Search results for "receptor kinase"

showing 10 items of 54 documents

Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6.

2015

Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 level…

0301 basic medicineDendritic spineVesicular Inhibitory Amino Acid Transport Proteinsdrug effects [Synapses]Tropomyosin receptor kinase BHippocampal formationgenetics [Carrier Proteins]pharmacology [Brain-Derived Neurotrophic Factor]Hippocampusmetabolism [Vesicular Inhibitory Amino Acid Transport Proteins]Mtap2 protein ratMice0302 clinical medicineNeurotrophic factorsdrug effects [Synaptic Vesicles]genetics [Nerve Tissue Proteins]Cells Culturedultrastructure [Neurons]NeuronsChemistryLong-term potentiationSynaptic Potentialsphysiology [Neurons]physiology [Dendritic Spines]Cell biologyultrastructure [Dendritic Spines]metabolism [Receptor trkB]Synaptic VesiclesFilopodiaultrastructure [Synaptosomes]Disks Large Homolog 4 ProteinMicrotubule-Associated ProteinsCognitive NeuroscienceDendritic Spinesmetabolism [Disks Large Homolog 4 Protein]Nerve Tissue Proteinsgenetics [Receptor trkB]03 medical and health sciencesCellular and Molecular NeuroscienceOrgan Culture Techniquesphysiology [Synaptic Vesicles]metabolism [Vesicular Glutamate Transport Protein 1]TrkB protein ratdrug effects [Synaptic Potentials]Synaptic vesicle recyclingAnimalsHumansReceptor trkBddc:610metabolism [Synaptosomes]metabolism [Nerve Tissue Proteins]Viaat protein ratBrain-Derived Neurotrophic Factormetabolism [Microtubule-Associated Proteins]Rats030104 developmental biologygenetics [Synaptic Potentials]nervous systemcytology [Hippocampus]Synaptic plasticityultrastructure [Synapses]SynapsesVesicular Glutamate Transport Protein 1CPNE6 protein ratphysiology [Synapses]Carrier Proteins030217 neurology & neurosurgerymetabolism [Carrier Proteins]SynaptosomesCerebral cortex (New York, N.Y. : 1991)
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The Amino-Terminal Domain of GRK5 Inhibits Cardiac Hypertrophy through the Regulation of Calcium-Calmodulin Dependent Transcription Factors.

2018

We have recently demonstrated that the amino-terminal domain of G protein coupled receptor kinase (GRK) type 5, (GRK5-NT) inhibits NFκB activity in cardiac cells leading to a significant amelioration of LVH. Since GRK5-NT is known to bind calmodulin, this study aimed to evaluate the functional role of GRK5-NT in the regulation of calcium-calmodulin-dependent transcription factors. We found that the overexpression of GRK5-NT in cardiomyoblasts significantly reduced the activation and the nuclear translocation of NFAT and its cofactor GATA-4 in response to phenylephrine (PE). These results were confirmed in vivo in spontaneously hypertensive rats (SHR), in which intramyocardial adenovirus-med…

0301 basic medicineG-Protein-Coupled Receptor Kinase 5MalecalmodulinMutantWistarPlasma protein binding030204 cardiovascular system & hematologyCatalysilcsh:ChemistryPhenylephrine0302 clinical medicineRats Inbred SHRMyocytes Cardiaclcsh:QH301-705.5SpectroscopybiologyChemistrycardiac hypertrophyNFATComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineLeft VentricularComputer Science ApplicationsCell biologycardiac hypertrophy; transcription factors; calmodulin; GRKGRKHypertrophy Left VentricularCardiacProtein BindingInbred SHRCalmodulinCalmodulin; Cardiac hypertrophy; GRK; Transcription factors; Animals; Binding Sites; Calmodulin; Cell Line; G-Protein-Coupled Receptor Kinase 5; GATA4 Transcription Factor; Hypertrophy Left Ventricular; Male; Myocytes Cardiac; NFATC Transcription Factors; Phenylephrine; Protein Binding; Rats; Rats Inbred SHR; Rats Wistar; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryCatalysisArticleCell LineInorganic Chemistry03 medical and health sciencesG-Protein-Coupled Receptor Kinase 5transcription factorsAnimalsPhysical and Theoretical ChemistryRats WistarTranscription factorMolecular BiologyG protein-coupled receptor kinaseMyocytesBinding SitesNFATC Transcription FactorsOrganic ChemistryHypertrophyNFATC Transcription FactorsGATA4 Transcription FactorRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinTranscription factorInternational journal of molecular sciences
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NT3/TrkC Pathway Modulates the Expression of UCP-1 and Adipocyte Size in Human and Rodent Adipose Tissue

2021

Neurotrophin-3 (NT3), 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 (especially 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 (encoded by NTF3) was present in human re…

0301 basic medicineMaleAgingSympathetic Nervous SystemEndocrinology Diabetes and Metabolismbeta-adrenoceptorsAdipose tissueWhite adipose tissueTropomyosin receptor kinase Clcsh:Diseases of the endocrine glands. Clinical endocrinologychemistry.chemical_compound0302 clinical medicineEndocrinologyAdipocyteBrown adipose tissueUncoupling Protein 1Original ResearchbiologyChemistryCell Differentiationtropomyosin-related kinase receptor CCell biologymedicine.anatomical_structureAdipose Tissueembryonic structuresFemaleSignal Transductionanimal structuresadipocytesLipolysisUCP-1Mice TransgenicNeurotrophin-303 medical and health scienceswhite adipose tissueneurotrophin-3Receptors Adrenergic betamedicineLipolysisAnimalsHumansReceptor trkCRats WistarAgedCell Sizelcsh:RC648-665Body Weightbrown adipose tissue030104 developmental biologybiology.proteinBlood VesselsThermogenesis030217 neurology & neurosurgeryBiomarkersFrontiers in Endocrinology
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The TrkB agonist 7,8-dihydroxyflavone changes the structural dynamics of neocortical pyramidal neurons and improves object recognition in mice

2018

This is a pre-print of an article published in Brain Structure and Function. The final authenticated version is available online at: https://doi.org/10.1007/s00429-018-1637-x. BDNF and its receptor TrkB have important roles in neurodevelopment, neural plasticity, learning, and memory. Alterations in TrkB expression have been described in different CNS disorders. Therefore, drugs interacting with TrkB, specially agonists, are promising therapeutic tools. Among them, the recently described 7,8-dihydroxyflavone (DHF), an orally bioactive compound, has been successfully tested in animal models of these diseases. Recent studies have shown the influence of this drug on the structure of pyramidal …

0301 basic medicineMaleDendritic spineTrkB receptorNeocortexTropomyosin receptor kinase B78-Dihydroxyflavoneaxonal dynamicsMice0302 clinical medicineReceptorMembrane GlycoproteinsGeneral NeurosciencePyramidal CellsProtein-Tyrosine Kinases2-Photonbarrel cortexFemaleMicrogliaAnatomyAgonistHistologymedicine.drug_classDendritic SpinesMice TransgenicBiologyspine dynamicsrecognition memory03 medical and health sciencesBacterial ProteinsNeuroplasticitymedicinepyramidal neuronAnimalsMaze LearningParenchymal TissueRecognition memoryAnalysis of VarianceRecognition PsychologyBarrel cortexFlavonesAxonsLuminescent Proteins030104 developmental biologynervous systemAstrocytesen passant boutonsThy-1 AntigensNeuroscience030217 neurology & neurosurgery
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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Serotonin Heteroreceptor Complexes and Their Integration of Signals in Neurons and Astroglia—Relevance for Mental Diseases

2021

The heteroreceptor complexes present a novel biological principle for signal integration. These complexes and their allosteric receptor–receptor interactions are bidirectional and novel targets for treatment of CNS diseases including mental diseases. The existence of D2R-5-HT2AR heterocomplexes can help explain the anti-schizophrenic effects of atypical antipsychotic drugs not only based on blockade of 5-HT2AR and of D2R in higher doses but also based on blocking the allosteric enhancement of D2R protomer signaling by 5-HT2AR protomer activation. This research opens a new understanding of the integration of DA and 5-HT signals released from DA and 5-HT nerve terminal networks. The biologica…

0301 basic medicineReviewheteroreceptor complexesTropomyosin receptor kinase BReceptor tyrosine kinasechemistry.chemical_compound0302 clinical medicineG protein-coupled receptorsserotonin receptorsReceptor Serotonin 5-HT2ABiology (General)astrogliabiologyChemistryMental DisordersBrainGeneral MedicineAntidepressive AgentsdepressionG protein-coupled receptors; astroglia; depression; heteroreceptor complexes; rapid antidepressant drugs; receptor tyrosine kinase; serotonin receptors.medicine.symptomAntipsychotic AgentsSerotonergic NeuronsSignal TransductionProto-oncogene tyrosine-protein kinase Srcserotonin receptorheteroreceptor complexeQH301-705.5Astroglia; Depression; G protein-coupled receptors; Heteroreceptor complexes; Rapid antidepressant drugs; Receptor tyrosine kinase; Serotonin receptors;Allosteric regulationserotonin receptors heteroreceptor complexes depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptors.depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptorsHeteroreceptorNO03 medical and health sciencesmedicineAnimalsHumansReceptor Fibroblast Growth Factor Type 1rapid antidepressant drugsG protein-coupled receptorReceptors Dopamine D2Dopaminergic NeuronsTyrosine phosphorylationReceptor Cross-TalkReceptor Galanin Type 1Receptor Galanin Type 2030104 developmental biologyMechanism of actionAstrocytesreceptor tyrosine kinasebiology.proteinReceptors Serotonin 5-HT1Neuroscience030217 neurology & neurosurgeryCells
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Optical activation of TrkB neurotrophin receptor in mouse ventral hippocampus promotes plasticity and facilitates fear extinction

2021

AbstractSuccessful extinction of traumatic memories depends on neuronal plasticity in the fear extinction network. However, the mechanisms involved in the extinction process remain poorly understood. Here, we investigated the fear extinction network by using a new optogenetic technique that allows temporal and spatial control of neuronal plasticity in vivo. We optimized an optically inducible TrkB (CKII-optoTrkB), the receptor of the brain-derived neurotrophic factor, which can be activated upon blue light exposure to increase plasticity specifically in pyramidal neurons. The activation of CKII-optoTrkB facilitated the induction of LTP in Schaffer collateral-CA1 synapses after brief theta-b…

0303 health sciencesHippocampusLong-term potentiationExtinction (psychology)Tropomyosin receptor kinase BOptogeneticsBiology03 medical and health sciences0302 clinical medicinenervous systemNeurotrophic factorsNeuroplasticitybiology.proteinNeuroscience030217 neurology & neurosurgery030304 developmental biologyNeurotrophin
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Brothers in arms: proBDNF/BDNF and sAPPα/Aβ-signaling and their common interplay with ADAM10, TrkB, p75NTR, sortilin, and sorLA in the progression of…

2021

Abstract Brain-derived neurotrophic factor (BDNF) is an important modulator for a variety of functions in the central nervous system (CNS). A wealth of evidence, such as reduced mRNA and protein level in the brain, cerebrospinal fluid (CSF), and blood samples of Alzheimer’s disease (AD) patients implicates a crucial role of BDNF in the progression of this disease. Especially, processing and subcellular localization of BDNF and its receptors TrkB and p75 are critical determinants for survival and death in neuronal cells. Similarly, the amyloid precursor protein (APP), a key player in Alzheimer’s disease, and its cleavage fragments sAPPα and Aβ are known for their respective roles in neuropro…

ADAM10Clinical BiochemistryNerve Tissue ProteinsTropomyosin receptor kinase BReceptors Nerve Growth FactorBiochemistryNeuroprotectionADAM10 ProteinAmyloid beta-Protein PrecursorNeurotrophic factorsAlzheimer DiseaseAmyloid precursor proteinHumansReceptor trkBMolecular BiologyLDL-Receptor Related ProteinsAmyloid beta-PeptidesMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorMembrane ProteinsMembrane Transport ProteinsAdaptor Proteins Vesicular Transportnervous systembiology.proteinSignal transductionAmyloid Precursor Protein SecretasesNeuroscienceAmyloid precursor protein secretaseNeurotrophinBiological chemistryReferences
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Different expression of adrenoceptors and GRKs in the human myocardium depends on heart failure etiology and correlates to clinical variables.

2012

Downregulation of β1- adrenergic receptors (β1-ARs) and increased expression/function of G-protein-coupled receptor kinase 2 (GRK2) have been observed in human heart failure, but changes in expression of other ARs and GRKs have not been established. Another unresolved question is the incidence of these compensatory mechanisms depending on heart failure etiology and treatment. To analyze these questions, we quantified the mRNA/protein expressions of six ARs (α1A, α1B, α1D, β1, β2, and β3) and three GRKs (GRK2, GRK3, and GRK5) in left (LV) and right ventricle (RV) from four donors, 10 patients with ischemic cardiomyopathy (IC), 14 patients with dilated cardiomyopathy (DC), and 10 patients wit…

AdultCardiomyopathy DilatedMalemedicine.medical_specialtyGenotypePhysiologyCardiomyopathyMyocardial IschemiaVentricular Function LeftPhysiology (medical)Internal medicinemedicineHumansRNA MessengerHeart FailureAnalysis of VarianceEjection fractionIschemic cardiomyopathybiologybusiness.industryBeta adrenergic receptor kinaseMyocardiumDilated cardiomyopathyStroke VolumeStroke volumeMiddle Agedmedicine.diseaseG-Protein-Coupled Receptor KinasesReceptors AdrenergicEndocrinologymedicine.anatomical_structurePhenotypeVentricleSpainHeart failurebiology.proteinCardiologyLinear ModelsFemaleCardiology and Cardiovascular MedicinebusinessCardiomyopathiesAmerican journal of physiology. Heart and circulatory physiology
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Changes in Adrenoceptor and GRK Expression in Patients With Chronic Pulmonary Regurgitation.

2019

INTRODUCTION AND OBJECTIVES Pulmonary regurgitation (PR) is a frequent complication after repair of congenital heart disease. Lymphocyte expression of adrenoceptors (β1 and β2) and kinases (GRK2, GRK3, and GRK5) reflects the neurohumoral changes that occur in heart failure (HF). The main objective of this study was to describe the gene expression of these molecules in circulating lymphocytes in patients with severe PR. METHODS A prospective study was conducted to analyze lymphocyte expression of these molecules in patients with severe PR and compare it with expression in healthy controls and patients with advanced HF. RESULTS We studied 35 patients with severe PR, 22 healthy controls, and 1…

AdultMalemedicine.medical_specialtyHeart diseaseLymphocyteMagnetic Resonance Imaging Cine030204 cardiovascular system & hematologyGastroenterology03 medical and health sciences0302 clinical medicineInternal medicineGene expressionmedicineHumansProspective StudiesProspective cohort studybiologyKinasebusiness.industryBeta adrenergic receptor kinaseGeneral MedicineMiddle Agedmedicine.diseaseG-Protein-Coupled Receptor KinasesPulmonary Valve InsufficiencyReceptors Adrenergicmedicine.anatomical_structureGene Expression RegulationHeart failureChronic Diseasebiology.proteinRNAFemaleComplicationbusinessFollow-Up StudiesRevista espanola de cardiologia (English ed.)
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