Search results for "030305 genetics & heredity"

showing 10 items of 50 documents

Evaluation of DNA Methylation Episignatures for Diagnosis and Phenotype Correlations in 42 Mendelian Neurodevelopmental Disorders

2020

Contains fulltext : 218274.pdf (Publisher’s version ) (Closed access) Genetic syndromes frequently present with overlapping clinical features and inconclusive or ambiguous genetic findings which can confound accurate diagnosis and clinical management. An expanding number of genetic syndromes have been shown to have unique genomic DNA methylation patterns (called "episignatures"). Peripheral blood episignatures can be used for diagnostic testing as well as for the interpretation of ambiguous genetic test results. We present here an approach to episignature mapping in 42 genetic syndromes, which has allowed the identification of 34 robust disease-specific episignatures. We examine emerging pa…

0301 basic medicine[SDV]Life Sciences [q-bio]Computational biology030105 genetics & heredityBiologyPediatricsArticleCohort Studiesmolecular diagnostics03 medical and health sciencessymbols.namesakeGenetic HeterogeneityGene duplicationGeneticsHumansHunter-McAlpine syndromeGenetics (clinical)Mass screening030304 developmental biologyEpiSignGenetics0303 health sciencesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]DNA methylationGenetic heterogeneity030305 genetics & heredityCorrectionSyndromeDNA MethylationMolecular diagnosticsPhenotypePenetranceHuman genetics3. Good healthepisignaturegenomic DNA030104 developmental biologyPhenotypeNeurodevelopmental DisordersDNA methylationuncertain clinical casesMendelian inheritancesymbolsIdentification (biology)VUS classification
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Visualizing Human Protein‐Protein Interactions and Subcellular Localizations on Cell Images Through CellMap

2020

Visualizing protein data remains a challenging and stimulating task. Useful and intuitive visualization tools may help advance biomolecular and medical research; unintuitive tools may bar important breakthroughs. This protocol describes two use cases for the CellMap (http://cellmap.protein.properties) web tool. The tool allows researchers to visualize human protein-protein interaction data constrained by protein subcellular localizations. In the simplest form, proteins are visualized on cell images that also show protein-protein interactions (PPIs) through lines (edges) connecting the proteins across the compartments. At a glance, this simultaneously highlights spatial constraints that prot…

0303 health sciencesgenetic structuresComputer scienceCells030305 genetics & heredityProteinsA proteinComputational biologyBiochemistryWeb toolProtein subcellular localization predictionVisualizationProtein–protein interaction03 medical and health sciencesImaging Three-DimensionalStructural BiologyProtein Interaction MappingHumansProtocol (object-oriented programming)SoftwareSubcellular Fractions030304 developmental biologyCurrent Protocols in Bioinformatics
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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Not All Floating-Harbor Syndrome Cases are Due to Mutations in Exon 34 of SRCAP

2013

International audience; Floating-Harbor syndrome (FHS) is a rare disorder characterized by short stature, delayed bone age, speech delay, and dysmorphic facial features. We report here the molecular analysis of nine cases, fulfilling the diagnostic criteria for FHS. Using exome sequencing, we identified SRCAP as the disease gene in two cases and subsequently found SRCAP truncating mutations in 6/9 cases. All mutations occurred de novo and were located in exon 34, in accordance with the recent report of Hood et al. However, the absence of SRCAP mutations in 3/9 cases supported genetic heterogeneity of FH syndrome. Importantly, no major clinical differences were observed supporting clinical h…

AdultHeart Septal Defects VentricularMaleDNA Mutational AnalysisBiologyShort statureCraniofacial Abnormalitiesgenetic heterogeneity03 medical and health sciencesExonGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildFloating-Harbor syndromeGenetics (clinical)Exome sequencingGrowth Disorders030304 developmental biologyDisease geneGeneticsAdenosine Triphosphatases0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsGenetic heterogeneity030305 genetics & heredityBone ageExonsmedicine.diseaseSRCAP3. Good healthFloating–Harbor syndromeSpeech delayMutationFemalemedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Mutation spectrum and clinical investigation of achromatopsia patients with mutations in the GNAT2 gene

2019

Achromatopsia (ACHM) is a hereditary cone photoreceptor disorder characterized by the inability to discriminate colors, nystagmus, photophobia, and low-visual acuity. Six genes have been associated with this rare autosomal recessively inherited disease, including the GNAT2 gene encoding the catalytic α-subunit of the G-protein transducin which is expressed in the cone photoreceptor outer segment. Out of a cohort of 1,116 independent families diagnosed with a primary clinical diagnosis of ACHM, we identified 23 patients with ACHM from 19 independent families with likely causative mutations in GNAT2, representing 1.7% of our large ACHM cohort. In total 22 different potentially disease-causing…

AdultMaleAchromatopsiagenetic structuresAdolescentChild preschoolDNA Copy Number VariationsColor Vision DefectsBiologymedicine.disease_causeHeterotrimeric GTP-Binding Proteins/genetics03 medical and health sciencesExonGene duplicationGeneticsmedicineHumansGenetic Predisposition to DiseaseCopy-number variationColor Vision Defects/geneticsChildGenetics (clinical)030304 developmental biologyAgedGenetics0303 health sciencesGNAT2MutationSettore MED/30 - Malattie Apparato Visivo030305 genetics & heredityBreakpointInfantSequence Analysis DNAExonsMiddle Agedmedicine.diseaseHeterotrimeric GTP-Binding ProteinsPhotoreceptor outer segmenteye diseasesPedigreeSettore BIO/18 - GeneticaSequence Analysis DNA/methodsyoung adultFemalesense organsachromatopsia copy number variations GNAT2 mutations transducinmutation
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Phenotype associated with TAF2 biallelic mutations: a clinical description of four individuals and review of the literature

2021

International audience; Transcription factor IID is a multimeric protein complex that is essential for the initiation of transcription by RNA polymerase II. One of its critical components, the TATA-binding protein-associated factor 2, is encoded by the gene TAF2. Pathogenic variants of this gene have been shown to be responsible for the Mental retardation, autosomal recessive 40 syndrome. This syndrome is characterized by severe intellectual disability, postnatal microcephaly, pyramidal signs and thin corpus callosum. Until now, only three families have been reported separately. Here we report four individuals, from two unrelated families, who present with severe intellectual disability and…

AdultMaleAdolescentFoot Deformities CongenitalDevelopmental DisabilitiesAutosomal recessiveIntellectual disabilityPostnatal microcephaly[SDV.GEN] Life Sciences [q-bio]/GeneticsBiologyCorpus Callosum03 medical and health sciencesNeurodevelopmental disorderNeurodevelopmental disorderIntellectual disabilityGeneticsmedicineHumansMissense mutationGlobal developmental delayTAF2ChildGeneAllelesGenetics (clinical)Exome sequencing030304 developmental biologyGeneticsTATA-Binding Protein Associated Factors0303 health sciences[SDV.GEN]Life Sciences [q-bio]/Genetics030305 genetics & heredityGeneral Medicinemedicine.diseasePhenotypeChild PreschoolTAF2MicrocephalyFemaleTranscription Factor TFIID
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Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
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Deciphering exome sequencing data: Bringing mitochondrial DNA variants to light

2019

The expanding use of exome sequencing (ES) in diagnosis generates a huge amount of data, including untargeted mitochondrial DNA (mtDNA) sequences. We developed a strategy to deeply study ES data, focusing on the mtDNA genome on a large unspecific cohort to increase diagnostic yield. A targeted bioinformatics pipeline assembled mitochondrial genome from ES data to detect pathogenic mtDNA variants in parallel with the "in-house" nuclear exome pipeline. mtDNA data coming from off-target sequences (indirect sequencing) were extracted from the BAM files in 928 individuals with developmental and/or neurological anomalies. The mtDNA variants were filtered out based on database information, cohort …

AdultMaleMitochondrial DNAAtaxiaAdolescentDevelopmental Disabilities[SDV]Life Sciences [q-bio]BiologyDNA MitochondrialGenomeHaplogroupYoung Adult03 medical and health sciencesExome SequencingGeneticsmedicineHumansChildExomeGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSAged030304 developmental biologyAged 80 and overGenetics0303 health sciences030305 genetics & heredityInfant NewbornComputational BiologyGenetic VariationInfantMiddle AgedPhenotypeEarly DiagnosisChild PreschoolFemaleNervous System Diseasesmedicine.symptom
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Pharmacokinetics, pharmacodynamics, and safety of moss-aGalactosidase A in patients with Fabry disease.

2019

Moss-aGalactosidase A (moss-aGal) is a moss-derived version of human α-galactosidase developed for enzyme replacement therapy in patients with Fabry disease. It exhibits a homogenous N-glycosylation profile with >90% mannose-terminated glycans. In contrast to mammalian cell produced α-galactosidase, moss-aGal does not rely on mannose-6-phosphate receptor mediated endocytosis but targets the mannose receptor for tissue uptake. We conducted a phase 1 clinical trial with moss-aGal in six patients with confirmed diagnosis of Fabry disease during a 28-day schedule. All patients received a single dose of 0.2 mg/kg moss-aGal by i.v.-infusion. Primary endpoints of the trial were safety and pharmaco…

AdultMalePhases of clinical researchPharmacologyExcretion03 medical and health sciencesPharmacokineticsGermanyGeneticsmedicineHumansEnzyme Replacement TherapyInfusions IntravenousGenetics (clinical)030304 developmental biology0303 health sciencesKidneySphingolipidsbusiness.industry030305 genetics & heredityEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseasemedicine.anatomical_structureTreatment OutcomePharmacodynamicsalpha-GalactosidaseFabry DiseaseFemaleGlycolipidsbusinessMannose receptorJournal of inherited metabolic disease
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De novo 15q21.1q21.2 deletion identified through FBN1 MLPA and refined by 244K array-CGH in a female teenager with incomplete Marfan syndrome

2010

International audience; Interstitial deletions involving the 15q21.1 band are very rare. Only 4 of these cases have been studied using molecular cytogenetic techniques in order to confirm the deletion of the whole FBN1 gene. The presence of clinical features of the Marfan syndrome (MFS) spectrum associated with mental retardation has been described in only 2/4 patients. Here we report on a 16-year-old female referred for suspicion of MFS (positive thumb and wrist sign, scoliosis, joint hyperlaxity, high-arched palate with dental crowding, dysmorphism, mitral insufficiency with dystrophic valve, striae). She had therefore 3 minor criteria according to the Ghent nosology. She also had speech …

AdultMalemusculoskeletal diseasesProbandMarfan syndromecongenital hereditary and neonatal diseases and abnormalitiesAdolescent[SDV]Life Sciences [q-bio]Fibrillin-1BiologyFibrillinsBioinformaticsPolymerase Chain ReactionMarfan SyndromeLoss of heterozygosity03 medical and health sciencesTransforming Growth Factor betaIntellectual DisabilityGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationAlleleChildGeneIn Situ Hybridization FluorescenceGenetics (clinical)Oligonucleotide Array Sequence AnalysisSequence Deletion030304 developmental biologyGeneticsChromosomes Human Pair 15Comparative Genomic Hybridization0303 health sciencesMicrofilament Proteins030305 genetics & heredityGeneral Medicinemedicine.diseasePedigree3. Good healthPhenotypeMutationMicrosatelliteFemaleDNA ProbesHaploinsufficiencyMicrosatellite RepeatsEuropean Journal of Medical Genetics
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