Search results for " sodium channel"

showing 8 items of 28 documents

Heterozygous nonsense SCN5A mutation W822X explains a simultaneous sudden infant death syndrome.

2008

The sudden, unexpected, and unexplained death of both members of a set of healthy twins (simultaneous sudden infant death syndrome (SSIDS)) is defined as a case in which both infants meet the definition of sudden infant death syndrome individually. A search of the world medical literature resulted in only 42 reported cases of SSIDS. We report the case of a pair of identical, male, monozygotic twins, 138 days old, who suddenly died, meeting the full criteria of SSIDS and where a genetic screen was performed, resulting in a heterozygous nonsense SCN5A mutation (W822X) in both twins. Immunohistochemistry was performed on cardiac tissue samples utilizing polyclonal antibodies anti-Na+ CP type V…

MalePathologymedicine.medical_specialtyNav1.5 protein functionv1.5 protein functionmedia_common.quotation_subject2734Nonsense mutationNonsenseNa+ channel functionMuscle ProteinsSocio-culturaleBiology+Nav1.5 protein function; Na+ channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutation; Codon Nonsense; Diseases in Twins; Humans; Infant; Male; Muscle Proteins; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channels; Sudden Infant Death; 2734Sudden deathSodium ChannelsNAV1.5 Voltage-Gated Sodium ChannelPathology and Forensic MedicinePathogenesisSCN5A gene mutationDiseases in TwinsmedicineHumansSimultaneous sudden infant death syndromeSCN5A gene mutationW822X mutationNa+ channel functionNav1.5 protein functionNaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein function CodonMolecular BiologyCellular localizationmedia_commonSimultaneous sudden infant death syndromeSettore BIO/16 - Anatomia UmanaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein functionW822X mutationInfantCell BiologyGeneral MedicineSudden infant death syndromeNonsenseTerminal deoxynucleotidyl transferaseCodon NonsenseImmunohistochemistryNa; v; 1.5 protein function; Na; +; channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutationchannel functionSudden Infant Death
researchProduct

Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
researchProduct

Putative excitatory and putative inhibitory inputs are localised in different dendritic domains in aDrosophilaflight motoneuron

2012

Input-output computations of individual neurons may be affected by the three-dimensional structure of their dendrites and by the targeting of input synapses to specific parts of their dendrites. However, only few examples exist where dendritic architecture can be related to behaviorally relevant computations of a neuron. By combining genetic, immunohistochemical, and confocal laser scanning methods this study estimates the location of the spike initiating zone and the dendritic distribution patterns of putative synaptic inputs on an individually identified Drosophila flight motorneuron, MN5. MN5 is a monopolar neuron with more than 4000 dendritic branches. The site of spike initiation was e…

Motor NeuronsDendritic spikeGABAA receptorGeneral NeuroscienceAction PotentialsDendritesVoltage-Gated Sodium ChannelsReceptors NicotinicBiologyReceptors GABA-AInhibitory postsynaptic potentialArticleTonic (physiology)SynapseProtein TransportDrosophila melanogastermedicine.anatomical_structureSynapsesmedicineExcitatory postsynaptic potentialAnimalsDrosophila ProteinsGABAergicNeuronNeuroscienceEuropean Journal of Neuroscience
researchProduct

Commonalities and distinctions between two neurodevelopmental disorder subtypes associated with SCN2A and SCN8A variants and literature review.

2022

This study was aimed to analyze the commonalities and distinctions of voltage-gated sodium channels, Nav1.2, Nav1.6, in neurodevelopmental disorders. An observational study was performed including two patients with neurodevelopmental disorders. The demographic, electroclinical, genetic, and neuropsychological characteristics were analyzed and compared with each other and then with the subjects carrying the same genetic variants reported in the literature. The clinical features of one of them argued for autism spectrum disorder and developmental delay, the other for intellectual disability, diagnoses confirmed by the neuropsychological assessment. The first patient was a carrier of SCN2A (p.…

SCN8AEpilepsyNAV1.2 Voltage-Gated Sodium ChannelAutism Spectrum Disorderautism spectrum disordersObservational Studies as TopicPhenotypeNAV1.6 Voltage-Gated Sodium ChannelNeurodevelopmental DisordersIntellectual DisabilityHumansEEGwhole-exome sequencingSCN2AMolecular geneticsgenomic medicine
researchProduct

Polymorphism and solvates of flecainide base

2013

Flecainide base is pharmaceutically active substance used for production of flecainide acetate which is known in market as Tambacor, Almarytm, Apocard, Ecrinal or Flecaine. It is determined that flecainide base forms four polymorphic forms abbreviated as Ib, IIb, IIIb and IVb. Flecainide base form Ib is thermodynamically stable form at laboratory temperature while form IIIb is stable at higher temperatures. Flecainide form Ib absorbs water in its structure between layers and forms non-stoichiometric hydrate. Flecainide base binds with organic solvents and form monosolvates. Flecainide base form Ib crystallizes in orthorhombic crystals with lattice parameters a = 27.88 Å, b = 13.78 Å, c = 9.…

Voltage-Gated Sodium Channel BlockersFlecainideChemistryWaterPharmaceutical ScienceGeneral MedicineFlecainide Acetatelaw.inventionCrystallographyX-Ray DiffractionPolymorphism (materials science)lawX-ray crystallographymedicineThermodynamicsMoleculeOrthorhombic crystal systemCrystallizationCrystallizationHydrateAnti-Arrhythmia AgentsFlecainidemedicine.drugPharmaceutical Development and Technology
researchProduct

Age-dependent epileptic encephalopathy associated with an unusual co-occurrence of ZEB2 and SCN1A variants.

2020

Mowat-Wilson syndrome is a genetic disorder associated with a variable phenotype including peculiar facial features associated with intellectual disability, epilepsy, language impairment, and multiple congenital anomalies caused by heterozygous mutation of the ZEB2 gene. The ZEB2 protein is a complex transcription factor that encompasses multiple functional domains that interact with the regulatory regions of target genes including those involved in brain development. Recently, it has been documented that ZEB2 regulates the differentiation of interneuron progenitors migrating from the medial ganglionic eminence to cortical layers by repression of the Nkx2-1 homeobox transcription factor. It…

ZEB2genotype-phenotype correlationSettore MED/38 - Pediatria Generale E SpecialisticaSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityHumansMowat-Wilson syndromeEEGgenotype-phenotype correlationSCN1AHirschsprung DiseaseEEGChildGenetic Association StudiesZEB2Zinc Finger E-box Binding Homeobox 2EpilepsyEEG; epilepsy; GABAergic interneurons; genotype-phenotype correlation; Mowat-Wilson syndrome; SCN1A; ZEB2FaciesElectroencephalographySettore MED/39 - Neuropsichiatria InfantileGABAergic interneuronsMowat-Wilson syndromeepilepsyNAV1.1 Voltage-Gated Sodium ChannelGABAergic interneuronsMicrocephalySettore MED/26 - NeurologiaFemaleEpileptic disorders : international epilepsy journal with videotape
researchProduct

The Sea Urchin sns Insulator Blocks CMV Enhancer following Integration in Human Cells

2001

Insulators are a new class of genetic elements that attenuate enhancer function directionally. Previously, we characterized in sea urchin a 265-bp-long insulator, termed sns. To test insulator activity following stable integration in human cells, we placed sns between the CMV enhancer and a tk promoter up-stream of a GFP transgene of plasmid or retroviral vectors. In contrast to controls, cells transfected or transduced with insulated constructs displayed a barely detectable fluorescence. Southern blot and PCR ruled out vector rearrangement following integration into host DNA; RNase protection confirmed the enhancer blocking activity. Finally, we demonstrate that two cis-acting sequences, p…

animal structuresSea UrchinVirus IntegrationTransgeneMolecular Sequence DataBiophysicsCytomegalovirusSettore BIO/11 - Biologia MolecolareSimian virus 40BiologyTransfectionPolymerase Chain ReactionBiochemistrySodium ChannelsNAV1.8 Voltage-Gated Sodium ChannelPlasmidTumor Cells CulturedAnimalsHumansEnhancer trapDNA Polymerase Chain ReactionEnhancerBinding Sites; DNA Polymerase Chain Reaction; Recombinant Proteins; Sea Urchins;Tumor Cells Cultured; Enhancer Elements Genetic; Virus Integration;Molecular BiologyVirus IntegrationSouthern blotBinding SitesBase SequenceBinding SiteCell BiologyTransfectionRecombinant ProteinMolecular biologyRecombinant ProteinsChromatinSettore BIO/18 - GeneticaEnhancer Elements GeneticSea UrchinsDNA ViralBiochemical and Biophysical Research Communications
researchProduct

Pyrrethroid resistance in Varroa destructor: Investigating the role of mutations in the voltage-gated sodium channel

2022

Entre les majors amenaces de l'apicultura contemporània es troba el parasitisme de Varroa destructor, Anderson & Trueman (Acari: Varroidae). Aquest àcar ectoparàsit altament especialitzat s'alimenta directament de les pupes i els adults de l'abella mel·lífera europea, Apis mellifera L. (Hymenoptera: Apidae), la qual cosa debilita greument a les abelles i les indueix una immunosupressió que desemboca en brots d'infeccions preexistents o vectorizades pels àcars que comprometen la viabilitat de les colònies. El control dels àcars V. destructor es un problema agreujat pel limitat número de tractaments de control disponibles i l'evolució de la resistència a aquests en les poblacions d'àcars. Enc…

varroa destructorpyrethroidvoltage-gated sodium channelUNESCO::CIENCIAS DE LA VIDAVarroa mite:CIENCIAS AGRARIAS [UNESCO]kdr-type mutation:CIENCIAS DE LA VIDA [UNESCO]UNESCO::CIENCIAS AGRARIASpyrethroid resistance
researchProduct