Search results for "KCNQ"

showing 10 items of 13 documents

New insights into the pathogenesis of Beckwith-Wiedemann and Silver-Russell syndromes: contribution of small copy number variations to 11p15 imprinti…

2011

International audience; The imprinted 11p15 region is organized in two domains, each of them under the control of its own imprinting control region (ICR1 for the IGF2/H19 domain and ICR2 for the KCNQ1OT1/CDKN1C domain). Disruption of 11p15 imprinting results in two fetal growth disorders with opposite phenotypes: the Beckwith-Wiedemann (BWS) and the Silver-Russell (SRS) syndromes. Various 11p15 genetic and epigenetic defects have been demonstrated in BWS and SRS. Among them, isolated DNA methylation defects account for approximately 60% of patients. To investigate whether cryptic copy number variations (CNVs) involving only part of one of the two imprinted domains account for 11p15 isolated…

MaleBeckwith–Wiedemann syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsMESH: Base SequenceMESH: DNA MethylationCopy-number variationImprinting (psychology)[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)GeneticsComparative Genomic Hybridization0303 health sciencesKCNQ1OT1MESH: Polymorphism Single Nucleotide030305 genetics & hereditycopy number variation11p15 regionPedigreegenomic imprintingMESH: Silver-Russell SyndromeDNA methylationBeckwith-Wiedemann syndromeFemaleMESH: DNA Copy Number VariationsMESH: Beckwith-Wiedemann SyndromeAdultDNA Copy Number VariationsMESH: PedigreeBiologyPolymorphism Single Nucleotide03 medical and health sciences[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansEpigenetics030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: HumansBase SequenceChromosomes Human Pair 11MESH: AdultDNA Methylationmedicine.diseaseMESH: MaleMESH: Genomic ImprintingMESH: Comparative Genomic HybridizationUniparental IsodisomySilver-Russell syndromeMESH: Chromosomes Human Pair 11Genomic imprintingMESH: Femalefetal growthfetal growth.
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Genome-wide meta-analyses of multiancestry cohorts identify multiple new susceptibility loci for refractive error and myopia

2013

Author version made available in accordance with the publisher's policy.

Candidate geneRefractive errorBone Morphogenetic Protein 2Genome-wide association studyVARIANTSGenomeGenome-wide association studies0302 clinical medicineRisk FactorsMyopiaGRIA4Genetics0303 health sciencesKCNQ Potassium ChannelsDisease geneticsEYE GROWTHASSOCIATIONRETINAL-PIGMENT EPITHELIUMRefractive ErrorsGenetic load3. Good healthADAPTED MOUSE RETINAMeta-analysisACIDPOTASSIUM CHANNELEXPRESSIONSingle-nucleotide polymorphismBiologyWhite PeopleArticle03 medical and health sciencesAsian PeoplemedicineGeneticsHumansGenetic Predisposition to DiseaseReceptors AMPAgene; myopia; refractive030304 developmental biologyHomeodomain Proteinsta1184ta3121medicine.diseaseGENEAlcohol OxidoreductasesSERINE-PROTEASEbiology.protein030221 ophthalmology & optometrySusceptibility locusTrans-ActivatorsEye disorderLamininSerine ProteasesGWAS; meta-analyses; refractive error; myopiaGenome-Wide Association StudyNature Genetics
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Esophageal atresia and Beckwith–Wiedemann syndrome in one of the naturally conceived discordant newborn twins: first report

2018

Key Clinical Message Recent studies report a high incidence of monozygotic twinning in Beckwith–Wiedemann syndrome. A phenotypical discordance in monozygotic twins is rare. Twinning and Beckwith–Wiedemann syndrome show higher incidence in children born after assisted reproductive techniques. We report on the first observation of esophageal atresia and Beckwith–Wiedemann syndrome in one of the naturally conceived discordant monozygotic twins.

0301 basic medicinePediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesbuccal swabAssisted reproductive techniquesBuccal swabBeckwith–Wiedemann syndromeCase ReportCase Reports030105 genetics & heredity03 medical and health sciencesmedicinebusiness.industryIncidence (epidemiology)Monozygotic TwinningGeneral MedicineKCNQ1OT1 genemedicine.disease030104 developmental biologyAtresiaAssisted reproductive techniques buccal swab hypomethylation KCNQ1OT1 gene phenotypical discordance.phenotypical discordanceKCNQ1OT1 genebusinesshypomethylation
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Immunohistochemical analysis of KCNQ3 potassium channels in mouse brain.

2005

KCNQ-type potassium channels generate the so-called M-current regulating excitability in many neurons. Mutations in KCNQ2/KCNQ3 channels can cause benign familial neonatal convulsions (BFNC). We describe the immunohistochemical staining of adult and developing mouse brain using an antibody directed against the N-terminus of KCNQ3 channels (KCNQ3N). A widespread KCNQ3N immunoreactivity predominantly of neuropil but also of somata was detected in different regions of the adult mouse brain, in particular in the hippocampus, cortex, thalamus and cerebellum. This staining pattern appeared gradually and became more intense during development. In the pyramidal cell layer of the hippocampus, the im…

medicine.medical_specialtyCerebellumPathologyCentral nervous systemThalamusBlotting WesternHippocampusBiologyKCNQ3 Potassium ChannelMiceCortex (anatomy)Internal medicinemedicineNeuropilAnimalsGeneral NeuroscienceBrainGene Expression Regulation DevelopmentalImmunohistochemistryPotassium channelMice Inbred C57BLEndocrinologymedicine.anatomical_structureParvalbuminsnervous systemAnimals Newbornsense organsPyramidal cellNeuroscience letters
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Immunohistochemical analysis of KCNQ2 potassium channels in adult and developing mouse brain

2005

The syndrome of benign familial neonatal convulsions (BFNC) is characterized by seizures starting within the first days of life and disappearing within weeks to months. BFNC is caused by loss-of-function mutations in the potassium channels KCNQ2 and KCNQ3 which can well explain the resulting neuronal hyperexcitability. However, it is not understood why seizures predominantly occur in the neonatal period. A potential explanation might be a change in the expression pattern of these channels during development. We therefore performed an immunohistochemical analysis of mouse brain slices at different stages of postnatal development using an antibody recognizing the C-terminus of the KCNQ2 chann…

Mossy fiber (hippocampus)medicine.medical_specialtyThalamusCentral nervous systemHippocampusBiologyHippocampal formationHippocampusMidbrainMiceEpilepsyInternal medicineNeural PathwaysmedicineAnimalsKCNQ2 Potassium ChannelTissue DistributionMolecular BiologyGeneral NeuroscienceBrainGene Expression Regulation Developmentalmedicine.diseaseImmunohistochemistryAxonsMice Inbred C57BLGlobus pallidusEndocrinologymedicine.anatomical_structurenervous systemMossy Fibers HippocampalNeurology (clinical)Developmental BiologyBrain Research
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A novel mutation in KCNQ3-related benign familial neonatal epilepsy: electroclinical features and neurodevelopmental outcome.

2019

Benign familial neonatal epilepsy (BFNE) is caused, in about 5% of families, by mutations in the KCNQ3 gene encoding voltage-gated potassium channel subunits. Usually, newborns with BFNE show a normal neurological outcome, but recently, refractory seizures and/or developmental disability have been reported suggesting phenotype variability associated with KCNQ3-related BFNE. Here, we describe a proband from a BFNE family carrying a novel variant in the KCNQ3 gene. Regarding the paucity of data in the literature, we describe the presented case with a view to further establishing: (1) a genotype/phenotype correlation in order to define a BFNE phenotype associated with favourable outcome; (2) a…

MaleGenotypeelectroclinical featureInfantElectroencephalographygenotype-phenotype correlationSettore MED/39 - Neuropsichiatria InfantileEpilepsy Benign NeonatalKCNQ3 Potassium ChannelKCNQSettore MED/38 - Pediatria Generale E SpecialisticaPhenotypevoltage-gated potassium channelsSettore M-PSI/08 - Psicologia ClinicaHumansbenign familial neonatal epilepsyEpileptic SyndromesEpileptic disorders : international epilepsy journal with videotape
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A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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Activation of PPARβ/δ prevents hyperglycaemia-induced impairment of Kv7 channels and cAMP-mediated relaxation in rat coronary arteries.

2016

PPARβ/δ activation protects against endothelial dysfunction in diabetic models. Elevated glucose is known to impair cAMP-induced relaxation and Kv channel function in coronary arteries (CA). Herein, we aimed to analyse the possible protective effects of the PPARβ/δ agonist GW0742 on the hyperglycaemic-induced impairment of cAMP-induced relaxation and Kv channel function in rat CA. As compared with low glucose (LG), incubation under high glucose (HG) conditions attenuated the relaxation induced by the adenylate cyclase activator forskolin in CA and this was prevented by GW0742. The protective effect of GW0742 was supressed by a PPARβ/δ antagonist. In myocytes isolated from CA under LG, forsk…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPDK4Protein Serine-Threonine Kinasesmedicine.disease_causeGW0742Diabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineCyclic AMPAnimalsHumansPPAR deltaRats WistarPPAR-betaForskolinAntagonistPyruvate Dehydrogenase Acetyl-Transferring KinaseGeneral MedicineHyperpolarization (biology)Coronary VesselsPotassium channelRatsVasodilationThiazoles030104 developmental biologyEndocrinologychemistryHyperglycemiaKCNQ1 Potassium ChannelReactive Oxygen SpeciesOxidative stressClinical science (London, England : 1979)
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Benign familial infantile epilepsy associated with KCNQ3 mutation: a rare occurrence or an underestimated event?

2020

Abstract Benign familial infantile epilepsy (BFIE) is the most genetically heterogeneous phenotype among early-onset familial infantile epilepsies. It has an autosomal dominant inheritance pattern with incomplete penetrance. Although PRRT2 is the most mutated gene detected in families with BFIE, other mutations in KCNQ2, SCN2A, and GABRA6 genes have also been described. To date, KCNQ3 mutations have been detected in only four patients with BFIE. Here, we describe the clinical pattern and course of an additional individual with BFIE associated with a novel missense heterozygous KCNQ3 c.1850G>C variant inherited by his unaffected father. The incidence of KCNQ3 mutations among BFIE patients…

MaleGABRA6Mutation Missensemedicine.disease_causeKCNQ3 Potassium ChannelEpilepsymutation.medicineHumansMissense mutationBFIEGeneticsBenign familial infantile epilepsyMutationKCNQ3biologybusiness.industryGenetic heterogeneityInfantGeneral Medicinemedicine.diseasePenetranceEpilepsy Benign NeonatalNeurologybenign familial infantile epilepsybiology.proteinincidenceNeurology (clinical)businessPRRT2
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The DNA methylation profile of human spermatogonia at single-cell- and single-allele-resolution refutes its role in spermatogonial stem cell function…

2019

Human spermatogonial stem cells (hSSCs) have potential in fertility preservation of prepubertal boys or in treatment of male adults suffering from meiotic arrest. Prior to therapeutic application, in vitro propagation of rare hSSCs is mandatory. As the published data points to epigenetic alterations in long-term cell culture of spermatogonia (SPG), an initial characterisation of their DNA methylation state is important. Testicular biopsies from five adult normogonadotropic patients were converted into aggregate-free cell suspensions. FGFR3-positive (FGFR3+) SPG, resembling a very early stem cell state, were labelled with magnetic beads and isolated in addition to unlabelled SPG (FGFR3-). DN…

0301 basic medicineHomeobox protein NANOGMaleEmbryologyBiologyEpigenesis Genetic03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansReceptor Fibroblast Growth Factor Type 3EpigeneticsSpermatogenesisMolecular BiologyAllelesMEG3030219 obstetrics & reproductive medicineKCNQ1OT1Stem CellsObstetrics and GynecologyCell DifferentiationCell BiologyMethylationDNA MethylationMolecular biologySpermatozoaSpermatogonia030104 developmental biologymedicine.anatomical_structureReproductive MedicineDNA methylationGenomic imprintingGerm cellDevelopmental BiologyMolecular human reproduction
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