Search results for " trkC"

showing 7 items of 7 documents

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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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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Sensing life: regulation of sensory neuron survival by neurotrophins

2002

Neurotrophins are a family of structurally and functionally related neurotrophic factors which, in mammals, include: nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 (NT-3), and NT-4/5. In addition to their canonical role in promoting neuronal survival, these molecules appear to regulate multiple aspects of the development of the nervous system in vertebrates, including neuronal differentiation, axon elongation and target innervation, among others. Actions of neurotrophins and of their receptors in vivo are being analyzed by loss-of-function or gain-of-function experiments in mice. Here, we review the phenotypes of the primary sensory system in these mutant mouse strai…

Nervous systemGenetically modified mouseCell SurvivalMice TransgenicSensory systemReceptors Nerve Growth FactorMiceCellular and Molecular NeuroscienceNeurotrophic factorsmedicineAnimalsReceptor trkCNerve Growth FactorsNeurons AfferentAxonMolecular BiologyMice KnockoutPharmacologyMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorCell BiologyAnatomyProtein-Tyrosine KinasesSensory neuronmedicine.anatomical_structureNerve growth factornervous systembiology.proteinMolecular MedicineNeuroscienceSignal TransductionNeurotrophinCellular and Molecular Life 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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Activation of TRK Genes in Ewingʼs Sarcoma Trk A Receptor Expression Linked to Neural Differentiation

1997

Trk receptors have been identified by immunohistochemical methods in primitive neuroectodermal tumor (PNET)/Ewing's sarcoma (ES). However, the presence of different members of the Trk family of receptors in PNET/ES has not been specified. We have examined whether Trk A, B, and C receptors are specifically expressed in ES both with and without features of neural differentiation. Ten ES tumors (five primary tumors of bone and five extraosseous tumors transplanted into nude mice) were investigated for expression of Trk receptors by immunohistochemistry and reverse transcription-polymerase chain reaction. One primary ES and the five grafted ES tumors exhibited signs of neural differentiation; t…

animal structuresReceptor expressionReceptors Nerve Growth FactorSarcoma EwingBiologyPathology and Forensic MedicineMiceProto-Oncogene ProteinsmedicineAnimalsNeuroectodermal Tumors PrimitiveReceptor trkCReceptor trkAReceptorReceptor Ciliary Neurotrophic FactorMolecular BiologyNeuronsMembrane ProteinsReceptor Protein-Tyrosine KinasesEwing's sarcomaCell DifferentiationCell BiologyProtein-Tyrosine Kinasesmedicine.diseaseMolecular biologyGene Expression Regulation Neoplasticenzymes and coenzymes (carbohydrates)nervous systemTrk receptorPrimitive neuroectodermal tumorembryonic structuresImmunohistochemistrySarcomaImmunostainingDiagnostic Molecular Pathology
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Expression of neurotrophins, GDNF, and their receptors in rat thyroid tissue

1999

Levels of mRNA for neurotrophins (brain-derived neurotrophic factor, BDNF; neurotrophin 3, NT-3; neurotrophin 4, NT-4) and their receptors (trkA, trkB, trkC) and for glial cell line-derived neurotrophic factor (GDNF) and its receptors (ret, GDNFR-alpha) were measured in rat thyroid tissue by ribonuclease protection assays. In thyroid tissue the NT-3 mRNA level was threefold lower and the NT-4 mRNA level sixfold higher than those detected in adult rat hippocampus, while BDNF mRNA was undetectable. Very low levels of mRNA for truncated trkB and trkC receptors and no catalytic trkA, trkB or trkC were found. In conclusion NT-3 and NT-4, but not the corresponding functional receptors, are expres…

endocrine systemmedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsHistologyendocrine system diseasesThyroid GlandGene ExpressionNerve Tissue ProteinsReceptors Nerve Growth FactorNeurotrophin-3Tropomyosin receptor kinase AFollicular cellPathology and Forensic MedicineNeurotrophin 3Proto-Oncogene ProteinsInternal medicinemedicineGlial cell line-derived neurotrophic factorAnimalsDrosophila ProteinsHumansLow-affinity nerve growth factor receptorReceptor trkCGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsRNA MessengerReceptor trkAReceptor Ciliary Neurotrophic FactorbiologyBrain-Derived Neurotrophic FactorProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesCell BiologyRatsCell biologyEndocrinologynervous systemProto-Oncogene Proteins c-retbiology.proteinGDNF family of ligandsNeurotrophinCell and Tissue Research
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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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