational Analysis DNA Primers/chemistry Female Gene Silencing Heterozygote Humans Male Pedigree Point Mutation* Polymerase Chain Reactioncleidocranial dysplasiaCodon NonsenseCBFA1/RUNX2HumansPoint MutationChromosomes Human Pair 6Femalegene mutationGene SilencingCleidocranial DysplasiaDNA Primers
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Cathepsin C gene: First compound heterozygous patient with Papillon-Lefèvre syndrome and a novel symptomless mutation.

2001

Papillon-Lefevre syndrome (PLS) has recently been shown to be caused by mutations in the cathepsin C gene resulting in periodontal disease and palmoplantar keratosis. Thirteen different homozygous mutations have been characterised in PLS patients of different ethnic origin. In the present paper, a PLS patient is described who carries two novel mutations (706G>T and 872G>A) in the paternal and maternal chromosomes, respectively. This is the first compound patient described so far. In addition, a novel symptomless mutation (458C>T) in the cathepsin C gene is described in three homozygous individuals. Thus, not all mutations should be considered as a cause of disease, whether case studies or g…

MaleHeterozygoteHaim–Munk syndromeDNA Mutational AnalysisMolecular Sequence DataMutation MissensePapillon–Lefèvre syndromeBiologyCompound heterozygositymedicine.disease_causePapillon-Lefevre DiseaseCathepsin CCathepsin CPapillon-Lefevre DiseaseGene FrequencyGeneticsmedicineHumansAlleleAllele frequencyAllelesGenetics (clinical)Family HealthGeneticsMutationDNAmedicine.diseaseMutationFemale
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Hydrops, fetal pleural effusions and chylothorax in three patients with CBL mutations.

2014

Fetal hydrops, fetal pleural effusions, hydrothorax, and chylothorax, may be associated with various genetic disorders, in particular with the Noonan, cardio-facio-cutaneous and Costello syndromes. These syndromes, collectively called RASopathies, are caused by mutations in the RAS/MAPK pathway, which is known to play a major role in lymphangiogenesis. Recently, germline mutations in the Casitas B-cell lymphoma (CBL) gene were reported in 25 patients and of these, 20 had juvenile myelomonocytic leukemia (JMML). The disorder was named "CBL syndrome" or "Noonan syndrome-like disorder with or without juvenile myelomonocytic leukemia" (NSLL). To date, prenatal abnormalities have not been report…

MaleHeterozygoteHydrops FetalisDNA Mutational AnalysisRASopathyChylothoraxGermline mutationhemic and lymphatic diseasesHydrops fetalisGeneticsmedicineHumansProto-Oncogene Proteins c-cblGenetics (clinical)FetusJuvenile myelomonocytic leukemiabusiness.industryChylothoraxFaciesInfantmedicine.diseaseLymphomaPleural EffusionPhenotypeChild PreschoolImmunologyMutationHydrothoraxFemaleRNA Splice SitesbusinessAmerican journal of medical genetics. Part A
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Frontotemporal dementia: the post-tau era.

2006

As scientists have begun to decipher the molecular genetic bases of hereditary frontotemporal dementia (FTD), it has become clear that the biology of these human neurodegenerative diseases has a complexity not previously suspected. FTD has been found to be linked to several chromosomal loci including those in chromosome 9, chromosome 17, and chromosome 3. The article by Guyant-Marechal et al. in this issue of Neurology reports the clinical, pathologic, and molecular characteristics of a form of FTD associated with inclusion body myopathy and Paget disease of the bone observed in members of two families and expands our knowledge on genetically determined FTD.1 The disorder is associated with…

MaleHeterozygoteMultiple Organ FailureDNA Mutational AnalysisChromosome 9Cell Cycle ProteinsChromosome Disorderstau ProteinsBiologyRisk AssessmentMyositis Inclusion BodyExonRisk FactorsValosin Containing ProteinmedicinePrevalenceHumansGenetic Predisposition to DiseaseGeneRetrospective StudiesGeneticsAdenosine TriphosphatasesIncidenceChromosomeSyndromeMiddle Agedmedicine.diseaseOsteitis DeformansPhenotypePedigreeChromosome 17 (human)Chromosome 3MutationDementiaFemaleNeurology (clinical)FranceFrontotemporal dementiaNeurology
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Leigh syndrome due to compound heterozygosity of dihydrolipoamide dehydrogenase gene mutations. Description of the first E3 splice site mutation.

2003

Item does not contain fulltext A boy with recurrent episodes of hypoglycaemia and ataxia, microcephaly, mental retardation, permanent lactic acidaemia, intermittent 2-oxoglutaric aciduria as well as elevation of serum branched chain amino acids was diagnosed with dihydrolipoamide dehydrogenase (E3) deficiency. Analysis of genomic DNA revealed compound heterozygosity for two novel mutations: I393T in exon 11, located at the interface domain of the protein and possibly interfering with its dimerisation, and IVS9+1G>A located at a consensus splice site. A heterozygous polymorphism was also detected. In the patient's cDNA the I393T mutation and the polymorphism appeared to be homozygous, indica…

MaleHeterozygoteMutation MissensePyruvate Dehydrogenase ComplexGene mutationBiologyCompound heterozygosityLoss of heterozygositymedicineHumansLeigh diseaseMuscle SkeletalDihydrolipoamide DehydrogenaseGeneticsSplice site mutationDihydrolipoamide dehydrogenasePyruvate Dehydrogenase (Lipoamide)Fibroblastsmedicine.diseasePyruvate dehydrogenase complexRenal disorders [UMCN 5.4]Genetic defects of metabolism [UMCN 5.1]Child PreschoolPediatrics Perinatology and Child HealthRNA Splice SitesLeigh DiseaseCellular energy metabolism [UMCN 5.3]
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