Search results for "Growth factors"

showing 10 items of 118 documents

Central nicotinic receptors, neurotrophic factors and neuroprotection

2000

The multiple combinations of nAChR subunits identified in central nervous structures possess distinct pharmacological and physiological properties. A growing number of data have shown that compounds interacting with neuronal nAChRs have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improving of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's and Parkinson's disease. Taken together experimental and clinical data largely ind…

Cell SurvivalAgonist-antagonistCentral nervous systemReceptors Nicotiniccomplex mixturesNeuroprotectionBehavioral NeuroscienceNeurotrophic factorsmental disordersmedicineAnimalsHumansNerve Growth FactorsAcetylcholine receptorNeuronsRegulation of gene expressionbiologymusculoskeletal neural and ocular physiologyBrainHaplorhinimedicine.diseaseRatsNeuroprotective Agentsmedicine.anatomical_structurenervous systembiology.proteinFibroblast Growth Factor 2sense organsAlzheimer's diseasePsychologyNeuroscienceNeurotrophinBehavioural Brain Research
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Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone.

2009

We sought to address the fundamental question of how stem cell microenvironments can regulate self-renewal. We found that Notch was active in astroglia-like neural stem cells (NSCs), but not in transit-amplifying progenitors of the murine subependymal zone, and that the level of Notch transcriptional activity correlated with self-renewal and multipotency. Moreover, dividing NSCs appeared to balance renewal with commitment via controlled segregation of Notch activity, leading to biased expression of known (Hes1) and previously unknown (Egfr) Notch target genes in daughter cells. Pigment epithelium-derived factor (PEDF) enhanced Notch-dependent transcription in cells with low Notch signaling,…

Cell divisionTranscription GeneticNotch signaling pathwayGene ExpressionBiologyMicePEDFEpendymaSubependymal zoneBasic Helix-Loop-Helix Transcription FactorsAnimalsNuclear Receptor Co-Repressor 1Nerve Growth FactorsProgenitor cellHES1Receptor Notch1Eye ProteinsCells CulturedSerpinsHomeodomain ProteinsNeuronsTranscription Factor HES-1General NeuroscienceAge FactorsTranscription Factor RelACell DifferentiationNeural stem cellErbB ReceptorsAdult Stem CellsTranscription Factor HES-1NeuroscienceSignal TransductionNature neuroscience
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Neurotrophin secretion: current facts and future prospects

2003

The proteins of the mammalian neurotrophin family (nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5)) were originally identified as neuronal survival factors. During the last decade, evidence has accumulated implicating them (especially BDNF) in addition in the regulation of synaptic transmission and synaptogenesis in the CNS. However, a detailed understanding of the secretion of neurotrophins from neurons is required to delineate their role in regulating synaptic function. Some crucial questions that need to be addressed include the sites of neurotrophin secretion (i.e. axonal versus dendritic; synaptic versus extrasyna…

Central Nervous SystemNeuronsNeuronal PlasticityArc (protein)biologyCell SurvivalGeneral NeuroscienceSynaptogenesisLong-term potentiationAMPA receptorNeurotransmissionCell Linenervous systemNeurotrophic factorsTrk receptorbiology.proteinAnimalsHumansNerve Growth FactorsPeptidesNeuroscienceForecastingNeurotrophinProgress in Neurobiology
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EGFL7 ligates αvβ3 integrin to enhance vessel formation

2013

Angiogenesis, defined as blood vessel formation from a preexisting vasculature, is governed by multiple signal cascades including integrin receptors, in particular integrin αVβ3. Here we identify the endothelial cell (EC)-secreted factor epidermal growth factor-like protein 7 (EGFL7) as a novel specific ligand of integrin αVβ3, thus providing mechanistic insight into its proangiogenic actions in vitro and in vivo. Specifically, EGFL7 attaches to the extracellular matrix and by its interaction with integrin αVβ3 increases the motility of EC, which allows EC to move on a sticky underground during vessel remodeling. We provide evidence that the deregulation of EGFL7 in zebrafish embryos leads …

EGF Family of ProteinsEmbryo NonmammalianAngiogenesisAmino Acid MotifsImmunologyIntegrinGene ExpressionMice NudeEndothelial Growth FactorsBiochemistryCollagen receptorMiceCell MovementCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansImmunoprecipitationPhosphorylationZebrafishbiologyReverse Transcriptase Polymerase Chain ReactionChemistryCalcium-Binding ProteinsInfarction Middle Cerebral ArteryVenous plexusCell BiologyHematologyIntegrin alphaVbeta3ImmunohistochemistryExtracellular MatrixCell biologyEndothelial stem cellHEK293 Cellsmedicine.anatomical_structureIntegrin alpha MImmunologybiology.proteinBlood VesselsRNA InterferenceIntegrin beta 6Protein BindingBlood vesselBlood
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Neuromuscular junction disassembly and muscle fatigue in mice lacking neurotrophin-4

2001

Neurotrophin-4 (NT-4) is produced by slow muscle fibers in an activity-dependent manner and promotes growth and remodeling of adult motorneuron innervation. However, both muscle fibers and motor neurons express NT-4 receptors, suggesting bidirectional NT-4 signaling at the neuromuscular junction. Mice lacking NT-4 displayed enlarged and fragmented neuromuscular junctions with disassembled postsynaptic acetylcholine receptor (AChR) clusters, reduced AChR binding, and acetylcholinesterase activity. Electromyographic responses, posttetanic potentiation, and action potential amplitude were also significantly reduced in muscle fibers from NT-4 knock-out mice. Slow-twitch soleus muscles from thes…

End-plate potentialNeuromuscular JunctionElectromyographyBiologyNeuromuscular junctionCellular and Molecular NeuroscienceMicePostsynaptic potentialmedicineAnimalsReceptors CholinergicNerve Growth FactorsMuscle SkeletalMolecular BiologyAcetylcholine receptorMice KnockoutMotor Neuronsmedicine.diagnostic_testMuscle fatigueElectromyographyAge FactorsLong-term potentiationneuromuscular junction; neurotrophin-4; synaptic transmissionCell Biologymedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle FatigueAcetylcholinesteraseTetanic stimulationNeuroscienceMuscle Contraction
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Activation of gp 130 by IL-6/soluble IL-6 receptor induces neuronal differentiation

1998

Interleukin-6 (IL-6) on target cells binds to the specific IL-6 receptor (IL-6R) and subsequently induces homodimerization of the signal-transducing protein gp130. Cells which express gp130 but no IL-6R and which therefore do not respond to IL-6 can be stimulated by the complex of IL-6 and soluble IL-6R (slL-6R). Here we show that on rat pheochromocytoma cells (PC12), the combination of IL-6 and slL-6R but not IL-6 alone induces expression of c-fos, GAP-43 and neuron-specific enolase followed by neuron-specific differentiation and formation of a neuronal network. The differentiation was dose-and time-dependent and followed the same kinetics as nerve-growth factor (NGF)-induced differentiati…

EnolaseGene ExpressionBiologyBinding CompetitivePC12 CellsAntibodiesGAP-43 ProteinAntigens CDNeutralization TestsCytokine Receptor gp130NeuritesAnimalsHumansNerve Growth FactorsReceptorNeuronsMessenger RNAMembrane GlycoproteinsInterleukin-6General NeuroscienceCell DifferentiationGlycoprotein 130Receptors Interleukin-6Molecular biologyRecombinant ProteinsRatsCell biologySolubilitynervous systemTrk receptorInterleukin-6 receptorSignal transductionProto-Oncogene Proteins c-fosTyrosine kinaseEuropean Journal of Neuroscience
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Mistranslation Drives Alterations in Protein Levels and the Effects of a Synonymous Variant at the Fibroblast Growth Factor 21 Locus.

2021

This article also appears in: Health, Medical, and Life Sciences Virtual Issue for Advanced Science.

FGF21General Chemical EngineeringGeneral Physics and AstronomyMedicine (miscellaneous)CODON USAGE BIAS02 engineering and technology01 natural sciencesGLUCOSEACTIVATIONPF-05231023ComputingMilieux_COMPUTERSANDEDUCATIONGeneral Materials SciencegeneticsCells CulturedINSULIN-RESISTANCEFull PaperFatty liverQGeneral Engineeringfibroblast growth factor 21 genetics metabolic metabolic associated fatty liver disease Cells Cultured Enzyme-Linked Immunosorbent Assay Fatty Liver Fibroblast Growth Factors Humans Inflammation LiverFull Papers021001 nanoscience & nanotechnologyPhenotype3. Good healthLiverOBESITY221 Nano-technology0210 nano-technologyReprogrammingEXPRESSIONmedicine.medical_specialtySettore MED/12 - GASTROENTEROLOGIAScienceEnzyme-Linked Immunosorbent Assayfibroblast growth factor 21Biology010402 general chemistryBiochemistry Genetics and Molecular Biology (miscellaneous)metabolic associated fatty liver diseaseInsulin resistancemetabolicInternal medicinemedicineHumansSecretionFGF21 RESISTANCEAlleleInflammationmedicine.disease0104 chemical sciencesFatty LiverFibroblast Growth FactorsEndocrinologyRNA SECONDARY STRUCTURETRANSLATIONHormoneAdvanced science (Weinheim, Baden-Wurttemberg, Germany)
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The b1 isoform of protocadherin-gamma (Pcdhgamma) interacts with the microtubule-destabilizing protein SCG10.

2004

Due to their structural characteristics and their diversity, the 22 members of the protocadherin-gamma (Pcdhgamma) family have been suggested to contribute to the establishment of specific connections in the nervous system. Here, we focus on a single isoform, Pcdhgamma-b1. Its expression is found in different brain regions and in developing spinal cord it is restricted to scattered cells, whereas all cells are labeled using an antibody that recognizes all Pcdhgamma isoforms. As a first step to understanding the signaling mechanisms downstream of Pcdhgamma, we identify the microtubule-destabilizing protein SCG10 as a cytoplasmic interactor for Pcdhgamma-b1 and other isoforms of the Pcdhgamma…

Gene isoformNervous systemSubfamilyRecombinant Fusion ProteinsBiophysicsTwo-hybridProtocadherinCadherin Related ProteinsBiologyBiochemistryMicrotubulesMiceProtocadherinStructural BiologyMicrotubuleTwo-Hybrid System TechniquesChlorocebus aethiopsGeneticsmedicineAnimalsProtein IsoformsInteractorNerve Growth FactorsGrowth coneMolecular BiologyNeuronsProtocadherin-gammaCalcium-Binding ProteinsIntracellular Signaling Peptides and ProteinsBrainCell BiologySCGIOCadherinsMolecular biologyCell biologySCG10medicine.anatomical_structureCytoplasmCOS CellsStathminGrowth coneSignal TransductionFEBS letters
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Physical exercise in the prevention and treatment of Alzheimer's disease

2020

Highlights • Low levels of physical activity are a risk factor associated with Alzheimer's disease. • Older adults who exercise are more likely to maintain cognition. • Exercise modulates amyloid β turnover, inflammation, synthesis, and release of neurotrophins, and cerebral blood flow.

GerontologyAgingPsychological interventionPhysical Therapy Sports Therapy and RehabilitationPhysical exercisetau ProteinsDiseaseReviewLifestyle factorsExercise traininglcsh:GV557-1198.99503 medical and health sciences0302 clinical medicineCognitionAlzheimer DiseaseRisk FactorsmedicineDementiaAerobic exerciseAnimalsHumansOrthopedics and Sports Medicine030212 general & internal medicineHealthy LifestyleNerve Growth Factorslcsh:Sports medicineExerciseAerobic exerciselcsh:SportsInflammationAmyloid beta-Peptidesbusiness.industryMechanism (biology)BrainMultidomain interventionsCognition030229 sport sciencesmedicine.diseaseMental healthResistance exercise3. Good healthExercise TherapyCerebrovascular CirculationDementialcsh:RC1200-1245business[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Cytomegalovirus inhibits the engraftment of donor bone marrow cells by downregulation of hemopoietin gene expression in recipient stroma

1998

ABSTRACT Cytomegalovirus (CMV) disease after bone marrow (BM) transplantation is often associated with BM graft failure. There are two possible reasons for such a correlation. First, a poor hematopoietic reconstitution of unrelated etiology could promote the progression of CMV infection by the lack of immune control. Alternatively, CMV infection could interfere with the engraftment of donor BM cells in recipient BM stroma. Evidence for a causative role of CMV in BM aplasia came from studies in long-term BM cultures and from the murine in vivo model of CMV-induced aplastic anemia. A deficiency in the expression of essential stromal hemopoietins, such as stem cell factor (SCF), has indicated …

Graft RejectionMaleStromal cellImmunologyPopulationCytomegalovirusDown-RegulationViral Pathogenesis and ImmunityStem cell factorBiologyHematopoietic Cell Growth FactorsMicrobiologyMiceVirologymedicineAnimalsAplastic anemiaeducationBone Marrow Transplantationeducation.field_of_studyMice Inbred BALB CHematopoietic Cell Growth Factorsmedicine.diseaseTransplantationHaematopoiesisTransplantation Isogeneicmedicine.anatomical_structureInsect ScienceImmunologyCytomegalovirus InfectionsFemaleBone marrowStromal Cells
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