Search results for " trkB"

showing 6 items of 16 documents

A common thread for pain and memory synapses? Brain-derived neurotrophic factor and trkB receptors.

2003

Recent evidence indicates that trophic factors can exert fast effects on neurones and so alter synaptic plasticity. Here, we focus on brain-derived neurotrophic factor (BDNF), which exerts a modulatory action at hippocampal synapses that are involved in learning and memory, and at the first pain synapse between primary sensory neurones and dorsal horn neurones. Hippocampal and sensory neurones share some properties for the release of endogenous BDNF. In the Schaffer collateral pathway of the hippocampus, binding of BDNF to high-affinity trkB receptors is essential for the induction of long-term potentiation, a specific type of synaptic plasticity. However, the consequences of BDNF binding t…

PharmacologyBrain-derived neurotrophic factorBrain-Derived Neurotrophic FactorPainLong-term potentiationTropomyosin receptor kinase BToxicologyHippocampusSynapsemedicine.anatomical_structurenervous systemSchaffer collateralNeurotrophic factorsMemorySynaptic plasticityMetaplasticitySynapsesmedicineHumansReceptor trkBNeurons AfferentPsychologyNeuroscienceTrends in pharmacological sciences
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Entrectinib: a potent new TRK, ROS1, and ALK inhibitor

2015

Abstract: Introduction: Receptor tyrosine kinases (RTKs) and their signaling pathways, control normal cellular processes; however, their deregulation play important roles in malignant transformation. In advanced non-small cell lung cancer (NSCLC), the recognition of oncogenic activation of specific RTKs, has led to the development of molecularly targeted agents that only benefit roughly 20% of patients. Entrectinib is a pan-TRK, ROS1 and ALK inhibitor that has shown potent anti-neoplastic activity and tolerability in various neoplastic conditions, particularly NSCLC. Areas covered: This review outlines the pharmacokinetics, pharmacodynamics, mechanism of action, safety, tolerability, pre-cl…

Receptor Protein-Tyrosine KinasesEntrectinibNTRK1NTRK2NTRK3Receptor tyrosine kinaseEntrectinibMalignant transformationAntineoplastic AgentNeoplasmsProtein-Tyrosine KinaseALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor; trkA; Receptor; trkB; Receptor; trkC; Pharmacology; Pharmacology (medical)Anaplastic Lymphoma KinasePharmacology (medical)salivary gland cancerProto-Oncogene ProteinbiologyTrkAPharmacology. TherapyTrkCTrkBGeneral MedicineProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinaseBenzamidesmedicine.symptomROS1ReceptorHumanIndazolesmedicine.drug_classprecision medicineAntineoplastic Agentscolorectal cancerBenzamideProto-Oncogene ProteinsmedicineROS1AnimalsHumansReceptor trkBReceptor trkCReceptor trkAnon-small cell lung cancerPharmacologyAnimalReceptor Protein-Tyrosine KinasesALK inhibitorIndazoleMechanism of actionALKTrk receptorbiology.proteinCancer researchNeoplasmALK; colorectal cancer; Entrectinib; non-small cell lung cancer; NTRK1; NTRK2; NTRK3; precision medicine; ROS1; salivary gland cancer; TrkA; TrkB; TrkC; Animals; Antineoplastic Agents; Benzamides; Humans; Indazoles; Neoplasms; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Receptor trkA; Receptor trkB; Receptor trkC; Pharmacology; Pharmacology (medical)Expert Opinion on Investigational Drugs
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p27Kip1participates in the regulation of endoreplication in differentiating chick retinal ganglion cells

2015

Nuclear DNA duplication in the absence of cell division (i.e. endoreplication) leads to somatic polyploidy in eukaryotic cells. In contrast to some invertebrate neurons, whose nuclei may contain up to 200,000-fold the normal haploid DNA amount (C), polyploid neurons in higher vertebrates show only 4C DNA content. To explore the mechanism that prevents extra rounds of DNA synthesis in these latter cells we focused on the chick retina, where a population of tetraploid retinal ganglion cells (RGCs) has been described. We show that differentiating chick RGCs that express the neurotrophic receptors p75 and TrkB while lacking retinoblastoma protein, a feature of tetraploid RGCs, also express p27K…

Retinal Ganglion CellsretinaEndocycleCell divisionCellular differentiationChick EmbryoRetinoblastoma ProteinendoreduplicationMicevertebrateRNA Small InterferingpolyploidyMice KnockoutRGCeducation.field_of_studyCell DifferentiationEndoreduplicationCell cycleImmunohistochemistryNuclear DNAendocycleneurogenesiscell cycleRNA InterferenceCyclin-Dependent Kinase Inhibitor p27NeurogenesisPopulationDown-RegulationCell cycleBiologyRetinal ganglionRetinaPolyploidyReportAnimalsReceptor trkBEndoreduplicationeducationMolecular BiologyPloidiesDNA synthesisVertebrateCyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cell BiologyMinichromosome Maintenance Complex Component 7Molecular biologyeye diseasessense organsChickensDevelopmental BiologyCell Cycle
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Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor.

2004

The Trk family of receptor tyrosine kinases and the p75 receptor (p75NTR) mediate the effects of neurotrophins on neuronal survival, differentiation and synaptic plasticity. The neurotrophin BDNF and its cognate receptor tyrosine kinase, TrkB.FL, are highly expressed in neurons of the central nervous system. At later stages in postnatal development the truncated TrkB splice variants (TrkB.T1, TrkB.T2) become abundant. However, the signalling and function of these truncated receptors remained largely elusive.We show that overexpression of TrkB.T1 in hippocampal neurons induces the formation of dendritic filopodia, which are known precursors of synaptic spines. The induction of filopodia by T…

Time FactorsGreen Fluorescent ProteinsReceptors Nerve Growth FactorTropomyosin receptor kinase ATransfectionTropomyosin receptor kinase CHippocampusModels BiologicalPC12 CellsReceptor Nerve Growth FactorReceptor tyrosine kinaseLow-affinity nerve growth factor receptorAnimalsReceptor trkBNerve Growth FactorsPseudopodiaCloning MolecularNeuronsbiologyDose-Response Relationship Drugmusculoskeletal neural and ocular physiologyCell DifferentiationCell BiologyDendritesImmunohistochemistryDendritic filopodiaCell biologyProtein Structure TertiaryRatsnervous systemMicroscopy FluorescenceTrk receptorembryonic structuresNeurotrophin bindingCOS Cellsbiology.proteinsense organsNeurotrophinProtein BindingSignal TransductionJournal of cell science
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Astrocytes in culture express the full-length Trk-B receptor and respond to brain derived neurotrophic factor by changing intracellular calcium level…

2000

Abstract Although cultured astroglial cells were reported to express exclusively the truncated non-catalytic Trk B receptor for brain-derived neurotrophic factor (BDNF), we detect here, using a sensitive ribonuclease protection assay, mRNAs for both truncated (TrkB–T) and the full length catalytic (TrkB–fl) form of BDNF receptor in developing cortical astrocytes and neurons in culture. Cortical neurons and immature astroglia, such as radial glia and proliferating astrocytes, express both the protein and mRNAs for TrkB-fl and TrkB-T, whereas the differentiation of astrocytes leads to a decrease in the trkB-fl mRNA, being the truncated TrkB the predominant receptor in differentiating and conf…

Tropomyosin receptor kinase BBiologyFetusNeurotrophic factorsmedicineAnimalsReceptor trkBRNA MessengerReceptorCells CulturedBrain-derived neurotrophic factorEthanolmusculoskeletal neural and ocular physiologyGeneral NeuroscienceBrain-Derived Neurotrophic FactorCentral Nervous System DepressantsGene Expression Regulation DevelopmentalCell DifferentiationCell biologyRatsmedicine.anatomical_structurenervous systemAstrocytesembryonic structuresbiology.proteinNeurogliaCalciumSignal transductionNeuroscienceNeurotrophinAstrocyteNeuroscience letters
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Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
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