Search results for "VARIATION"

showing 10 items of 2124 documents

Bi-allelic LoF NRROS Variants Impairing Active TGF-β1 Delivery Cause a Severe Infantile-Onset Neurodegenerative Condition with Intracranial Calcifica…

2020

Negative regulator of reactive oxygen species (NRROS) is a leucine-rich repeat-containing protein that uniquely associates with latent transforming growth factor beta-1 (TGF- β1) and anchors it on the cell surface; this anchoring is required for activation of TGF-β1 in macrophages and microglia. We report six individuals from four families with bi-allelic variants in NRROS. All affected individuals had neurodegenerative disease with refractory epilepsy, developmental regression, and reduced white matter volume with delayed myelination. The clinical course in affected individuals began with normal development or mild developmental delay, and the onset of seizures occurred within the first ye…

Male0301 basic medicineInflammationBiologyintracranial calcificationneuroinflammationTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineReportTGF-β1NRROSGeneticsmedicineHumansAllelesGenetics (clinical)NeuroinflammationBrain DiseasesMicrogliaMacrophagesNeurodegenerationneurodegenerationCalcinosisGenetic VariationInfantNeurodegenerative Diseasesmedicine.diseaseNFKB1Latent TGF-beta binding proteinHEK293 Cells030104 developmental biologymedicine.anatomical_structureLatent TGF-beta Binding ProteinsImmunologyKnockout mouseFemaleMicrogliamutationmedicine.symptomDevelopmental regression030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Inheritance patterns of ATCCT repeat interruptions in spinocerebellar ataxia type 10 (SCA10) expansions

2017

Spinocerebellar ataxia type 10 (SCA10), an autosomal dominant cerebellar ataxia disorder, is caused by a non-coding ATTCT microsatellite repeat expansion in the ataxin 10 gene. In a subset of SCA10 families, the 5'-end of the repeat expansion contains a complex sequence of penta- and heptanucleotide interruption motifs which is followed by a pure tract of tandem ATCCT repeats of unknown length at its 3'-end. Intriguingly, expansions that carry these interruption motifs correlate with an epileptic seizure phenotype and are unstable despite the theory that interruptions are expected to stabilize expanded repeats. To examine the apparent contradiction of unstable, interruption-positive SCA10 e…

Male0301 basic medicineMolecular biologyInheritance Patternslcsh:MedicineGene ExpressionArtificial Gene Amplification and ExtensionPolymerase Chain ReactionDatabase and Informatics MethodsSequencing techniquesAutosomal dominant cerebellar ataxiaMedicine and Health SciencesDNA sequencinglcsh:ScienceGeneticsMovement DisordersMultidisciplinaryNeurodegenerative DiseasesGenomicsPedigreePhenotypeNeurologyMutation (genetic algorithm)Spinocerebellar ataxiaFemaleSequence AnalysisResearch ArticleBioinformaticsBiologyAtaxin-1003 medical and health sciencesSequence Motif AnalysisMicrosatellite RepeatGeneticsmedicineHumansSpinocerebellar AtaxiasRepeated SequencesAlleleAllelesSequence (medicine)EpilepsyBase SequenceBiology and life scienceslcsh:RDideoxy DNA sequencingGenetic Variationmedicine.diseaseResearch and analysis methodsMolecular biology techniques030104 developmental biologyTandem Repeat Sequence AnalysisAtaxinMutationlcsh:QAtaxiaTrinucleotide repeat expansionMicrosatellite RepeatsPLOS ONE
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Incorporating Functional Genomic Information to Enhance Polygenic Signal and Identify Variants Involved in Gene-by-Environment Interaction for Young …

2018

BACKGROUND: Characterizing aggregate genetic risk for alcohol misuse and identifying variants involved in gene-by-environment (G × E) interaction effects has so far been a major challenge. We hypothesized that functional genomic information could be used to enhance detection of polygenic signal underlying alcohol misuse and to prioritize identification of single nucleotide polymorphisms (SNPs) most likely to exhibit G × E effects.METHODS: We examined these questions in the young adult FinnTwin12 sample (n = 1,170). We used genomewide association estimates from an independent sample to derive 2 types of polygenic scores for alcohol problems in FinnTwin12. Genomewide polygenic scores included…

Male0301 basic medicineMultifactorial InheritanceTwinsMedicine (miscellaneous)AlcoholToxicologyBioinformaticschemistry.chemical_compound0302 clinical medicineGene–environment interactionYoung adultta515FinlandGeneticsalcoholta3142GenomicsgenomiikkaPhenotypeAlcoholismPsychiatry and Mental health/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGenomic informationgeneettiset tekijätfunctional genomicsFunctional genomicsAdultympäristötekijätSingle-nucleotide polymorphismBiologyta3111Polymorphism Single NucleotideArticleYoung Adult03 medical and health sciencesSDG 3 - Good Health and Well-beingHumansGenetic Predisposition to Diseasenuoret aikuisetGenetic Variationalkoholiongelmatpolygenic scores030104 developmental biologychemistryGenomewide associationgene-environment interplayGene-Environment Interaction030217 neurology & neurosurgeryGenome-Wide Association StudyAlcoholism, Clinical and Experimental Research
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Genome-wide associations for birth weight and correlations with adult disease

2016

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10(-8)). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genet…

Male0301 basic medicineNetherlands Twin Register (NTR)AgingDatasets as TopicPhysiologyBlood PressureGenome-wide association studyCoronary Artery DiseaseType 2 diabetesBioinformaticsCHARGE Consortium Hematology Working GroupCohort Studies0302 clinical medicineBirth WeightInsulinGlucose homeostasis030212 general & internal medicineeducation.field_of_studyMultidisciplinaryAnthropometry3. Good healthPhenotype/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleGlycogenSignal TransductionAdulthypertensionGenotypeGeneral Science & TechnologyBirth weightintrauterine growthPopulationQuantitative trait locusBiologyArticlequantitative traitGenomic Imprinting03 medical and health sciencesFetusSDG 3 - Good Health and Well-beingEarly Growth Genetics (EGG) ConsortiumMD MultidisciplinaryGenetic variation/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicineHumansmetabolic disordersGenetic Predisposition to DiseaseeducationgenomeGenetic associationGenetic Variationbirth weightta3121Chromatin Assembly and Disassemblymedicine.diseaseta3123Glucose030104 developmental biologyDiabetes Mellitus Type 2Genetic Locigenome-wide association studiesadult diseaseGenome-Wide Association Study
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The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
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Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
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Genetic investigation of amyotrophic lateral sclerosis patients in south Italy: a two-decade analysis

2020

Amyotrophic lateral sclerosis (ALS) is a multifactorial disease characterized by the interplay of genetic and environmental factors. In the majority of cases, ALS is sporadic, whereas familial forms occur in less than 10% of patients. Herein, we present the results of molecular analyses performed in a large cohort of Italian ALS patients, focusing on novel and already described variations in ALS-linked genes. Our analysis revealed that more than 10% of tested patients carried a mutation in one of the major ALS genes, with C9orf72 hexanucleotide expansion being the most common mutation. In addition, our study confirmed a significant association between ALS patients carrying the ATNX-1 interm…

Male0301 basic medicineSanger sequencingAgingTime FactorsDiseaseCohort Studies03 medical and health sciencessymbols.namesake0302 clinical medicineRisk FactorsC9orf72HumansMedicineAmyotrophic lateral sclerosisRisk factorGenePathologicalAtaxin-1Genetic Association StudiesAmyotrophic lateral sclerosiSanger sequencingGeneticsDNA Repeat ExpansionC9orf72 ProteinMolecular analysibusiness.industryMolecular analysisGeneral NeuroscienceGenetic VariationAmyotrophic lateral sclerosismedicine.disease030104 developmental biologyItalyMutation (genetic algorithm)symbolsFemaleNeurology (clinical)Geriatrics and Gerontologybusiness030217 neurology & neurosurgeryDevelopmental BiologyNeurobiology of Aging
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Heritability and genome-wide association analyses of sleep duration in children: The EAGLE Consortium.

2016

STUDY OBJECTIVES: Low or excessive sleep duration has been associated with multiple outcomes, but the biology behind these associations remains elusive. Specifically, genetic studies in children are scarce. In this study, we aimed to: (1) estimate the proportion of genetic variance of sleep duration in children attributed to common single nucleotide polymorphisms (SNPs), (2) identify novel SNPs associated with sleep duration in children, and (3) investigate the genetic overlap of sleep duration in children and related metabolic and psychiatric traits.METHODS: We performed a population-based molecular genetic study, using data form the EArly Genetics and Life course Epidemiology (EAGLE) Cons…

Male0301 basic medicineTime FactorsAdolescentSleep Duration/Sleep QualityPopulationSingle-nucleotide polymorphismGenome-wide association studyPolymorphism Single NucleotideWhite PeopleSNP heritabilityCohort Studies03 medical and health sciencesQuantitative Trait Heritable0302 clinical medicine030225 pediatricsPhysiology (medical)Genetic variationHumansSNPMedicineLongitudinal StudiesChildeducationeducation.field_of_studybusiness.industryExcessive sleepHeritabilitygenome-wide association study (GWAS)medicine.disease3. Good healthpathway analysismeta-analysis030104 developmental biologyDiabetes Mellitus Type 2Child PreschoolMeta-analysisFemaleNeurology (clinical)Sleepbusinesschildhood sleep durationSnp Heritability ; Genome-wide Association Study (gwas) ; Meta-analysis ; Childhood Sleep Duration ; Pathway AnalysisGenome-Wide Association StudyDemography
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EGFR gene copy number decreases during anti-EGFR antibody therapy in colorectal cancer

2018

Epidermal growth factor receptor (EGFR) gene copy number (GCN) increase is associated with a favorable anti-EGFR antibody treatment response in RAS wild-type metastatic colorectal cancer. However, there are limited and comparative data regarding the EGFR GCN in primary colorectal cancer tumors and corresponding metastases or the effect of anti-EGFR antibody treatment on EGFR GCN in recurrent disease. In addition, little is known about the potential EGFR GCN changes during anti-EGFR therapy in comparison with other treatment regimens. EGFR GCN was analyzed by EGFR immunohistochemistry-guided silver in situ hybridization in primary and corresponding recurrent local or metastatic tumors from 8…

Male0301 basic medicineTime FactorsColorectal cancerBLOCKADEGene DosageCetuximabmedicine.disease_causeAntineoplastic Agents Immunological0302 clinical medicinePREDICTS RESPONSEMedicineHETEROGENEITYBENEFITCopy-number variationEpidermal growth factor receptorIn Situ Hybridization FluorescenceAged 80 and overbiologyPanitumumabvasta-aineetMiddle AgedImmunohistochemistry3. Good healthErbB ReceptorsGene Expression Regulation NeoplasticTreatment OutcomeRAS MUTATIONSChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleKRASAntibodyColorectal NeoplasmsAdultgene copy numbermedicine.drug_classCETUXIMAB THERAPY3122 Cancerssilver in situ hybridizationDown-Regulationcolorectal cancerIn situ hybridizationAdenocarcinomaMonoclonal antibodyta3111Pathology and Forensic MedicineProto-Oncogene Proteins p21(ras)03 medical and health sciencesKRASHumansWILD-TYPEMETAANALYSISAgedRetrospective Studiessyöpähoidotbusiness.industrymedicine.diseaseta3122Blockadeperäsuolisyöpä030104 developmental biologymonoclonal antibodyMutationCancer researchbiology.protein3111 BiomedicineNeoplasm Recurrence Localbusinessepidermal growth factor receptorACQUIRED-RESISTANCEHuman Pathology
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CNTN6 mutations are risk factors for abnormal auditory sensory perception in autism spectrum disorders

2017

International audience; Contactin genes CNTN5 and CNTN6 code for neuronal cell adhesion molecules that promote neurite outgrowth in sensory-motor neuronal pathways. Mutations of CNTN5 and CNTN6 have previously been reported in individuals with autism spectrum disorders (ASDs), but very little is known on their prevalence and clinical impact. In this study, we identified CNTN5 and CNTN6 deleterious variants in individuals with ASD. Among the carriers, a girl with ASD and attention-deficit/hyperactivity disorder was carrying five copies of CNTN5. For CNTN6, both deletions (6/1534 ASD vs 1/8936 controls; P=0.00006) and private coding sequence variants (18/501 ASD vs 535/33480 controls; P=0.000…

Male0301 basic medicinegenetic structuresAutism Spectrum Disorder[ SDV.MHEP.PSM ] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental health[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.MHEP.PSM] Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthmedicine.disease_causeChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGeneticsMutationPsychiatry and Mental healthSchizophrenia[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology[ SCCO.NEUR ] Cognitive science/NeuroscienceAuditory PerceptionMedical geneticsOriginal ArticleFemalePsychopharmacologymedicine.symptomPsychologyAdultmedicine.medical_specialtyAdolescentDNA Copy Number Variations[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsPolymorphism Single Nucleotidebehavioral disciplines and activities03 medical and health sciencesCellular and Molecular NeuroscienceContactinsmental disordersmedicineHumansDementiaGenetic Predisposition to DiseaseMolecular Biology[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceHyperacusis[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[ SDV.SP.PHARMA ] Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacologymedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAttention Deficit Disorder with Hyperactivity[SDV.MHEP.PSM]Life Sciences [q-bio]/Human health and pathology/Psychiatrics and mental healthMutationBehavioral medicine[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyAutismNeuroscienceMolecular Psychiatry
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