Search results for "Heredity"

showing 10 items of 247 documents

Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits

2020

The genetic background of childhood body mass index (BMI), and the extent to which the well-known associations of childhood BMI with adult diseases are explained by shared genetic factors, are largely unknown. We performed a genome-wide association study meta-analysis of BMI in 61,111 children aged between 2 and 10 years. Twenty-five independent loci reached genome-wide significance in the combined discovery and replication analyses. Two of these, located nearNEDD4LandSLC45A3, have not previously been reported in relation to either childhood or adult BMI. Positive genetic correlations of childhood BMI with birth weight and adult BMI, waist-to-hip ratio, diastolic blood pressure and type 2 d…

MaleGenetic-variationNedd4 Ubiquitin Protein LigasesPooled AnalysisBlood Pressure0302 clinical medicineHuman geneticsMendelian RandomizationYoung adultChildhealth care economics and organizationsBody mass indexAdiposityGenetics & Heredity0303 health sciencesStatistics1184 Genetics developmental biology physiologyGenomicsadulto3. Good healthCardiovascular DiseasesChild PreschoolPhysical SciencesMenarchegenetic-variationpresión sanguíneaMonosaccharide Transport ProteinsGenetic locieducationenfermedades cardiovascularesProstate-specific AntigenGenetic correlation03 medical and health sciencesSDG 3 - Good Health and Well-beingDiabetes MellitusGeneticsHumansprostate-specific antigenStatistical MethodsMolecular BiologyEcology Evolution Behavior and Systematicschildhood0604 Genetics[SDV.GEN]Life Sciences [q-bio]/GeneticsScience & TechnologyEarly Growth Genetics ConsortiumBiology and Life SciencesComputational Biologynutritional and metabolic diseasesSingle nucleotide polymorphismsMendelian Randomization AnalysisBiological TissueDiabetes Mellitus Type 2estudio de asociación genómica completagenetic factorsmendelian randomizationanálisis de la aleatorización mendelianaproteínas de transporte de monosacáridosBody mass index030217 neurology & neurosurgeryMathematicsDemographyDevelopmental BiologyCardiovascular RiskCancer ResearchobesityPhysiologyhumanosadolescenteOverweightQH426-470Genome-wide association studiesWaist–hip ratioMathematical and Statistical TechniquesMedicine and Health Sciencesbody mass index (BMI)Genetics of diseaseGenetics (clinical)2. Zero hungeradiposityMetaanalysisPhysiological ParametersConnective Tissue/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemalemedicine.symptomAnatomypooled analysisLife Sciences & BiomedicineResearch ArticleAdultcardiovascular riskAdolescentBirth weightmenarquiaAdipose tissueBiology3121 Internal medicineResearch and Analysis MethodsmedicineoverweightGenetic Predisposition to DiseaseObesity030304 developmental biologyMenarcheWaist-Hip Ratioíndice de masa corporalBody WeightCardiometabolic Risk Factorspredisposición genética a la enfermedadHeritabilityOverweightGenome Analysisyoung-adultsGenome-wide Associationíndice cintura-caderaYoung-adultsgenome-wide associationGenome-Wide Association StudyPLoS genetics
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Signatures of selection in the genome of Swedish warmblood horses selected for sport performance

2019

Abstract Background A growing demand for improved physical skills and mental attitude in modern sport horses has led to strong selection for performance in many warmblood studbooks. The aim of this study was to detect genomic regions with low diversity, and therefore potentially under selection, in Swedish Warmblood horses (SWB) by analysing high-density SNP data. To investigate if such signatures could be the result of selection for equestrian sport performance, we compared our SWB SNP data with those from Exmoor ponies, a horse breed not selected for sport performance traits. Results The genomic scan for homozygous regions identified long runs of homozygosity (ROH) shared by more than 85%…

MaleGenotyping TechniquesPerformanceDIVERSITYBreedingRuns of HomozygosityHorseGenomeHISTORYInbreedingHOMOZYGOSITYGenetics & Heredity0303 health sciencesSnp dataeducation.field_of_studyHomozygoteRUNSASSOCIATIONGenomics04 agricultural and veterinary sciencesBreedDIFFERENTIATIONWarmbloodFemaleLife Sciences & BiomedicineTRAITSResearch ArticleSportsBiotechnologyGENESlcsh:QH426-470lcsh:BiotechnologyPopulationBiologyRuns of homozygosityPolymorphism Single Nucleotide03 medical and health scienceslcsh:TP248.13-248.65GeneticsAnimalsHorsesFunctional studieseducationSelection (genetic algorithm)030304 developmental biologyScience & Technology0402 animal and dairy scienceSelection signature040201 dairy & animal sciencelcsh:GeneticsBiotechnology & Applied MicrobiologyEvolutionary biologyWIDE SCANHaplotype homozygosityBMC Genomics
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NOTCH, a new signaling pathway implicated in holoprosencephaly.

2011

International audience; Genetics of Holoprosencephaly (HPE), a congenital malformation of the developing human forebrain, is due to multiple genetic defects. Most genes that have been implicated in HPE belong to the sonic hedgehog signaling pathway. Here we describe a new candidate gene isolated from array comparative genomic hybridization redundant 6qter deletions, DELTA Like 1 (DLL1), which is a ligand of NOTCH. We show that DLL1 is co-expressed in the developing chick forebrain with Fgf8. By treating chick embryos with a pharmacological inhibitor, we demonstrate that DLL1 interacts with FGF signaling pathway. Moreover, a mutation analysis of DLL1 in HPE patients revealed a three-nucleoti…

MaleMESH: Signal TransductionCandidate gene[SDV.GEN] Life Sciences [q-bio]/GeneticsChick EmbryoMESH: Amino Acid SequenceMESH: Base SequenceHoloprosencephalyMESH: Animals[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Sequence DeletionGenetics0303 health sciencesReceptors NotchMESH: Androstenediols030305 genetics & heredityMESH: Infant NewbornIntracellular Signaling Peptides and ProteinsGeneral MedicineMESH: Sequence DeletionMESH: Chick EmbryoCell biologyembryonic structuresFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MESH: Membrane ProteinsSignal transductionMESH: HoloprosencephalySignal TransductionAdultmusculoskeletal diseasesCell signalingcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresMolecular Sequence DataNotch signaling pathwayMESH: Sequence AlignmentBiologyArticle03 medical and health sciencesFGF8[SDV.BDD] Life Sciences [q-bio]/Development BiologyHoloprosencephalyAndrostenediolsGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequenceMolecular Biology030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Molecular Sequence DataMESH: HumansBase SequenceInfant NewbornMembrane ProteinsMESH: Adultmedicine.diseaseMESH: MaleForebrainMutation testingMESH: Receptors NotchSequence AlignmentMESH: Female
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Identifying Genetic Traces of Historical Expansions: Phoenician Footprints in the Mediterranean

2008

10 páginas, 1 figura, 4 páginas.-- et al.

MaleMediterranean climatePopulation DynamicsPopulationHomelandBiologyPolymorphism Single NucleotideHaplogroup03 medical and health sciencesMediterranean seaGene FrequencyReportEthnicityMediterranean SeaGeneticsHumansAnalytical strategyGenetics(clinical)educationAllelesHistory AncientGenetics (clinical)Historical record030304 developmental biologyGenetics0303 health scienceseducation.field_of_studyChromosomes Human YGeography030305 genetics & heredityEmigration and Immigrationlanguage.human_languageGenealogyGenetics PopulationHaplotypeslanguagePhoenician
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Widening of the genetic and clinical spectrum of Lamb-Shaffer syndrome, a neurodevelopmental disorder due to SOX5 haploinsufficiency

2020

International audience; PURPOSE: Lamb-Shaffer syndrome (LAMSHF) is a neurodevelopmental disorder described in just over two dozen patients with heterozygous genetic alterations involving SOX5, a gene encoding a transcription factor regulating cell fate and differentiation in neurogenesis and other discrete developmental processes. The genetic alterations described so far are mainly microdeletions. The present study was aimed at increasing our understanding of LAMSHF, its clinical and genetic spectrum, and the pathophysiological mechanisms involved.METHODS: Clinical and genetic data were collected through GeneMatcher and clinical or genetic networks for 41 novel patients harboring various ty…

MaleMedizinHaploinsufficiencyL-SOX5VARIANTS0302 clinical medicineNeurodevelopmental disorderIntellectual disabilityMissense mutation2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)GeneticsPediatricGenetics & Heredity0303 health sciencesPedigreeFAMILYDNA-Binding Proteinsdevelopmental delayTRANSCRIPTION FACTORSPhenotypeintellectual disabilityChild Preschoolmissense variantsFemalemissense variants.HaploinsufficiencySOXD Transcription FactorsAdultEXPRESSIONAdolescentIntellectual and Developmental Disabilities (IDD)Clinical SciencesMutation MissenseautismCell fate determinationBiologyLONG FORMSEQUENCEArticle03 medical and health sciencesYoung AdultRare DiseasesClinical ResearchCARTILAGEIntellectual DisabilitymedicineGeneticsAnimalsHumansLanguage Development DisordersGenetic Predisposition to DiseasePreschoolTranscription factorGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMUTATIONSHuman GenomeInfantmedicine.diseaseBrain DisordersNeurodevelopmental DisordersDeciphering Developmental Disorder StudyMutationAutismepilepsyMissense030217 neurology & neurosurgeryGENERATIONGenetics in Medicine
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Muscle-Related Polymorphisms (MSTN rs1805086 and ACTN3 rs1815739) Are Not Associated with Exceptional Longevity in Japanese Centenarians

2016

Myostatin (MSTN) and α-actinin-3 (ACTN3) genes are potentially associated with preservation of muscle mass and oxidative capacity, respectively. To explore the possible role of these genes in exceptional longevity (EL), the allele/genotype frequency distribution of two polymorphisms in MSTN (rs1805086, K153R) and ACTN3 (rs1815739, R577X) was studied in Japanese centenarians of both sexes (n = 742) and healthy controls (n = 814). The rs1805086 R-allele (theoretically associated with muscle mass preservation at the expense of oxidative capacity) was virtually absent in the two groups, where genotype distributions were virtually identical. Likewise, no differences in allele (p = 0.838 (women);…

MaleMetabolic Processes0301 basic medicineAgingHeredityPhysiologyAging and Cancerlcsh:MedicinePolimorfismo genéticoGenética humanaBiochemistry0302 clinical medicineGene FrequencyJapanPolymorphism (computer science)GenotypeMedicine and Health SciencesMorphogenesisActininlcsh:ScienceMusculoskeletal SystemProtein Metabolismmedia_commonGeneticseducation.field_of_studyMultidisciplinaryMusclesCancer Risk FactorsLongevityMuscle DifferentiationGenetic MappingOncologyPopulation SurveillanceFemaleAnatomyResearch ArticleAsian Continental Ancestry Groupmedicine.medical_specialtyGenotypemedia_common.quotation_subjectLongevityAncianoPopulationMuscle TissueVariant GenotypesBiology03 medical and health sciencesAsian PeopleInternal medicineGeneticsmedicineHumansAlleleeducationAllele frequencyAllelesGenetic Association StudiesPolymorphism Geneticlcsh:RBiology and Life SciencesMyostatinGenotype frequencyBiological TissueMetabolism030104 developmental biologyEndocrinologySkeletal MusclesLongevidadlcsh:QPhysiological ProcessesXX GenotypeOrganism Development030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
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Search for genetic factors associated with susceptibility to multiple sclerosis.

2006

Multiple sclerosis (MS) is a cell-mediated autoimmune disease characterized by type-1 cytokine production. Environmental and individual genetic background might influence this response particularly in cytokine gene polymorphisms. We evaluated whether polymorphisms of interleukin (IL)-10, IL-12, and tumor necrosis factor (TNF)-alpha genes, which might play a role in MS pathogenesis, are associated with MS susceptibility. Genotype frequencies for all the analyzed polymorphisms were not differently distributed between cases and controls. It is reasonable to suppose that the cytokine single-nucleotide polymorphisms (SNPs) studied must be considered against a larger genetic background involving …

MaleMultiple Sclerosismedicine.medical_treatmentSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceGene FrequencymedicineSNPHumansGenetic Predisposition to DiseaseGeneticsAutoimmune diseasePolymorphism GeneticTumor Necrosis Factor-alphaGeneral NeuroscienceMultiple sclerosisInterleukinmedicine.diseaseInterleukin-12Genotype frequencyInterleukin-10tumor necrosis factor alpha genetic polymorphism genetic susceptibility genotype heredity human major clinical studyInterleukin 10CytokineCase-Control StudiesImmunologyCytokinesFemaleDisease SusceptibilityAnnals of the New York Academy of Sciences
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The Molecular Genetic Architecture of Self-Employment

2013

Economic variables such as income, education, and occupation are known to affect mortality and morbidity, such as cardiovascular disease, and have also been shown to be partly heritable. However, very little is known about which genes influence economic variables, although these genes may have both a direct and an indirect effect on health. We report results from the first large-scale collaboration that studies the molecular genetic architecture of an economic variable-entrepreneurship-that was operationalized using self-employment, a widely-available proxy. Our results suggest that common SNPs when considered jointly explain about half of the narrow-sense heritability of self-employment es…

MaleNetherlands Twin Register (NTR)Multifactorial InheritanceHeredityEpidemiologyEconomicsIntelligenceTwinsGenome-wide association studyCORONARY HEART-DISEASESocial and Behavioral SciencesTheoreticalMissing heritability problemModelsMISSING HERITABILITYMicroeconomicsTwins DizygoticSOCIOECONOMIC-STATUSRegistriesGenetics0303 health sciencesMultidisciplinaryStatistics05 social sciencesQRGenomicsSingle NucleotideOccupational and Industrial Health/dk/atira/pure/sustainabledevelopmentgoals/decent_work_and_economic_growth3. Good healthCARDIOVASCULAR-DISEASEGenetic EpidemiologyMeta-analysisScience & Technology - Other TopicsMedicineFemalePublic HealthBehavioral and Social Aspects of HealthResearch ArticlePersonalityEmploymentGenotypeClinical Research DesignGeneral Science & Technology515 PsychologyScienceeducationSingle-nucleotide polymorphismBiostatisticsBiologyPolymorphism Single NucleotideMonozygotic03 medical and health sciencesGenome Analysis Tools0502 economics and businessMD MultidisciplinaryGenome-Wide Association StudiesGenetics/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_DizygoticHumansStatistical MethodsHuman heightPolymorphismGENOME-WIDE ASSOCIATIONBiology030304 developmental biologyGenetic associationEDUCATIONAL-ATTAINMENTScience & TechnologyComplex TraitsMULTIDISCIPLINARY SCIENCESComputational BiologyHuman GeneticsSDG 8 - Decent Work and Economic GrowthTwins Monozygoticta3121HeritabilityModels TheoreticalGenetic architectureCOMMON SNPS EXPLAINLARGE PROPORTIONGenetic PolymorphismRISK-FACTORSGene-Environment Interaction3111 BiomedicineMeta-AnalysesHUMAN HEIGHTPopulation GeneticsMathematics050203 business & managementGenome-Wide Association Study
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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