Search results for " Nerve Growth Factor"

showing 10 items of 15 documents

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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A Key Regulatory Role of the Transcription Factor NFATc2 in Bronchial Adenocarcinoma via CD8+ T Lymphocytes

2009

AbstractThe Ca2+-regulated calcineurin/nuclear factor of activated T cells (NFAT) cascade controls alternative pathways of T-cell activation and peripheral tolerance. Here, we describe reduction of NFATc2 mRNA expression in the lungs of patients with bronchial adenocarcinoma. In a murine model of bronchoalveolar adenocarcinoma, mice lacking NFATc2 developed more and larger solid tumors than wild-type littermates. The extent of central tumor necrosis was decreased in the tumors in NFATc2(−/−) mice, and this finding was associated with reduced tumor necrosis factor-α and interleukin-2 (IL-2) production by CD8+ T cells. Adoptive transfer of CD8+ T cells of NFATc2(−/−) mice induced transforming…

CD4-Positive T-LymphocytesCancer ResearchAdoptive cell transferTranscription GeneticTransplantation HeterologousMice TransgenicReceptors Nerve Growth FactorAdenocarcinomaCD8-Positive T-LymphocytesBiologyReceptors Tumor Necrosis FactorTransforming Growth Factor beta1Interferon-gammaMiceGlucocorticoid-Induced TNFR-Related ProteinAnimalsHumansIL-2 receptorInterleukin-7 receptorMice Inbred BALB CReceptors Interleukin-7NFATC Transcription FactorsTumor Necrosis Factor-alphaBronchial NeoplasmsInterleukin-2 Receptor alpha SubunitPeripheral toleranceForkhead Transcription FactorsNFATCalcineurinDisease Models AnimalOncologyCancer researchInterleukin-2Tumor necrosis factor alphaCD8Cancer Research
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Regulatory activity of human CD4 CD25 T cells depends on allergen concentration, type of allergen and atopy status of the donor.

2005

Regulatory CD4+ CD25+ FoxP3-positive T cells (Treg) are functional in most atopic patients with allergic rhinitis and are able to inhibit T helper type 1 (Th1) and Th2 cytokine production of CD4+ CD25- T cells. This study was designed to analyse the following additional aspects: influence of allergen concentration, influence of the type of allergen, and influence of the atopy status of the donor on the strength of the regulatory activity. CD4+ CD25- T cells from healthy non-atopic controls or from grass-pollen-allergic or wasp-venom-allergic donors were stimulated alone or in the presence of Treg with autologous mature monocyte-derived dendritic cells which were pulsed with different concen…

CD4-Positive T-LymphocytesHypersensitivity ImmediateAllergymedicine.medical_treatmentImmunologyDose-Response Relationship Immunologicchemical and pharmacologic phenomenaWasp VenomsReceptors Nerve Growth FactorBiologymedicine.disease_causePoaceaeReceptors Tumor Necrosis FactorAtopyInterleukin 21AllergenTh2 CellsAntigenT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyHumansIL-2 receptorReceptorCells CulturedCell Proliferationhemic and immune systemsForkhead Transcription FactorsReceptors Interleukin-2Original ArticlesAllergensTh1 Cellsmedicine.diseaseCoculture TechniquesCytokineImmunologyCytokinesPollenImmunology
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NFATc2 and NFATc3 transcription factors play a crucial role in suppression of CD4+ T lymphocytes by CD4+ CD25+ regulatory T cells

2005

The phenotype of NFATc2(-/-) c3(-/-) (double knockout [DKO]) mice implies a disturbed regulation of T cell responses, evidenced by massive lymphadenopathy, splenomegaly, and autoaggressive phenomena. The population of CD4(+) CD25(+) T cells from DKO mice lacks regulatory capacity, except a small subpopulation that highly expresses glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR) and CD25. However, neither wild-type nor DKO CD4(+) CD25(+) regulatory T cells (T reg cells) are able to suppress proliferation of DKO CD4(+) CD25(-) T helper cells. Therefore, combined NFATc2/c3 deficiency is compatible with the development of CD4(+) CD25(+) T reg cells but renders c…

CD4-Positive T-LymphocytesT cellImmunologyPopulationchemical and pharmacologic phenomenaReceptors Nerve Growth FactorBiologyLymphocyte ActivationReceptors Tumor Necrosis FactorInterleukin 21MiceT-Lymphocyte SubsetsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptoreducationTranscription factorMice Knockouteducation.field_of_studyNFATC Transcription FactorsZAP70Brief Definitive ReportNuclear Proteinshemic and immune systemsReceptors Interleukin-2Molecular biologyCoculture TechniquesDNA-Binding Proteinsmedicine.anatomical_structureTranscription FactorsThe Journal of Experimental Medicine
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Proneurotrophin Binding to P75 Neurotrophin Receptor (P75ntr) Is Essential for Brain Lesion Formation and Functional Impairment after Experimental Tr…

2015

Traumatic brain injury (TBI) initiates an excessive mediator release of e.g. neurotrophins, which promote neuronal survival, differentiation, and modulate synaptic plasticity. Paradoxically, mature forms of neurotrophins promote neuronal survival, whereas unprocessed forms of neurotrophins induce cell death through p75 neurotrophin receptor (p75NTR) signaling. p75NTR is widely expressed during synaptogenesis and is subsequently downregulated in adulthood. Repair mechanisms after acute cerebral insults can reactivate its expression. Therefore, the influence of p75NTR on secondary brain damage was addressed. mRNA levels of p75NTR and its ligands were quantified in brain tissue up to 7 days af…

MaleProgrammed cell deathmedicine.medical_specialtyTraumatic brain injurySynaptogenesisReceptors Nerve Growth FactorBrain damageMiceInternal medicineAnimalsMedicineLow-affinity nerve growth factor receptorRNA MessengerMice KnockoutBehavior AnimalCell Deathbiologybusiness.industrymedicine.diseaseMice Inbred C57BLDisease Models AnimalEndocrinologyBrain InjuriesSynaptic plasticitybiology.proteinFemalesense organsNeurology (clinical)medicine.symptomSignal transductionbusinessNeuroscienceProtein BindingSignal TransductionNeurotrophinJournal of Neurotrauma
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Updated overview on interplay between physical exercise, neurotrophins, and cognitive function in humans

2019

Highlights • Physical exercise maintains or improves cognitive functions, and neurotrophin receptor signaling may play an important role. • A positive relationship exists between physical exercise and circulating brain-derived neurotrophic factor levels. • Less clear evidence has been found for a relationship between physical exercise and other neurotrophin levels, such as nerve growth factor, neurotrophin-3, and neurotrophin-4. • The postexercise variation of brain-derived neurotrophic factor might be associated with improvement of neurocognitive functioning. • Physical exercise may be an inexpensive and safe strategy for boosting brain-derived neurotrophic factor release, thus preserving …

Nerve Tissue ProteinsPhysical Therapy Sports Therapy and RehabilitationPhysical exerciseReceptors Nerve Growth Factorneurotrophins03 medical and health sciencesCognition0302 clinical medicineNeurotrophin 3Neurotrophic factorsphysical exerciseRegular PaperHumansMedicineAerobic exerciseOrthopedics and Sports MedicineNerve Growth Factors030212 general & internal medicineExercisephysical exercise neurotrophins cognitive functioncognitive functionSportbiologybusiness.industryBrain-Derived Neurotrophic FactorCognition030229 sport sciencesNerve growth factorSynaptic plasticitybiology.proteinbusinessNeuroscienceNeurocognitiveNeurotrophin
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Regulation of neurogenesis by neurotrophins in developing spinal sensory ganglia.

2002

Neurons and glia in spinal sensory ganglia derive from multipotent neural crest-derived stem cells. In contrast to neural progenitor cells in the central nervous system, neural crest progenitors coexist with differentiated sensory neurons all throughout the neurogenic period. Thus, developing sensory ganglia are advantageous for determining the possible influence of cell-cell interactions in the regulation of precursor proliferation and neurogenesis. Neurotrophins are important regulators of neuronal survival in the developing vertebrate nervous system and, in addition, they appear to influence precursor behavior in vitro. Studies in mice carrying mutations in neurotrophin genes provide a g…

Nervous systemCentral nervous systemSensory systemReceptors Nerve Growth FactorBiologyMiceNeurotrophic factorsGanglia SpinalmedicineAnimalsNerve Growth FactorsNeurons AfferentGeneral NeuroscienceStem CellsNeurogenesisNeural crestCell DifferentiationNeural stem cellmedicine.anatomical_structurenervous systemNeural Crestbiology.proteinNeuroscienceNeurogliaCell DivisionNeurotrophinBrain research bulletin
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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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Activation of the p75 neurotrophin receptor through conformational rearrangement of disulphide-linked receptor dimers.

2009

Ligand-mediated dimerization has emerged as a universal mechanism of growth factor receptor activation. Recent structural studies have shown that neurotrophins interact with dimers of the p75 neurotrophin receptor (p75NTR), but the actual mechanism of receptor activation has remained elusive. Here we show that p75NTR forms disulphide-linked dimers independently of neurotrophin binding through the highly conserved Cys257 in its transmembrane domain. Mutation of Cys257 abolished neurotrophin-dependent receptor activity but did not affect downstream signaling by the p75NTR/NgR/Lingo-1 complex in response to MAG, indicating the existence of distinct, ligand-specific activation mechanisms for p7…

Protein ConformationMutantNeuronesReceptor Nerve Growth FactorMiceProtein structureChlorocebus aethiopsNerve Growth FactorLow-affinity nerve growth factor receptorRNA Small InterferingReceptorskin and connective tissue diseasesReceptors neuralsCells CulturedNeuronsCell DeathGeneral NeuroscienceNF-kappa BCell biologyTransmembrane domainSIGNALINGOligopeptidesNeurotrophinProtein BindingSignal Transductionmusculoskeletal diseasesPROTEINSNeuroscience(all)Green Fluorescent ProteinsNerve Tissue ProteinsReceptors Nerve Growth FactorSuperior Cervical GanglionBiologyTransfectionMOLNEUROArticleGrowth factor receptorAnimalsHumansProtein Interaction Domains and MotifsReceptors Growth FactorCysteineBinding SitesMembrane Proteinsbiological factorsRatsnervous systemAnimals NewbornNeurotrophin bindingMutationbiology.proteinsense organsProtein MultimerizationrhoA GTP-Binding ProteinProteïnesNeuron
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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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