Search results for "Association studies"

showing 10 items of 216 documents

PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

2019

Abstract Background Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous functio…

0301 basic medicineMaleMicrocephalyMutation MissenseCase ReportNerve Tissue ProteinsBioinformaticsRisk AssessmentSeverity of Illness Index03 medical and health sciences0302 clinical medicineRare DiseasesSeizuresmedicineHumansGenetic Predisposition to DiseaseGenetic TestingExome sequencingGenetic Association StudiesBenign familial infantile epilepsyDysmorphic featuresbusiness.industryEpileptic encephalopathylcsh:RJ1-570InfantMembrane Proteinslcsh:PediatricsParoxysmal dyskinesiamedicine.diseaseBody Dysmorphic DisordersPrognosisPRRT2 mutationMagnetic Resonance Imaging030104 developmental biologyDyskinesiaMicrocephalymedicine.symptomPRRT2 mutation Dysmorphic features Microcephaly Epileptic encephalopathybusinessMyoclonus030217 neurology & neurosurgeryPRRT2Benign infantile epilepsy
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Mutation-specific pathophysiological mechanisms define different neurodevelopmental disorders associated with SATB1 dysfunction

2021

AbstractWhereas large-scale statistical analyses can robustly identify disease-gene relationships, they do not accurately capture genotype-phenotype correlations or disease mechanisms. We use multiple lines of independent evidence to show that different variant types in a single gene,SATB1, cause clinically overlapping but distinct neurodevelopmental disorders. Clinical evaluation of 42 individuals carryingSATB1variants identified overt genotype-phenotype relationships, associated with different pathophysiological mechanisms, established by functional assays. Missense variants in the CUT1 and CUT2 DNA-binding domains result in stronger chromatin binding, increased transcriptional repression…

0301 basic medicineMaleModels MolecularMISSENSE MUTATIONSCHROMATINTranscription GeneticCellMedizinDiseaseHaploinsufficiencymedicine.disease_cause0302 clinical medicineMissense mutationde novo variantsGenetics (clinical)INTERLEUKIN-2seizuresGenetics0303 health sciencesMutationChromatin bindingneurodevelopmental disordersMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]SATB1Phenotypemedicine.anatomical_structureintellectual disabilityFemaleHaploinsufficiencyteeth abnormalitiesProtein BindingNeuroinformaticsEXPRESSIONGENESMutation MissenseBiologyBINDING PROTEINREGION03 medical and health sciencesSATB1Protein DomainsReportGeneticsmedicineHPO-based analysisHumansGenetic Association StudiesHpo-based Analysis ; Satb1 ; Cell-based Functional Assays ; De Novo Variants ; Intellectual Disability ; Neurodevelopmental Disorders ; Seizures ; Teeth Abnormalities030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Matrix Attachment Region Binding Proteins030104 developmental biologyNeurodevelopmental DisordersMutationNanomedicine Radboud Institute for Molecular Life Sciences [Radboudumc 19]030217 neurology & neurosurgerycell-based functional assays
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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MICA-129 Dimorphism and Soluble MICA Are Associated With the Progression of Multiple Myeloma

2018

Natural killer (NK) cells are immune innate effectors playing a pivotal role in the immunosurveillance of multiple myeloma (MM) since they are able to directly recognize and kill MM cells. In this regard, among activating receptors expressed by NK cells, NKG2D represents an important receptor for the recognition of MM cells, being its ligands expressed by tumor cells, and being able to trigger NK cell cytotoxicity. The MHC class I-related molecule A (MICA) is one of the NKG2D ligands; it is encoded by highly polymorphic genes and exists as membrane-bound and soluble isoforms. Soluble MICA (sMICA) is overexpressed in the serum of MM patients, and its levels correlate with tumor progression. …

0301 basic medicineMaleModels MolecularProtein ConformationGenotypeImmunology and AllergyReceptorpredictive biomarkerOriginal ResearchAged 80 and overnatural killer cellsbiologyChemistryMiddle AgedImmunosurveillanceGene Expression Regulation NeoplasticKiller Cells Naturalmultiple myelomaNK Cell Lectin-Like Receptor Subfamily KDisease ProgressionFemaleNKG2D receptorProtein Bindinglcsh:Immunologic diseases. AllergyGenotypeImmunologyEnzyme-Linked Immunosorbent AssayMICA polymorphismImmunophenotyping03 medical and health sciencesStructure-Activity RelationshipImmune systemMHC class IHumansGenetic Predisposition to DiseaseAllelesGenetic Association StudiesAgedPolymorphism GeneticHistocompatibility Antigens Class INKG2DMolecular biologyMolecular Typingstomatognathic diseases030104 developmental biologyAmino Acid SubstitutionTumor progressionbiology.proteinmultiple myeloma natural killer cells NKG2D receptor MICA polymorphism predictive biomarkerGene polymorphismlcsh:RC581-607Frontiers in Immunology
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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Combined effects of the PNPLA3 rs738409, TM6SF2 rs58542926, and MBOAT7 rs641738 variants on NAFLD severity: a multicenter biopsy-based study.

2016

The PNPLA3 p.I148M, TM6SF2 p.E167K, and MBOAT7 rs641738 variants represent genetic risk factors for nonalcoholic fatty liver disease (NAFLD). Here we investigate if these polymorphisms modulate both steatosis and fibrosis in patients with NAFLD. We recruited 515 patients with NAFLD (age 16–88 years, 280 female patients). Liver biopsies were performed in 320 patients. PCR-based assays were used to genotype the PNPLA3, TM6SF2, and MBOAT7 variants. Carriers of the PNPLA3 and TM6SF2 risk alleles showed increased serum aspartate aminotransferase and alanine transaminase activities (P 0.05). The MBOAT7 variant was solely associated with increased fibrosis (P = 0.046). In the multivariate model, v…

0301 basic medicineMalePathologyBiopsyBiochemistryGastroenterologySeverity of Illness Index0302 clinical medicineEndocrinologyFibrosisNon-alcoholic Fatty Liver DiseaseGenotypeNonalcoholic fatty liver diseaseAged 80 and overeducation.field_of_studybiologyFatty liverMiddle AgedLiver030211 gastroenterology & hepatologyFemaleAdultmedicine.medical_specialtyAdolescentGenotypePolymorphism Single Nucleotide03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAdiponutrinGenetic Predisposition to DiseaseeducationAllelesGenetic Association StudiesAgedbusiness.industryMembrane ProteinsCell BiologyLipasemedicine.diseaseFibrosisFatty Liver030104 developmental biologyAlanine transaminasebiology.proteinSteatosisbusinessPatient-Oriented and Epidemiological ResearchAcyltransferasesTM6SF2Journal of lipid research
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Large national series of patients with Xq28 duplication involving MECP2: Delineation of brain MRI abnormalities in 30 affected patients.

2016

International audience; Xq28 duplications encompassing MECP2 have been described in male patients with a severe neurodevelopmental disorder associated with hypotonia and spasticity, severe learning disability, stereotyped movements, and recurrent pulmonary infections. We report on standardized brain magnetic resonance imaging (MRI) data of 30 affected patients carrying an Xq28 duplication involving MECP2 of various sizes (228 kb to 11.7 Mb). The aim of this study was to seek recurrent malformations and attempt to determine whether variations in imaging features could be explained by differences in the size of the duplications. We showed that 93% of patients had brain MRI abnormalities such …

0301 basic medicineMalePathologyMethyl-CpG-Binding Protein 2[SDV]Life Sciences [q-bio]030105 genetics & heredityCorpus callosumLateral ventricles0302 clinical medicineGene DuplicationIKBKGFLNAChildGenetics (clinical)GeneticsBrain Diseasesmedicine.diagnostic_testMiddle AgedPrognosisMagnetic Resonance ImagingHypotonia3. Good healthPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structurePhenotypeXq28 duplicationChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentGenotypeBiologygenotype-phenotype correlationWhite matter03 medical and health sciencesYoung AdultGeneticsmedicineHumansGenetic Association StudiesChromosomes Human X[ SDV ] Life Sciences [q-bio]Infant NewbornInfantMagnetic resonance imagingHyperintensitynervous system diseasesMental Retardation X-LinkedMECP2 gene030217 neurology & neurosurgeryAmerican journal of medical genetics. Part A
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HLA-C1 ligands are associated with increased susceptibility to systemic lupus erythematosus.

2017

Recently, the role of killer cell immunoglobulin-like receptor (KIR) in autoimmune diseases has received increasing attention. The present study was undertaken to determine the association of KIR genes and the human leukocytes antigen (HLA) ligands with Systemic Lupus Erythematosus (SLE) and accompanying oxidative stress. Presence or absence of 17 KIR and 5 HLA loci was performed using the polymerase chain reaction-sequence specific primer (PCR-SSP) method by case-control study. A total of 45 SLE patients, and 60 healthy controls, all of Sicilian descent, were enrolled. Plasma values of the anti-oxidant molecule Taurine were determined in all subjects by capillary electrophoresis UV detecti…

0301 basic medicineMaleTaurineTaurineCellSLEDiseasemedicine.disease_causechemistry.chemical_compound0302 clinical medicineReceptors KIRImmunology and AllergyLupus Erythematosus SystemicReceptorSicilyGeneral MedicineMiddle AgedKIRHLAmedicine.anatomical_structureDisease ProgressionFemaleCase-Control StudieHumanAdultNKImmunologyGenetic Association StudieHuman leukocyte antigenHLA-C Antigens03 medical and health sciencesYoung AdultAntigenmedicineHumansGeneGenetic Association StudiesSettore MED/04 - Patologia Generale030203 arthritis & rheumatologyHLA-C Antigenbusiness.industryOxidative StreSettore MED/16 - ReumatologiaOxidative Stress030104 developmental biologychemistryCase-Control StudiesImmunologybusinessOxidative stressHuman immunology
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Homocysteine concentration in coronary artery disease: Influence of three common single nucleotide polymorphisms.

2017

Whether single nucleotide polymorphisms (SNPs) of homocysteine metabolism enzymes influence the rate of cardiovascular (CV) events in coronary artery disease (CAD) patients remains controversial.In this analysis, 1126 subjects from the AtheroGene study with CAD and 332 control subjects without known CAD were included. The following SNPs were investigated: methylentetrahydrofolate reductase (MTHFR-C667T), methionin synthetase (MS-D919G), and cystathionin beta synthetase (CBS-I278T). The endpoint was the combination of cardiovascular death, stroke, and non-fatal myocardial infarction (N = 286). The median follow-up time was 6.4 years. Kaplan-Meier curve analysis showed an increasing event rat…

0301 basic medicineMaleTime FactorsHomocysteineEndocrinology Diabetes and MetabolismMyocardial InfarctionMedicine (miscellaneous)Coronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyReductaseGastroenterology5-Methyltetrahydrofolate-Homocysteine S-MethyltransferaseCoronary artery diseasechemistry.chemical_compound0302 clinical medicineGene FrequencyRisk FactorsMyocardial infarctionStrokeHomocysteineGeneticsNutrition and DieteticsbiologyHomozygoteMiddle AgedStrokePhenotypeArea Under CurveDisease ProgressionFemaleCardiology and Cardiovascular Medicinemedicine.medical_specialtyHeterozygoteCystathionine beta-SynthaseSingle-nucleotide polymorphismPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesMethylenetetrahydrofolate Reductase (NADPH2)AgedProportional Hazards ModelsChi-Square DistributionCurve analysismedicine.disease030104 developmental biologychemistryROC CurveMethylenetetrahydrofolate reductaseCase-Control Studiesbiology.proteinBiomarkersNutrition, metabolism, and cardiovascular diseases : NMCD
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Genetic and constitutional factors are major contributors to substantia nigra hyperechogenicity

2017

9 páginas, 2 figuras, 4 tablas

0301 basic medicineMalemedicine.medical_specialtyMovement disordersScienceSubstantia nigraDiseaseComorbidityArticle03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansGenetic Predisposition to DiseaseFamily historyAmyotrophic lateral sclerosisPsychiatryGenetic Association StudiesGenetic testingAgedUltrasonographyMultidisciplinarymedicine.diagnostic_testbusiness.industryQCase-control studyRNeurodegenerative DiseasesMiddle Agedmedicine.diseaseComorbiditySubstantia Nigra030104 developmental biologyCase-Control StudiesMutationMedicineFemalemedicine.symptombusiness030217 neurology & neurosurgeryBiomarkers
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