Search results for "Contactins"

showing 3 items of 3 documents

Sympathetic neurons can produce and respond to interleukin 6

1998

Neuronal expression of cytokines is an area of active investigation in the contexts of development, disease, and normal neural function. Although cultured rat sympathetic neurons respond very weakly to exogenous interleukin 6 (IL-6), we find that addition of soluble IL-6 receptor (sIL-6R) and IL-6 enhances neuronal survival in the absence of nerve growth factor. Neutralizing monoclonal antibodies against IL-6 block these effects. Addition of IL-6 and sIL-6R also induces a subset of neuropeptide and transmitter synthetic enzyme mRNAs identical to that demonstrated for leukemia inhibitory factor, ciliary neurotrophic factor, and oncostatin M. Both of these effects are duplicated by addition o…

Superior cervical ganglionmedicine.medical_specialtyCell SurvivalRecombinant Fusion ProteinsSuperior Cervical GanglionCiliary neurotrophic factorPC12 CellsRats Sprague-DawleyMiceParacrine signallingContactinsInternal medicinemedicineAnimalsNerve Growth FactorsRNA MessengerInterleukin 6Autocrine signallingNeural Cell Adhesion MoleculesCells CulturedNeuronsMultidisciplinarybiologyInterleukin-6Neuropeptides3T3 CellsBiological SciencesReceptors Interleukin-6RatsCell biologyAutocrine CommunicationNerve growth factorEndocrinologyAnimals Newbornbiology.proteinNeural cell adhesion moleculeLeukemia inhibitory factorCaltech Library ServicesProceedings of the National Academy of Sciences
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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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Activation of oligodendroglial Fyn kinase enhances translation of mRNAs transported in hnRNP A2-dependent RNA granules.

2008

Central nervous system myelination requires the synthesis of large amounts of myelin basic protein (MBP) at the axon–glia contact site. MBP messenger RNA (mRNA) is transported in RNA granules to oligodendroglial processes in a translationally silenced state. This process is regulated by the trans-acting factor heterogeneous nuclear ribonucleoprotein (hnRNP) A2 binding to the cis-acting A2 response element (A2RE). Release of this repression of MBP mRNA translation is thus essential for myelination. Mice deficient in the Src family tyrosine kinase Fyn are hypomyelinated and contain reduced levels of MBP. Here, we identify hnRNP A2 as a target of activated Fyn in oligodendrocytes. We show that…

Heterogeneous nuclear ribonucleoproteinCell Adhesion Molecules NeuronalRecombinant Fusion ProteinsBiologyHeterogeneous ribonucleoprotein particleCytoplasmic GranulesProto-Oncogene Proteins c-fynResponse Elementsenvironment and public healthRNA TransportCell LineMiceFYNContactinsGenes ReporterReportHeterogeneous-Nuclear Ribonucleoprotein Group A-BProtein biosynthesisAnimalsRNA MessengerPhosphorylationLuciferasesNeural Cell Adhesion MoleculesResearch ArticlesMessenger RNARNATranslation (biology)Cell BiologyMolecular biologyMyelin basic proteinEnzyme ActivationOligodendroglianervous systemProtein Biosynthesisbiology.proteinProtein BindingThe Journal of cell biology
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