Search results for "Tropomyosin"

showing 10 items of 38 documents

Subtype-specific endothelin-A and endothelin-B receptor desensitization correlates with differential receptor phosphorylation.

1998

In the rat cardiovascular system endothelin-1 (ET-1) elicits prolonged physiologic responses mediated by the ET A receptor, whereas the effects mediated by the ET B receptor are transient. The molecular mechanisms for the subtype-specific responses are not yet clear. However, post-translational modifications such as phosphorylation and palmitoylation may play an important role. In Sf9 cells overexpressing the human ET A and ET B receptors, both subtypes are palmitoylated. However, only the ET B but not the ET A receptor is phosphorylated in a ligand-dependent manner. Because phosphorylation is believed to play an important role in ligand-dependent receptor inactivation, we analyzed whether …

Endothelin Receptor Antagonistsmedicine.medical_specialtyTropomyosin receptor kinase BCHO CellsBiologyEstrogen-related receptor alphaInternal medicineCricetinaemedicineEnzyme-linked receptorAnimalsHumansCloning MolecularPhosphorylationReceptorProtease-activated receptor 2Insulin-like growth factor 1 receptorPharmacologyReceptors EndothelinInterleukin-13 receptorReceptor Endothelin AReceptor Endothelin BCell biologyRatsInterleukin 10KineticsEndocrinologyCardiology and Cardiovascular MedicineSignal TransductionJournal of cardiovascular pharmacology
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Mutations in the β-tropomyosin (TPM2) gene – a rare cause of nemaline myopathy

2002

Nemaline myopathy is a clinically and genetically heterogeneous muscle disorder. In the nebulin gene we have detected a number of autosomal recessive mutations. Both autosomal dominant and recessive mutations have been detected in the genes for alpha -actin and alpha -tropomyosin 3. A recessive mutation causing nemaline myopathy among the Old Order Amish has recently been identified in the gene for slow skeletal muscle troponin T. As linkage studies had shown that at least one further gene exists for nemaline myopathy, we investigated another tropomyosin gene expressed in skeletal muscle, the beta -tropomyosin 2 gene. Screening 66 unrelated patients, using single strand conformation polymor…

Genetic MarkersMaleGenetic LinkageProtein ConformationBiopsyMolecular Sequence DataMutation MissenseTropomyosinmacromolecular substancesMuscle disorderMyopathies NemalineTPM203 medical and health sciencesNebulin0302 clinical medicineNemaline myopathymedicineAnimalsHumansAmino Acid SequenceMuscle SkeletalNemaline bodiesPolymorphism Single-Stranded ConformationalGenetics (clinical)DNA Primers030304 developmental biologyGenetics0303 health sciencesSequence Homology Amino AcidbiologyReverse Transcriptase Polymerase Chain Reactionmusculoskeletal systemmedicine.diseaseMolecular biologyTropomyosinCongenital myopathyPedigree3. Good healthHaplotypesNeurologyMutationPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)Sequence Alignment030217 neurology & neurosurgeryCentral core diseaseNeuromuscular Disorders
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NT3/TrkC pathway modulates the expression of UCP-1 and adipocyte size in human and murine adipose tissue

2020

ABSTRACTNT3, through activation of its tropomyosin-related kinase receptor C (TrkC), modulates neuronal survival and neural stem cell differentiation. It is widely distributed in peripheral tissues (specially vessels and pancreas) and this ubiquitous pattern suggests a role for NT3, outside the nervous system and related to metabolic functions. The presence of the NT3/TrkC pathway in the adipose tissue (AT) has never been investigated. Present work studies in human and murine adipose tissue (AT) the presence of elements of the NT3/TrkC pathway and its role on lipolysis and adipocyte differentiation. qRT-PCR and immunoblot indicate that NT3 was present in human retroperitoneal AT and decreas…

Genetically modified mousechemistry.chemical_compoundanimal structureschemistryAdipocyteembryonic structuresLipolysisAdipose tissueReceptorThermogenesisTropomyosin receptor kinase CNeural stem cellCell biology
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Sciences within European Young Researcher Community272The neuro-cardiac interaction defines an extracellular microdomain required for neurotrophic si…

2016

# 272 The neuro-cardiac interaction defines an extracellular microdomain required for neurotrophic signaling {#article-title-2} Purpose: Sympathetic neurons (SNs) innervate the myocardium with a defined topology that allows physiological modulation of cardiac activity. Limiting amounts of neurotrophins released by cardiac cells control SN viability and myocardial distribution, whose impairment has been described in a number of heart diseases (e.g. myocardial infarction, heart failure). Therefore, the fine control of cardiac innervation is crucial to ensure the physiological sympathetic function. It has been demonstrated that SNs directly interact with cardiomyocytes (CMs). Although it has b…

Genetically modified mousemedicine.medical_specialtybiologyTyrosine hydroxylasePhysiologyPhysiologyTropomyosin receptor kinase AAngiotensin IIEndocrinologymedicine.anatomical_structurePhysiology (medical)Internal medicinebiology.proteinmedicineMyocyteNeuronCardiology and Cardiovascular MedicineHomeostasisNeurotrophinCardiovascular Research
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Spatial shaping of cochlear innervation by temporally regulated neurotrophin expression.

2001

Previous work suggested qualitatively different effects of neurotrophin 3 (NT-3) in cochlear innervation patterning in different null mutants. We now show that all NT-3 null mutants have a similar phenotype and lose all neurons in the basal turn of the cochlea. To understand these longitudinal deficits in neurotrophin mutants, we have compared the development of the deficit in the NT-3 mutant to the spatial–temporal expression patterns of brain-derived neurotrophic factor (BDNF) and NT-3, using lacZ reporters in each gene and with expression of the specific neurotrophin receptors, trkB and trkC. In the NT-3 mutant, almost normal numbers of spiral ganglion neurons form, but fiber outgrowth t…

HeterozygoteCell SurvivalCell CountNeurotrophin-3Tropomyosin receptor kinase BTropomyosin receptor kinase CArticleMiceNeurotrophin 3Neurotrophic factorsGenes ReportermedicineAnimalsReceptor trkBReceptor trkCNeurons AfferentCochleaSpiral ganglionBrain-derived neurotrophic factorAfferent PathwaysbiologyGeneral NeuroscienceBrain-Derived Neurotrophic FactorHomozygoteGene Expression Regulation DevelopmentalImmunohistochemistryMice Mutant StrainsCochleamedicine.anatomical_structurePhenotypenervous systemAnimals NewbornLac OperonMutationbiology.proteinSpiral GanglionNeuroscienceNeurotrophin
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The expression mechanism of the residual LTP in the CA1 region of BDNF k.o. mice is insensitive to NO synthase inhibition

2011

Abstract BDNF and nitric oxide signaling both contribute to long-term potentiation (LTP) at glutamatergic synapses, but to date, few studies analyzed the interaction of both signaling cascades in the same synaptic pathway. Here we addressed the question whether the residual LTP in the CA1 region of hippocampal slices from heterozygous BDNF knockout mice (BDNF +/− ) is dependent on nitric oxide (NO) signaling. Extracellular recording of synaptic field potentials elicited by presynaptic Schaffer collateral stimulation was performed in the CA1 region of hippocampal slices of 4- to 6-week-old mice, and LTP was induced by a theta burst stimulation protocol. Application of the nitric oxide inhibi…

Long-Term PotentiationBiophysicsTropomyosin receptor kinase BIn Vitro TechniquesBiologyNitric oxideMicechemistry.chemical_compoundmedicineAnimalsEnzyme InhibitorsCA1 Region HippocampalMolecular BiologyMice KnockoutBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factormusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsLong-term potentiationElectric StimulationCell biologyMice Inbred C57BLNG-Nitroarginine Methyl EsterSynaptic fatiguemedicine.anatomical_structureAnimals Newbornnervous systemchemistrySchaffer collateralSynaptic plasticityRetrograde signalingNeurology (clinical)Nitric Oxide SynthaseNeuroscienceDevelopmental BiologyBrain Research
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Brain BDNF levels are dependent on cerebrovascular endothelium-derived nitric oxide

2016

International audience; Scientific evidence continues to demonstrate a link between endothelial function and cognition. Besides, several studies have identified a complex interplay between nitric oxide (NO) and brain-derived neurotrophic factor (BDNF), a neurotrophin largely involved in cognition. Therefore, this study investigated the link between cerebral endothelium-derived NO and BDNF signaling. For this purpose, levels of BDNF and the phosphorylated form of endothelial NO synthase at serine 1177 (p-eNOS) were simultaneously measured in the cortex and hippocampus of rats subjected to either bilateral common carotid occlusion (n=6), physical exercise (n=6) or a combination of both (n=6) …

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHippocampusPhysical exerciseTropomyosin receptor kinase BHippocampusNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemphysical exercisenitric oxideNeurotrophic factorsPhysical Conditioning AnimalInternal medicinemedicineAnimalsReceptor trkBRats WistarCerebral CortexBrain-derived neurotrophic factorbiologyChemistry[SCCO.NEUR]Cognitive science/NeuroscienceGeneral Neurosciencebrain-derived neurotrophic factorTrkB[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemRatsCerebrovascular Disorders030104 developmental biologyEndocrinologymedicine.anatomical_structurecarotid arteries occlusionnervous system[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinEndothelium VascularNeuroscience030217 neurology & neurosurgeryNeurotrophinEuropean Journal of Neuroscience
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''Comparative Effect of Treadmill Exercise on Mature BDNF Production in Control versus Stroke Rats''

2012

Quirie, Aurore | Hervieu, Marie | Garnier, Philippe | Demougeot, Celine | Mossiat, Claude | Bertrand, Nathalie | Martin, Alain | Marie, Christine | Prigent-Tessier, Anne; International audience; ''Physical exercise constitutes an innovative strategy to treat deficits associated with stroke through the promotion of BDNF-dependent neuroplasticity. However, there is no consensus on the optimal intensity/duration of exercise. In addition, whether previous stroke changes the effect of exercise on the brain is not known. Therefore, the present study compared the effects of a clinically-relevant form of exercise on cerebral BDNF levels and localization in control versus stroke rats. For this purpo…

MaleBEHAVIORAL RECOVERYTropomyosin receptor kinase BBiochemistryHippocampus0302 clinical medicineNerve Growth FactorHippocampus (mythology)StrokeCerebral Cortex0303 health sciencesNeuronal PlasticityMultidisciplinaryMOTOR RECOVERYQRTRKBNeurochemistryStrokemedicine.anatomical_structureNeurologyOrgan SpecificityCerebral cortex[ SCCO.NEUR ] Cognitive science/NeuroscienceMedicineNeurochemicalsmedicine.symptomResearch ArticleEXPRESSIONmedicine.medical_specialtyHIPPOCAMPAL PLASTICITYCORTEXCerebrovascular DiseasesAnimal TypesScienceBlotting WesternSynaptophysinEnzyme-Linked Immunosorbent AssayPhysical exerciseCONTROLLED-TRIALLesion03 medical and health sciencesPhysical Conditioning AnimalInternal medicineNeuroplasticitymedicineAnimalsLaboratory AnimalsSports and Exercise MedicineProtein PrecursorsRats WistarBiologyIschemic Stroke030304 developmental biologyBrain-derived neurotrophic factorbusiness.industry[SCCO.NEUR]Cognitive science/NeuroscienceBrain-Derived Neurotrophic FactorTRKB''AXONAL-TRANSPORTmedicine.diseaseCorpus StriatumRatsDisease Models AnimalEndocrinology''FOCAL BRAIN ISCHEMIAnervous systemFOCAL BRAIN ISCHEMIAExercise TestPhysical therapyBlood VesselsVeterinary ScienceEndothelium Vascularbusiness030217 neurology & neurosurgerySynaptic PlasticityNeuroscienceNEUROTROPHIC FACTOR
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Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

2014

International audience; Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabo…

MalePlasminlcsh:MedicineTropomyosin receptor kinase BBiochemistryMechanical Treatment of SpecimensHippocampusTissue plasminogen activator[SCCO]Cognitive scienceCell SignalingNeurotrophic factorsNeurobiology of Disease and RegenerationMedicine and Health SciencesMembrane Receptor SignalingFibrinolysinBRAINlcsh:ScienceMultidisciplinaryNeuromodulationNeurotransmitter Receptor SignalingNeurochemistryLong-term potentiationNeurotransmittersDENDRITIC GROWTHNEURONAL DEATHRECEPTORSElectroporationNeurologySpecimen DisruptionTranexamic AcidTissue Plasminogen ActivatorACTIVATORTPANMDA receptor[ SCCO ] Cognitive scienceLONG-TERM POTENTIATIONResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyN-MethylaspartateResearch and Analysis MethodsNeuropharmacologyDevelopmental NeuroscienceInternal medicinemedicineAnimalsReceptor trkBProtein PrecursorsRats WistarSPATIAL MEMORYBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factorlcsh:RBiology and Life SciencesCell BiologySYNAPTIC-PLASTICITYRetractionEndocrinologynervous systemSpecimen Preparation and TreatmentSynaptic plasticitylcsh:QMolecular NeuroscienceDizocilpine MaleateNEUROTROPHIC FACTORNeuroscienceSynaptic PlasticityPLoS ONE
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Ipsilateral versus contralateral spontaneous post-stroke neuroplastic changes: involvement of BDNF?

2013

International audience; Stroke is a leading cause of death and disability in industrialized countries. Although surviving patients exhibit a certain degree of restoration of function attributable to brain plasticity, the majority of stroke survivors has to struggle with persisting deficits. In order to potentiate post-stroke recovery, several rehabilitation therapies have been undertaken and many experimental studies have reported that brain-derived neurotrophic factor (BDNF) is central to many facets of neuroplastic processes. However, although BDNF role in brain plasticity is well characterized through strategies that manipulate its content, the involvement of this neurotrophin in spontan…

MaleTime FactorsSynaptophysinHippocampusTropomyosin receptor kinase BHippocampal formationBrain Ischemia03 medical and health sciences0302 clinical medicineNeurotrophic factorsNeuroplasticitymedicineAnimalsRats WistarStroke030304 developmental biology0303 health sciencesNeuronal PlasticitybiologyGeneral NeuroscienceBrain-Derived Neurotrophic Factor[SCCO.NEUR]Cognitive science/NeuroscienceBrainmedicine.diseaseRatsStrokenervous system[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinSynaptophysinPsychologyNeuroscience030217 neurology & neurosurgeryNeurotrophin
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