Search results for " Nerve Growth Factor"

showing 5 items of 15 documents

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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Posttraumatic Propofol Neurotoxicity Is Mediated via the Pro–Brain-Derived Neurotrophic Factor-p75 Neurotrophin Receptor Pathway in Adult Mice*

2016

Objectives:The gamma-aminobutyric acid modulator propofol induces neuronal cell death in healthy immature brains by unbalancing neurotrophin homeostasis via p75 neurotrophin receptor signaling. In adulthood, p75 neurotrophin receptor becomes down-regulated and propofol loses its neurotoxic effect. H

musculoskeletal diseases0301 basic medicineBrain-derived neurotrophic factorProgrammed cell deathbiologybusiness.industryNeurotoxicityCaspase 3PharmacologyCritical Care and Intensive Care Medicinemedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemAnesthesiamedicinebiology.proteinLow-affinity nerve growth factor receptorReceptorbusiness030217 neurology & neurosurgeryHomeostasisNeurotrophinCritical Care Medicine
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Tiam1 as a Signaling Mediator of Nerve Growth Factor-Dependent Neurite Outgrowth

2010

Nerve Growth Factor (NGF)-induced neuronal differentiation requires the activation of members of the Rho family of small GTPases. However, the molecular mechanisms through which NGF regulates cytoskeletal changes and neurite outgrowth are not totally understood. In this work, we identify the Rac1-specific guanine exchange factor (GEF) Tiam1 as a novel mediator of NGF/TrkA-dependent neurite elongation. In particular, we report that knockdown of Tiam1 causes a significant reduction in Rac1 activity and neurite outgrowth induced by NGF. Physical interaction between Tiam1 and active Ras (Ras- GTP), but not tyrosine phosphorylation of Tiam1, plays a central role in Rac1 activation by NGF. In add…

rac1 GTP-Binding ProteinTiam1; Nerve growth factor (NGF)GTPaseTropomyosin receptor kinase ABiochemistryPC12 CellsCell Biology/Cell Signalingchemistry.chemical_compoundChlorocebus aethiopsNerve Growth FactorTiam1Guanine Nucleotide Exchange FactorsT-Lymphoma Invasion and Metastasis-inducing Protein 1NGFNeuronsMultidisciplinaryUNESCO::CIENCIAS DE LA VIDA::Biología molecularQOtras Medicina BásicaRCell Differentiation//purl.org/becyt/ford/3.1 [https]Cell biologyNeoplasm ProteinsMedicina BásicaNeuronal differentiationNerve growth factor (NGF)COS CellsMedicine//purl.org/becyt/ford/3 [https]Guanine nucleotide exchange factorSignal transductionResearch ArticleSignal TransductionCIENCIAS MÉDICAS Y DE LA SALUDNeuriteScienceCell Biology/Neuronal Signaling MechanismsRAC1Biology:CIENCIAS DE LA VIDA::Biología molecular [UNESCO]Neuroscience/Neuronal Signaling MechanismsNeuritesAnimalsHumansReceptor trkATyrosine phosphorylationMolecular biologyRatsNerve growth factorchemistrynervous systemras ProteinsRac1 GTPasePLoS ONE
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