Search results for "Nerve Tissue Protein"

showing 10 items of 345 documents

Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell–cell Adhesion in the Postnatal Brain

2018

In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell–cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening andin vivoloss-of-function and gain-of-f…

Male0301 basic medicineanimal structuresRostral migratory streamNerve Tissue ProteinsProto-Oncogene Proteins c-fynAdherens junctionMice03 medical and health sciencesFYNNeural Stem CellsNeuroblastCell MovementCell AdhesionmedicineAnimalsCell adhesionResearch ArticlesChemistryGeneral NeurosciencefungiBrainCateninsCadherinsDAB1Granule cellOlfactory BulbOlfactory bulbCell biology030104 developmental biologymedicine.anatomical_structurenervous systemGene Knockdown Techniquesembryonic structuresFemaleThe Journal of Neuroscience
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

2018

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim…

Male0301 basic medicinemetabolism [Apoptosis Regulatory Proteins]FAIM2 protein humanlifeguard protein mouseIschemiaNerve Tissue Proteinspathology [Ischemic Attack Transient]physiology [Neuroprotection]PharmacologyBiochemistryNeuroprotectionmetabolism [Erythropoietin]metabolism [Ischemic Attack Transient]Brain ischemiaMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineAnimalsHumansddc:610ErythropoietinStrokeProtein kinase BPI3K/AKT/mTOR pathwayAgedpharmacology [Erythropoietin]Mice Knockoutmetabolism [Nerve Tissue Proteins]business.industryPenumbraMembrane ProteinsMiddle Agedmedicine.diseaseNeuroprotection030104 developmental biologyIschemic Attack TransientErythropoietinphysiopathology [Ischemic Attack Transient]FemaleDose-dependency ; Erythropoietin ; Fas-apoptotic Inhibitory Molecule 2 ; Ischemia-reperfusion ; Neuroprotection ; StrokeApoptosis Regulatory Proteinsbusinessmetabolism [Membrane Proteins]030217 neurology & neurosurgerymedicine.drug
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Analysis of N-terminal-pro-brain natriuretic peptide and C-reactive protein for risk stratification in stable and unstable coronary artery disease: r…

2004

Aims N-terminal-pro-brain natriuretic peptide (Nt-proBNP) is a reliable risk predictor in acute coronary artery disease (CAD). Little is known about patients with stable angina pectoris (SAP). We aimed to investigate the prognostic impact of Nt-proBNP in a population with CAD especially focussing on patients with SAP. Methods and results We obtained baseline samples from a prospective cohort of 904 consecutive patients with CAD. Cardiovascular events were registered during followup (median 2 years; maximum 3.7 years). Baseline Nt-proBNP was significantly higher among individuals with cardiovascular events compared with those without (711.5 vs. 238.8 pg/mL; P , 0.0001). A similar association…

MaleAcute coronary syndromemedicine.medical_specialtymedicine.drug_classPopulationNerve Tissue ProteinsCoronary Artery DiseaseRisk AssessmentAngina PectorisCohort StudiesCoronary artery diseasePredictive Value of TestsRisk FactorsInternal medicineNatriuretic Peptide BrainmedicineNatriuretic peptideHumansProspective Studiescardiovascular diseasesRisk factoreducationeducation.field_of_studybiologybusiness.industryC-reactive proteinMiddle AgedPrognosismedicine.diseaseBrain natriuretic peptideSurvival AnalysisPeptide FragmentsC-Reactive ProteinEndocrinologyQuartilebiology.proteinCardiologyFemaleCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
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Prospero mutants induce precocious sexual behavior in Drosophila males.

2007

0001-8244 (Print) Journal Article Research Support, Non-U.S. Gov't; Brain maturation, a developmental process influenced by both endogenous and environmental factors, can affect sexual behavior. In vertebrates and invertebrates, sexual maturation is under the influence of hormones and neuromodulators, but the role of developmental genes in this process is still poorly understood. We report that prospero (pros), a gene crucial for nervous system development, can change the age of onset of sexual behavior in Drosophila melanogaster males: adult males carrying a single copy of several pros mutations court females and mate at a younger age than control males. However, these pros mutations had n…

MaleAgingmedia_common.quotation_subjectSexual BehavioreducationNerve Tissue ProteinsTranscription Factors/*geneticsCrossesmedicine.disease_causeCourtship03 medical and health sciencesSexual Behavior Animal0302 clinical medicineGeneticGeneticsmedicineNuclear Proteins/*geneticsAnimal/*physiologySexual maturityAnimalsDrosophila ProteinsMatingHydrocarbons/analysisGenetics (clinical)Ecology Evolution Behavior and SystematicsCrosses Genetic030304 developmental biologymedia_commonGenetics0303 health sciencesMutationbiologyDrosophila Proteins/*geneticsNuclear ProteinsProsperobiology.organism_classificationPhenotypeNerve Tissue Proteins/*geneticshumanitiesHydrocarbonsDrosophila melanogasterPhenotypeMutationFemaleDrosophila melanogasterAge of onset030217 neurology & neurosurgeryDrosophila melanogaster/cytology/*genetics/growth & development/physiologyTranscription FactorsBehavior genetics
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The cognition‐enhancing activity of E1R , a novel positive allosteric modulator of sigma‐1 receptors

2013

Background and Purpose Here, we describe the in vitro and in vivo effects of (4R,5S)-2-(5-methyl-2-oxo-4-phenyl-pyrrolidin-1-yl)-acetamide (E1R), a novel positive allosteric modulator of sigma-1 receptors. Experimental Approach E1R was tested for sigma receptor binding activity in a [3H](+)-pentazocine assay, in bradykinin (BK)-induced intracellular Ca2+ concentration ([Ca2+]i) assays and in an electrically stimulated rat vas deferens model. E1R's effects on cognitive function were tested using passive avoidance (PA) and Y-maze tests in mice. A selective sigma-1 receptor antagonist (NE-100), was used to study the involvement of the sigma-1 receptor in the effects of E1R. The open-field test…

MaleAgonistAllosteric modulatormedicine.drug_classSigma receptorNerve Tissue ProteinsIn Vitro TechniquesMotor ActivityPharmacologyCell LineMiceCognitionVas DeferensAllosteric RegulationIn vivoAcetamidesmedicineAnimalsReceptors sigmaCalcium SignalingRats WistarReceptorNootropic AgentsPharmacologyMice Inbred BALB CMice Inbred ICRSigma-1 receptorBehavior AnimalChemistryBrainDrug SynergismReceptor antagonistPiracetamResearch PapersCholinergic NeuronsPyrrolidinonesRacetamRatsDisease Models AnimalNeuroprotective AgentsAmnesiamedicine.drugBritish Journal of Pharmacology
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The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling.

2021

Nondegradative ubiquitin chains attached to specific targets via Lysine 63 (K63) residues have emerged to play a fundamental role in synaptic function. The K63-specific deubiquitinase CYLD has been widely studied in immune cells and lately also in neurons. To better understand if CYLD plays a role in brain and synapse homeostasis, we analyzed the behavioral profile of CYLD-deficient mice. We found that the loss of CYLD results in major autism-like phenotypes including impaired social communication, increased repetitive behavior, and cognitive dysfunction. Furthermore, the absence of CYLD leads to a reduction in hippocampal network excitability, long-term potentiation, and pyramidal neuron s…

MaleAutism Spectrum DisorderNerve Tissue ProteinsHippocampal formationHippocampusDeubiquitinating enzymeSynapseMiceUbiquitinAutophagyAnimalsAutistic DisorderMechanistic target of rapamycinPI3K/AKT/mTOR pathwayNeuronsMultidisciplinarybiologyUbiquitinLysineTOR Serine-Threonine KinasesAutophagyMicrofilament ProteinsUbiquitinationLong-term potentiationBiological SciencesDeubiquitinating Enzyme CYLDMice Inbred C57BLSynapsesbiology.proteinFemaleNeuroscienceSignal TransductionProceedings of the National Academy of Sciences of the United States of America
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Mice lacking α-synuclein display functional deficits in the nigrostriatal dopamine system

2000

alpha-Synuclein (alpha-Syn) is a 14 kDa protein of unknown function that has been implicated in the pathophysiology of Parkinson's disease (PD). Here, we show that alpha-Syn-/- mice are viable and fertile, exhibit intact brain architecture, and possess a normal complement of dopaminergic cell bodies, fibers, and synapses. Nigrostriatal terminals of alpha-Syn-/- mice display a standard pattern of dopamine (DA) discharge and reuptake in response to simple electrical stimulation. However, they exhibit an increased release with paired stimuli that can be mimicked by elevated Ca2+. Concurrent with the altered DA release, alpha-Syn-/- mice display a reduction in striatal DA and an attenuation of …

MaleCalbindinsNeuroscience(all)DopamineDopamine AgentsLong-Term PotentiationPresynaptic TerminalsSynucleinsGene ExpressionGlutamic AcidSubstantia nigraNerve Tissue ProteinsNeurotransmissionMotor ActivityHippocampusSynaptic TransmissionReuptakechemistry.chemical_compoundMiceS100 Calcium Binding Protein GDopamineDopaminergic CellmedicineAnimalsAutoreceptorsAlpha-synucleinMice KnockoutNeuronsGeneral NeuroscienceRab3A GTP-Binding ProteinCorpus Striatumrab3A GTP-Binding Proteinnervous system diseasesMice Inbred C57BLSubstantia NigraAmphetaminechemistrynervous systemalpha-SynucleinCalciumFemaleBeta-synucleinNeuroscienceLocomotionmedicine.drug
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Neurogenin 3+ cells contribute to β-cell neogenesis and proliferation in injured adult mouse pancreas

2013

Abstract: We previously showed that injury by partial duct ligation (PDL) in adult mouse pancreas activates Neurogenin 3 (Ngn3)(+) progenitor cells that can differentiate to beta cells ex vivo. Here we evaluate the role of Ngn3(+) cells in beta cell expansion in situ. PDL not only induced doubling of the beta cell volume but also increased the total number of islets. beta cells proliferated without extended delay (the so-called 'refractory' period), their proliferation potential was highest in small islets, and 86% of the beta cell expansion was attributable to proliferation of pre-existing beta cells. At sufficiently high Ngn3 expression level, upto 14% of all beta cells and 40% of small i…

MaleCancer Researchmedicine.medical_specialtyendocrine systemCell- och molekylärbiologiImmunologyCellNerve Tissue Proteinsdigestive systemNeogenesisCellular and Molecular NeuroscienceMiceInternal medicineInsulin-Secreting CellsJournal ArticlemedicineBasic Helix-Loop-Helix Transcription FactorsAnimalsInsulinRegenerationProgenitor cellBeta (finance)PancreasCell ProliferationCell SizeMice Inbred BALB CbiologydiabetesCell growthResearch Support Non-U.S. Gov'tRegeneration (biology)Cell Biologybiology.organism_classificationCell biologytissue injurycell differentiationEndocrinologymedicine.anatomical_structureOriginal ArticleHuman medicinePancreasEx vivoCell and Molecular BiologyCell Death & Disease
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Functional Inactivation of the Genome-Wide Association Study Obesity Gene Neuronal Growth Regulator 1 in Mice Causes a Body Mass Phenotype

2012

To date, genome-wide association studies (GWAS) have identified at least 32 novel loci for obesity and body mass-related traits. However, the causal genetic variant and molecular mechanisms of specific susceptibility genes in relation to obesity are yet to be fully confirmed and characterised. Here, we examined whether the candidate gene NEGR1 encoding the neuronal growth regulator 1, also termed neurotractin or Kilon, accounts for the obesity association. To characterise the function of NEGR1 for body weight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-deficient mouse line as well as an ENU-mutagenised line carrying a loss-of-function mutation …

MaleCandidate geneMutantlcsh:MedicineGenome-wide association studymedicine.disease_causeEndoplasmic ReticulumEatingGene Knockout TechniquesMice0302 clinical medicineEndocrinologylcsh:ScienceObesity; NEGR1; GWAS; body weight control2. Zero hungerGenetics0303 health sciencesMutationMultidisciplinaryNeuronal growth regulator 1GenomicsPhenotypePhenotypeMedicineFemaleFunction and Dysfunction of the Nervous SystemResearch ArticleGenotypeHypothalamusNerve Tissue ProteinsBiologyMotor ActivityDiet High-FatCell Line03 medical and health sciencesGenetic MutationGenome Analysis ToolsmedicineGeneticsGenome-Wide Association StudiesCell AdhesionNeuritesAnimalsHumansObesityGene SilencingGeneBiologyAlleles030304 developmental biologyNutritionlcsh:RBody WeightMembrane ProteinsHuman GeneticsNeuroendocrinologyBody HeightMetabolic DisordersGenetics of DiseaseLean body masslcsh:QEnergy Metabolism030217 neurology & neurosurgeryGenome-Wide Association StudyPLoS ONE
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