Search results for "Pedigree"

showing 10 items of 313 documents

A genome scan for developmental dyslexia confirms linkage to chromosome 2p11 and suggests a new locus on 7q32

2003

Developmental dyslexia is a distinct learning disability with unexpected difficulty in learning to read despite adequate intelligence, education, and environment, and normal senses. The genetic aetiology of dyslexia is heterogeneous and loci on chromosomes 2, 3, 6, 15, and 18 have been repeatedly linked to it. We have conducted a genome scan with 376 markers in 11 families with 38 dyslexic subjects ascertained in Finland. Linkage of dyslexia to the vicinity of DYX3 on 2p was confirmed with a non-parametric linkage (NPL) score of 2.55 and a lod score of 3.01 for a dominant model, and a novel locus on 7q32 close to the SPCH1 locus was suggested with an NPL score of 2.77. The SPCH1 locus has p…

MaleCandidate geneGenotypeDNA Mutational AnalysisShort ReportLocus (genetics)BiologyDyslexia03 medical and health sciences0302 clinical medicineCommunication disorderDCDC2mental disordersGeneticsmedicineHumansLanguage disorderFinlandGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesGenome HumanDyslexiaChromosome MappingForkhead Transcription FactorsFOXP2medicine.diseasePedigreeRepressor ProteinsChromosomes Human Pair 2Learning disabilityFemaleLod Scoremedicine.symptomChromosomes Human Pair 7030217 neurology & neurosurgeryTranscription FactorsJournal of Medical Genetics
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Homozygous disruption of PDZD7 by reciprocal translocation in a consanguineous family: a new member of the Usher syndrome protein interactome causing…

2008

A homozygous reciprocal translocation, 46,XY,t(10;11),t(10;11), was detected in a boy with non-syndromic congenital sensorineural hearing impairment. Both parents and their four other children were heterozygous translocation carriers, 46,XX,t(10;11) and 46,XY,t(10;11), respectively. Fluorescence in situ hybridization of region-specific clones to patient chromosomes was used to localize the breakpoints within bacterial artificial chromosome (BAC) RP11-108L7 on chromosome 10q24.3 and within BAC CTD-2527F12 on chromosome 11q23.3. Junction fragments were cloned by vector ligation and sequenced. The chromosome 10 breakpoint was identified within the PDZ domain containing 7 (PDZD7) gene, disrupti…

MaleCandidate geneHeterozygoteUsher syndromePDZ domainMolecular Sequence DataChromosomal translocationBiologyTranslocation GeneticConsanguinityotorhinolaryngologic diseasesGeneticsmedicineHumansAmino Acid SequenceHearing LossMolecular BiologyGenetics (clinical)GeneticsGene RearrangementBacterial artificial chromosomemedicine.diagnostic_testBase SequenceChromosomes Human Pair 10Chromosomes Human Pair 11BreakpointHomozygoteChromosomeGeneral Medicinemedicine.diseaseMolecular biologyPedigreeChild PreschoolEar InnerFemaleUsher SyndromesFluorescence in situ hybridizationHuman molecular genetics
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A very mild phenotype of Charcot-Marie-Tooth disease type 4H caused by two novel mutations in FGD4

2019

Abstract Background Mutations in the FGD4 gene cause an autosomal recessive demyelinating peripheral neuropathy referred to as CMT4H, characterized by its onset in infancy or early-childhood and its slow progression. Methods The clinical and genetic status of two patients with CMT4H was studied, performing genetic testing with a panel of genes and analysing FGD4 mRNA expression by quantitative PCR. Results Two novel FGD4 variants (c.514delG and c.2211dupA) were identified in two mildly affected Spanish siblings with CMT4H, and with disease onset in late adolescence/adulthood (one of them remaining asymptomatic at 20). On examination, foot deformity was observed without weakness or sensory i…

MaleCharcot-Marie-ToothPathologymedicine.medical_specialtyAdolescentFGD4medicine.disease_causeAsymptomaticYoung Adult03 medical and health sciences0302 clinical medicineCharcot-Marie-Tooth DiseaseCharcot-Marie-Tooth disease type 4HCMT4HmedicineHumans030212 general & internal medicineAlleleFrameshift MutationGeneAllelesGenetic testingMutationmedicine.diagnostic_testbusiness.industrySiblingsCMTMicrofilament Proteinsmedicine.diseasePhenotypePedigreeNeuropathyPhenotypePeripheral neuropathyNeurologyFemaleNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgeryJournal of the Neurological Sciences
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X-linked primary ciliary dyskinesia due to mutations in the cytoplasmic axonemal dynein assembly factor PIH1D3

2017

By moving essential body fluids and molecules, motile cilia and flagella govern respiratory mucociliary clearance, laterality determination and the transport of gametes and cerebrospinal fluid. Primary ciliary dyskinesia (PCD) is an autosomal recessive disorder frequently caused by non-assembly of dynein arm motors into cilia and flagella axonemes. Before their import into cilia and flagella, multi-subunit axonemal dynein arms are thought to be stabilized and pre-assembled in the cytoplasm through a DNAAF2–DNAAF4–HSP90 complex akin to the HSP90 co-chaperone R2TP complex. Here, we demonstrate that large genomic deletions as well as point mutations involving PIH1D3 are responsible for an X-li…

MaleCytoplasmProtein FoldingAxoneme[SDV]Life Sciences [q-bio][SDV.GEN] Life Sciences [q-bio]/Genetics[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractouterGenes X-LinkedChilddefectsPhylogenyZebrafisharmsSequence DeletionvariantsIntracellular Signaling Peptides and ProteinsGenetic Diseases X-LinkedPedigreeMultidisciplinary Sciences[SDV] Life Sciences [q-bio]motilityChild PreschoolMicrotubule ProteinsSperm MotilityScience & Technology - Other TopicsFemaleAdultAdolescentinnerUK10K Rare Groupr2tp complexof-function mutationsArticleMicroscopy Electron TransmissionMD MultidisciplinaryExome SequencingAnimalsHumansPoint MutationCiliaHSP90 Heat-Shock Proteins[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyKartagener SyndromeInfant NewbornAxonemal DyneinsDisease Models AnimalHEK293 Cells[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractidentifies mutationsproteinApoptosis Regulatory ProteinsSequence AlignmentMolecular ChaperonesNature Communications
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High Variability of Fabry Disease Manifestations in an Extended Italian Family

2015

Fabry disease (FD) is an inherited metabolic disorder caused by partial or full inactivation of the lysosomal hydrolaseα-galactosidase A (α-GAL). The impairment ofα-GAL results in the accumulation of undegraded glycosphingolipids in lysosomes and subsequent cell and microvascular dysfunctions. This study reports the clinical, biochemical, and molecular characterization of 15 members of the same family. Eight members showed the exonic mutation M51I in the GLA gene, a disease-causing mutation associated with the atypical phenotype. The clinical history of this family highlights a wide phenotypic variability, in terms of involved organs and severity. The phenotypic variability of two male pati…

MaleDNA Mutational AnalysisFamilial Mediterranean feverlcsh:Medicinemedicine.disease_causePathogenesis0302 clinical medicineSettore BIO/13 - Biologia ApplicataFabry disease; GLA gene; LysoGb3glaFabry diseaseexonic mutation M51IGenetics0303 health sciencesMutationMetabolic disorderGeneral MedicineMiddle AgedPedigree3. Good healthItalyFemalemedicine.symptomResearch ArticleAdultArticle SubjectMolecular Sequence DataBiologyAsymptomaticGeneral Biochemistry Genetics and Molecular BiologyYoung Adult03 medical and health sciencesmedicineHumansFamilyGLA gene030304 developmental biologyfabry diseaseAlpha-galactosidaseBase SequenceGeneral Immunology and MicrobiologyMultiple sclerosislcsh:RLysoGb3medicine.diseaseFabry diseasealpha-GalactosidaseImmunologybiology.protein030217 neurology & neurosurgeryBioMed Research International
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SPG10 is a rare cause of spastic paraplegia in European families.

2008

Contains fulltext : 71099.pdf (Publisher’s version ) (Closed access) BACKGROUND: SPG10 is an autosomal dominant form of hereditary spastic paraplegia (HSP), which is caused by mutations in the neural kinesin heavy chain KIF5A gene, the neuronal motor of fast anterograde axonal transport. Only four mutations have been identified to date. OBJECTIVE: To determine the frequency of SPG10 in European families with HSP and to specify the SPG10 phenotype. PATIENTS AND METHODS: 80 index patients from families with autosomal dominant HSP were investigated for SPG10 mutations by direct sequencing of the KIF5A motor domain. Additionally, the whole gene was sequenced in 20 of these families. RESULTS: Th…

MaleDNA Mutational AnalysisKinesinsHEREDITARYmedicine.disease_cause0302 clinical medicineSpasticPerception and Action [DCN 1]Missense mutationKIF5AAge of OnsetChildFrameshift MutationMUTATIONGenes DominantGeneticsNeurologic Examination0303 health sciencesMutationSplice site mutationSITEExonsMiddle AgedAnterograde axonal transport3. Good healthPedigreeEuropePsychiatry and Mental healthPhenotypeATAXIASChild PreschoolFemaleChromosome DeletionMOTORFunctional Neurogenomics [DCN 2]AdultNeuromuscular diseaseGenotypeHereditary spastic paraplegiaMutation Missense03 medical and health sciencesCognitive neurosciences [UMCN 3.2]medicineHumansGait Disorders Neurologic030304 developmental biologyChromosome Aberrationsbusiness.industrySpastic Paraplegia HereditarySequence Analysis DNAmedicine.diseaseGENEPeripheral neuropathyGenetics PopulationSurgeryNeurology (clinical)RNA Splice Sitesbusiness030217 neurology & neurosurgeryJournal of neurology, neurosurgery, and psychiatry
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Deficient membrane integration of the novel p.N14D-GJB2mutant associated with non-syndromic hearing impairment

2006

Mutations in GJB2, the gene encoding for the Gap Junction protein Connexin 26 (Cx26), have been established as the major cause of hereditary, non-syndromic hearing impairment (HI). We report here the identification of a novel point mutation in GJB2, c.40A>G [p.N14D], detected in compound heterozygosity with the c.35delG mutation in two brothers with moderate non-syndromic sensorineural HI. The mother who carried one wildtype and a p.N14D allele displayed normal hearing. The mutation leads to substitution of the neutral amino acid asparagine (N) by the negatively charged aspartic acid (D) at amino acid number 14, a position that is conserved among Cx26 of different organisms and among many o…

MaleDNA Mutational AnalysisMutantGene ExpressionConnexinIn Vitro TechniquesBiologymedicine.disease_causeCompound heterozygosityConnexinsXenopus laevisAspartic acidotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCloning MolecularChildHearing LossGenetics (clinical)chemistry.chemical_classificationMutationPoint mutationCell MembraneWild typeGap JunctionsMolecular biologyPedigreeAmino acidConnexin 26Protein TransportchemistryChild PreschoolAntigens SurfaceMutationOocytesHuman Mutation
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Mutations in a new gene, encoding a zinc-finger protein, cause tricho-rhino-phalangeal syndrome type I

1999

Tricho-rhino-phalangeal syndrome type I (TRPS I, MIM 190350) is a malformation syndrome characterized by craniofacial and skeletal abnormalities and is inherited in an autosomal dominant manner. TRPS I patients have sparse scalp hair, a bulbous tip of the nose, a long flat philtrum, a thin upper vermilion border and protruding ears. Skeletal abnormalities include cone-shaped epiphyses at the phalanges, hip malformations and short stature. We assigned TRPS1 to human chromosome 8q24. It maps proximal of EXT1, which is affected in a subgroup of patients with multiple cartilaginous exostoses and deleted in all patients with TRPS type II (TRPS II, or Langer-Giedion syndrome, MIM 150230; ref.2-5)…

MaleDNA Complementaryanimal structuresLanger-Giedion SyndromeMolecular Sequence DataBiologyLanger–Giedion syndromeOpen Reading FramesTRPS1 geneotorhinolaryngologic diseasesGeneticsmedicineTricho–rhino–phalangeal syndromeHumansGeneZinc fingerGeneticsSyndrome typeChromosome MappingZinc Fingersmedicine.diseaseBlotting NorthernPedigreeTrichorhinophalangeal syndromeMutationTrichorhinophalangeal Syndrome Type IFemaleChromosomes Human Pair 8Nature genetics
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Biallelic pathogenic variants in the lanosterol synthase gene LSS involved in the cholesterol biosynthesis cause alopecia with intellectual disabilit…

2019

International audience; Purpose Lanosterol synthase (LSS) gene was initially described in families with extensive congenital cataracts. Recently, a study has highlighted LSS associated with hypotrichosis simplex. We expanded the phenotypic spectrum of LSS to a recessive neuroectodermal syndrome formerly named alopecia with mental retardation (APMR) syndrome. It is a rare autosomal recessive condition characterized by hypotrichosis and intellectual disability (ID) or developmental delay (DD), frequently associated with early-onset epilepsy and other dermatological features. Methods Through a multicenter international collaborative study, we identified LSS pathogenic variants in APMR individu…

MaleDevelopmental DisabilitiesIntellectual disabilitycholesterol pathwayWhole Exome Sequencingchemistry.chemical_compoundMissense mutationAge of OnsetChildIntramolecular TransferasesGenetics (clinical)Exome sequencingGeneticsSanger sequencing0303 health sciencesbiologyLanosterol030305 genetics & heredityLSS3. Good healthPedigreeCholesterolPhenotypeintellectual disabilityChild PreschoolAllelic ImbalanceCongenital cataractssymbolsFemaleSqualeneearly-onset epileptic encephalopathy03 medical and health sciencessymbols.namesakeLanosterolCholesterol pathwayExome SequencingmedicineHumans030304 developmental biologyEpilepsyInfantAlopeciaalopeciamedicine.diseaseEarly-onset epileptic encephalopathychemistryMutationbiology.proteinHypotrichosis[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology[SDV.MHEP.DERM]Life Sciences [q-bio]/Human health and pathology/DermatologyLanosterol synthase
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Two Cases of Thyroid Dysgenesis Caused by Different Novel PAX8 Mutations in the DNA-Binding Region: In Vitro Studies Reveal Different Pathogenic Mech…

2013

Mutations in PAX8, a transcription factor gene, cause thyroid dysgenesis (TD). The extreme variability of the thyroid phenotype makes it difficult to identify individuals harboring PAX8 gene mutations. Here we describe two patients with TD and report two novel PAX8 gene mutations (S54R and R133Q). We performed in vitro studies to functionally characterize these mutations.Using PAX8 expression vectors, we investigated whether the PAX8 mutants localized correctly to the nucleus. To analyze the DNA-binding properties of S54R and R133Q, electrophoretic mobility shift assays were performed. Furthermore, we measured whether the mutant PAX8 proteins were able to activate the thyroglobulin (TG)- an…

MaleEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMutantGene mutationBiologyThyroid dysgenesisPAX8 Transcription Factorchemistry.chemical_compoundEndocrinologyThyroid peroxidaseCongenital HypothyroidismmedicineHumansPaired Box Transcription FactorsChildGeneticsOriginal StudiesThyroid Dysfunction: Hypothyroidism Thyrotoxicosis and Thyroid Function TestsInfant Newbornmedicine.diseasePhenotypePedigreechemistryChild PreschoolThyroid Dysgenesisbiology.proteinFemaleThyroglobulinPAX8DNAThyroid
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