Search results for "Heterozygosity"

showing 10 items of 150 documents

Autosomal recessive mutations inTHOC6cause intellectual disability: syndrome delineation requiring forward and reverse phenotyping

2016

THOC6 is a part of the THO complex, which is involved in coordinating mRNA processing with export. The THO complex interacts with additional components to form the larger TREX complex (transcription export complex). Previously, a homozygous missense mutation in THOC6 in the Hutterite population was reported in association with syndromic intellectual disability. Using exome sequencing, we identified three unrelated patients with bi-allelic mutations in THOC6 associated with intellectual disability and additional clinical features. Two of the patients were compound heterozygous for a stop and a missense mutation, and the third was homozygous for a missense mutation; the missense mutations wer…

0301 basic medicineGeneticseducation.field_of_studyMicrocephalybusiness.industryPopulationTranscription export complex030105 genetics & heredityCompound heterozygositymedicine.disease03 medical and health sciences030104 developmental biologyIntellectual disabilityGeneticsMedicineMissense mutationbusinesseducationExomeGenetics (clinical)Exome sequencingClinical Genetics
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An improved genome assembly uncovers prolific tandem repeats in Atlantic cod

2016

AbstractBackground: The first Atlantic cod (Gadus morhua) genome assembly published in 2011 was one of the early genome assemblies exclusively based on high-throughput 454 pyrosequencing. Since then, rapid advances in sequencing technologies have led to a multitude of assemblies generated for complex genomes, although many of these are of a fragmented nature with a significant fraction of bases in gaps. The development of long-read sequencing and improved software now enable the generation of more contiguous genome assemblies.Results: By combining data from Illumina, 454 and the longer PacBio sequencing technologies, as well as integrating the results of multiple assembly programs, we have …

0301 basic medicineHeterozygoteAssembly algorithmsSequence assemblyGenomicsRepetitive DNABiologyGenome03 medical and health sciences0302 clinical medicineAssembly consolidationTandem repeatIndel polymorphismGeneticsAnimalsGadusLong-read sequencing technologyPromoter Regions GeneticMicrosatellitesRepeated sequenceGenePacBioGeneticsHeterozygosityDinucleotide repeatsMolecular Sequence AnnotationGenomicsSequence Analysis DNAbiology.organism_classification030104 developmental biologyGadus morhuaTandem Repeat SequencesEvolutionary biologyPyrosequencingAtlantic cod030217 neurology & neurosurgeryResearch ArticleBiotechnology
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Biallelic variants in LARS2 and KARS cause deafness and (ovario)leukodystrophy

2019

Supplemental Digital Content is available in the text.

0301 basic medicineLysine-tRNA LigaseMalePathologyMagnetic Resonance SpectroscopyMedizinmembrane proteins030204 cardiovascular system & hematologyMitochondrionDeafnessmedicine.disease_causeCompound heterozygosityCorrectionsLeukoencephalopathyMyelin0302 clinical medicineCytosolLeukoencephalopathies030212 general & internal medicineOvarian DiseasesTransfer RNA AminoacylationChildZebrafishMUTATIONExome sequencing10012MutationBrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineMiddle AgedDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]Magnetic Resonance ImagingMitochondriaProtein Transportendoplasmic reticulummedicine.anatomical_structureChild PreschoolTransfer RNAComputingMethodologies_DOCUMENTANDTEXTPROCESSING/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Biological AssayFemaleWRBRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Adultcardiomyopathiesmedicine.medical_specialtyMitochondrial diseaseAminoacylationMuscle disorderBiologyArticleMEDIATES INSERTIONAmino Acyl-tRNA Synthetases03 medical and health sciencesSDG 3 - Good Health and Well-beingmedicineAnimalsPoint MutationHumansAmino Acid SequenceAlleleAllelesCOMPLEXGenetic heterogeneitybusiness.industryArsenite Transporting ATPasesLeukodystrophyGenetic Variation10090Original ArticlesZebrafish Proteinsbiology.organism_classificationDILATED CARDIOMYOPATHYmedicine.diseasezebrafishGENEMolecular biologyDisease Models Animal030104 developmental biologyMembrane protein[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics10084Neurology (clinical)Transfer RNA AminoacylationMEMBRANEbusinessSequence Alignment030217 neurology & neurosurgeryexomeNeurology
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INTU -related oral-facial-digital syndrome type VI: a confirmatory report

2018

Oral-facial-digital (OFD) syndromes are a subgroup of ciliopathies distinguished by the co-occurrence of hamartomas and/or multiple frenula of the oral region and digital anomalies. Several clinical forms of OFD syndromes are distinguished by their associated anomalies and/or inheritance patterns, and at least 20 genetic types of OFD syndromes have been delineated. We describe here a child with preaxial and postaxial polydactyly, lingual hamartoma, a congenital heart defect, delayed development and cerebellar peduncles displaying the molar tooth sign. Whole-exome sequencing and SNP array identified compound heterozygous variants in the INTU gene, which encodes a protein involved in the posi…

0301 basic medicineMalePathologymedicine.medical_specialtyCiliary basal bodyCompound heterozygosityCiliopathies03 medical and health sciencesIntraflagellar transportCPLANEGeneticsmedicineInheritance PatternsHamartomaHumansINTU[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)business.industryInfant NewbornInfantMembrane ProteinsOrofaciodigital Syndromesmedicine.diseasePhenotypeMagnetic Resonance ImagingCytoskeletal Proteins030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNGSoral-facial-digital syndromebusinessSNP array
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Autosomal recessive variations of TBX6 , from congenital scoliosis to spondylocostal dysostosis

2017

International audience; Proximal 16p11.2 microdeletions are recurrent microdeletions with an overall prevalence of 0.03%. In patients with segmentation defects of the vertebra (SDV), a burden of this microdeletion was observed with TBX6 as a candidate gene for SDV. In a published cohort of patients with congenital scoliosis (CS), TBX6 haploinsufficiency was compound heterozygous with a common haplotype. Besides, a single three-generation family with spondylocostal dysostosis (SCD) was reported with a heterozygous stop-loss of TBX6. These observations questioned both on the inheritance mode and on the variable expressivity associated with TBX6-associated SDV. Based on a national recruitment …

0301 basic medicineMalePediatricsmedicine.medical_specialtyCandidate geneGenotypeScoliosis030105 genetics & heredityCompound heterozygosity03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineInheritance ModeMissense mutationHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildGenetics (clinical)GeneticsHernia Diaphragmaticbusiness.industryHaplotypeInfantmedicine.diseaseSpondylocostal dysostosisSpine3. Good healthPedigree030104 developmental biologyHaplotypesScoliosisChild PreschoolMutationFemalebusinessHaploinsufficiencyT-Box Domain Proteins[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Genome-wide diversity and runs of homozygosity in the “Braque Français, type Pyrénées” dog breed

2018

Objective Braque Français, type Pyrénées is a French hunting-dog breed whose origin is traced back to old pointing gun-dogs used to assist hunters in finding and retrieving game. This breed is popular in France, but seldom seen elsewhere. Despite the ancient background, the literature on its genetic characterization is surprisingly scarce. A recent study looked into the demography and inbreeding using pedigree records, but there is yet no report on the use of molecular markers in this breed. The aim of this work was to genotype a population of Braque Français, type Pyrénées dogs with the high-density SNP array to study the genomic diversity of the breed. Results The average observed (\docum…

0301 basic medicineMalelcsh:MedicineRuns of HomozygosityGenetic diversitySettore AGR/17 - Zootecnica Generale E Miglioramento Geneticotype PyrénéesSNPGenetic diversityMolecular markersInbreedingRuns of homozygosityHeterozygosityEffective population sizeDogInbreedingDogBraque Français type PyrénéesSNPGenetic diversityMolecular markersInbreedingRuns of homozygosityHeterozygositylcsh:QH301-705.5education.field_of_studyHeterozygosityGenomeHomozygote04 agricultural and veterinary sciencesGeneral Medicinetype PyrénéesBraque Français type PyrénéesBreedResearch NoteFemaleFranceInbreedingSNP arrayGenetic MarkersHeterozygotePopulationSNPBiologyRuns of homozygosityPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesDogsAnimalsGenetic variabilityeducationlcsh:Science (General)Genetic diversityDogBraque Françaislcsh:R0402 animal and dairy sciencebraque françaisMolecular markersGenetic Variation040201 dairy & animal science030104 developmental biologylcsh:Biology (General)Evolutionary biologyDog Braque Français type Pyrénées SNP Genetic diversity Molecular markers Inbreeding Runs of homozygosity Heterozygositylcsh:Q1-390BMC Research Notes
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Confirmation of PDZD7 as a Nonsyndromic Hearing Loss Gene.

2016

Objective PDZD7 was identified in 2009 in a family with apparent nonsyndromic sensorineural hearing loss. However, subsequent clinical reports have associated PDZD7 with digenic Usher syndrome, the most common cause of deaf-blindness, or as a modifier of retinal disease. No further reports have validated this gene for nonsyndromic hearing loss, intuitively calling correct genotype-phenotype association into question. This report describes a validating second case for biallelic mutations in PDZD7 causing nonsyndromic mild to severe sensorineural hearing loss. It also provides detailed audiometric and ophthalmologic data excluding Usher syndrome in both the present proband (proband 1) and the…

0301 basic medicineProbandMalemedicine.medical_specialtyHeterozygoteAdolescentHearing lossUsher syndromeHearing Loss SensorineuralOtoacoustic Emissions SpontaneousAudiologyCompound heterozygosity03 medical and health sciencesSpeech and Hearing0302 clinical medicineotorhinolaryngologic diseasesmedicineEvoked Potentials Auditory Brain StemHumansGenetic Predisposition to DiseaseChildAllelesmedicine.diagnostic_testbusiness.industryAudiogramSequence Analysis DNAmedicine.diseaseMinor allele frequency030104 developmental biologyOtorhinolaryngologyMutationAudiometry Pure-ToneSensorineural hearing lossFemaleAudiometrymedicine.symptombusinessCarrier Proteins030217 neurology & neurosurgeryEar and hearing
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CLINICAL CHARACTERISTICS AND PLASMA LIPIDS IN SUBJECTS WITH FAMILIAL COMBINED HYPOLIPIDEMIA: A POOLED ANALYSIS

2013

Background. Angiopoietin-like 3 (ANGPTL3) regulates lipoprotein metabolism by modulating extracellular lipases. Loss-of function mutations in ANGPTL3 gene cause familial combined hypolipidemia (FHBL2). The mode of inheritance and hepatic and vascular consequences of FHBL2 have not been fully elucidated. To get further insights on these aspects, we re-evaluated the clinical and the biochemical characteristics of all reported cases of FHBL2. Methods and Results. One hundred fteen FHBL2 individuals carrying 13 different mutations in the ANGPTL3 gene (14 homozygotes, 8 compound heterozygotes and 93 heterozygotes) and 402 controls were considered. Carriers of 2 mutant alleles had undetectable pl…

ANGPTL3 mutations; angiopoietin-like 3; cardiovascular disease; diabetes mellitus; fatty liverSettore MED/09 - Medicina InternaCompound heterozygosityBiochemistryCohort StudiesHypobetalipoproteinemiasEndocrinologyANGPTL3cardiovascular diseaseGenotypeChildLipoproteinclinical characteristicsAged 80 and overbiologydiabetes mellituFatty liverHomozygoteLipoprotein(a)Middle AgedANGPTL3 mutationLipidsCardiovascular Diseasesdiabetes mellitusANGPTL3 Familial combined hypolipidemia LipoproteinAdultmedicine.medical_specialtyHeterozygoteANGPTL3; Familial combined hypolipidemia; clinical characteristicsAdolescentEvinacumabQD415-436Young AdultDiabetes mellitusInternal medicinemedicineHumansANGPTL3 mutationsAlleleFamilial combined hypolipidemiaAgedAngiopoietin-Like Protein 3fatty liverangiopoietin-like 3Cell Biologymedicine.diseaseEndocrinologyAngiopoietin-like ProteinsGene Expression RegulationMutationbiology.proteinPatient-Oriented and Epidemiological ResearchAngiopoietinsLipoproteinLipoprotein(a)
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Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC-PGL syndromes: a clinicopathological and m…

2014

ObjectiveAlthough the succinate dehydrogenase (SDH)-related tumor spectrum has been recently expanded, there are only rare reports of non-pheochromocytoma/paraganglioma tumors in SDHx-mutated patients. Therefore, questions still remain unresolved concerning the aforementioned tumors with regard to their pathogenesis, clinicopathological phenotype, and even causal relatedness to SDHx mutations. Absence of SDHB expression in tumors derived from tissues susceptible to SDH deficiency is not fully elucidated.Design and methodsThree unrelated SDHD patients, two with pituitary adenoma (PA) and one with papillary thyroid carcinoma (PTC), and three SDHB patients affected by renal cell carcinomas (RC…

AdenomaAdultMalemedicine.medical_specialtyPathologySDHBEndocrinology Diabetes and MetabolismSDHALoss of HeterozygosityBiologyPheochromocytomaLoss of heterozygosityEndocrinologyParagangliomaInternal medicinemedicineHumansPituitary NeoplasmsThyroid NeoplasmsCarcinoma Renal CellGerm-Line MutationCarcinomaGeneral MedicineExonsMiddle Agedmedicine.diseaseNeuroblastic TumorCarcinoma Papillary3. Good healthNeoplasm ProteinsSuccinate DehydrogenaseEndocrinologyThyroid Cancer PapillaryMutationFemaleSDHDClear cellGene DeletionEuropean Journal of Endocrinology
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Multiple endocrine neoplasia type 1 gene expression is normal in sporadic adrenocortical tumors.

2000

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disorder with neoplasia of the anterior pituitary, the parathyroid, the endocrine pancreas and other endocrine tissues including the adrenal cortex. The tumor-suppressor gene causing this disease was identified at the gene locus 11q13. We recently reported that adrenocortical carcinomas frequently show loss of heterozygosity (LOH) of 11q13, but do not contain point mutations within the MEN1-coding region. To investigate whether reduced gene expression (for example by mutations within the MEN1 promoter) may contribute to the tumorigenesis of sporadic adrenocortical tumors, 24 adrenocortical specimen were studied by Northern …

Adenomamedicine.medical_specialtyCandidate geneendocrine system diseasesHydrocortisoneEndocrinology Diabetes and MetabolismGene ExpressionLoss of HeterozygosityBiologyLoss of heterozygosityEndocrinologyReference ValuesInternal medicineGene expressionAdrenal GlandsmedicineMultiple Endocrine Neoplasia Type 1Adrenocortical carcinomaHumansMEN1Northern blotRNA MessengerMultiple endocrine neoplasiaAldosteroneAdrenal cortexCarcinomaGeneral Medicinemedicine.diseaseAdrenal Cortex Neoplasmsmedicine.anatomical_structureEndocrinologyCancer researchEuropean journal of endocrinology
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