Search results for "Growth factor"

showing 10 items of 1300 documents

Detection of Fibroblast Growth Factor Receptor 1 (FGFR1) Transactivation by Muscarinic Acetylcholine Receptors (mAChRs) in Primary Neuronal Hippocamp…

2018

In addition to their canonical intracellular signals involved in the regulation of neuronal plasticity, G-protein coupled receptors can also rapidly transactivate tyrosine kinase receptors and their downstream intracellular signaling in absence of specific ligands. Here we describe our protocol for dissociating and maintaining hippocampal primary neurons in high- and low-density culture, followed by a description of methods employed to evaluate neurite outgrowth and protein phosphorylation associated with fibroblast growth factor receptor 1 transactivation by muscarinic acetylcholine receptors. Our goal was to provide the reader with detailed protocols of the abovementioned techniques and t…

TransactivationChemistryFibroblast growth factor receptor 1Tyrosine kinase receptorHippocampal formationHippocampusSettore BIO/09 - FisiologiaFibroblast growth factor receptorWestern blottingCell biologyMuscarinic acetylcholine receptorPrimary neuronal cultureTransactivationNeurite growthMuscarinic acetylcholine receptorPhosphorylationReceptor–receptor interactions
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Insulin-like growth factor 1 differentially regulates estrogen receptor-dependent transcription at estrogen response element and AP-1 sites in breast…

2007

Cross-talk between insulin-like growth factor 1 (IGF-1) and estrogen receptor alpha (ER) regulates gene expression in breast cancer cells, but the underlying mechanisms remain unclear. Here, we studied how 17-beta-estradiol (E2) and IGF-1 affect ER transcriptional machinery in MCF-7 cells. E2 treatment stimulated ER loading on the estrogen response element (ERE) in the pS2 promoter and on the AP-1 motif in the cyclin D1 promoter. On ERE, similar amounts of liganded ER were found at 1-24-h time points, whereas on AP-1, ER binding fluctuated over time. At 1 h, liganded ER was recruited to ERE together with histone acetyltransferases SRC-1 and p300, ubiquitin ligase E6-AP, histone methyltransf…

Transcription GeneticActive Transport Cell NucleusEstrogen receptorBreast NeoplasmsLigandsResponse ElementsBiochemistryCyclin D1Cell Line TumorHumansCyclin D1RNA MessengerInsulin-Like Growth Factor IHistone H3 acetylationMolecular BiologyHormone response elementbiologyEstradiolTumor Suppressor ProteinsEstrogen Receptor alphaCell BiologyUbiquitin ligaseCell biologyUp-RegulationTranscription Factor AP-1Histone methyltransferasebiology.proteinCancer researchMdm2Trefoil Factor-1Estrogen receptor alphahormones hormone substitutes and hormone antagonistsThe Journal of biological chemistry
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Transcription of different exons 1 of the human neuronal nitric oxide synthase gene is dynamically regulated in a cell- and stimulus-specific manner.

2003

An extensive screening of the human neuronal nitric oxide synthase (nNOS) mRNAs in various human tissues and cell lines unraveled an extreme complexity in the transcription of this gene. Using 5'rapid amplification of cDNA ends (5'-RACE), ten different exons 1 (named 1a-1l) were identified. They were spliced in a cell-specific manner to a common exon 2, which bears the translational start site. Three first exons (1 d, 1g and 1f) were used predominantly for the transcription of the nNOS gene (146 out of 197 5'-RACE clones contained these exons). Exon 1 k was found alone, but in many instances was interposed between exons 1 b, 1d, 1g, 1 i or 1j and the common exon 2. In addition to the cell-s…

Transcription GeneticClinical BiochemistryMolecular Sequence DataNitric Oxide Synthase Type IBiologyBiochemistryGene Expression Regulation EnzymologicExonDownregulation and upregulationEpidermal growth factorTranscription (biology)Complementary DNATumor Cells CulturedHumansRNA MessengerCloning MolecularMolecular BiologyGeneMessenger RNABase SequenceExonsMolecular biologyUp-RegulationAlternative SplicingBucladesineCell cultureNitric Oxide SynthaseBiological chemistry
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Transcriptional Activity and Nuclear Localization of Cabut, the Drosophila Ortholog of Vertebrate TGF-β-Inducible Early-Response Gene (TIEG) Proteins

2011

Background Cabut (Cbt) is a C2H2-class zinc finger transcription factor involved in embryonic dorsal closure, epithelial regeneration and other developmental processes in Drosophila melanogaster. Cbt orthologs have been identified in other Drosophila species and insects as well as in vertebrates. Indeed, Cbt is the Drosophila ortholog of the group of vertebrate proteins encoded by the TGF-s-inducible early-response genes (TIEGs), which belong to Sp1-like/Kruppel-like family of transcription factors. Several functional domains involved in transcriptional control and subcellular localization have been identified in the vertebrate TIEGs. However, little is known of whether these domains and fu…

Transcription GeneticNuclear Localization SignalsActive Transport Cell Nucleuslcsh:MedicineGene ExpressionBiochemistrybehavioral disciplines and activities03 medical and health sciencesModel Organisms0302 clinical medicineTransforming Growth Factor betaMolecular Cell Biologymental disordersGeneticsTranscriptional regulationAnimalsDrosophila Proteinslcsh:ScienceBiology030304 developmental biologyGeneticsZinc finger transcription factor0303 health sciencesMultidisciplinarybiologySchneider 2 cellslcsh:RfungiProteinsAnimal Modelsbiology.organism_classificationFusion proteinCellular StructuresDorsal closure3. Good healthRepressor ProteinsDrosophila melanogasterGene Expression RegulationVertebrateslcsh:QDrosophila melanogaster030217 neurology & neurosurgeryDrosophila ProteinNuclear localization sequenceTranscription FactorsResearch ArticleDevelopmental BiologyPLoS ONE
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Urokinase activates macrophage PON2 gene transcription via the PI3K/ROS/MEK/SREBP-2 signalling cascade mediated by the PDGFR-β

2009

Aims We have recently shown that urokinase plasminogen activator (uPA) increases oxidative stress (OS), cholesterol biosynthesis, and paraoxonase 2 (PON2) expression in macrophages via binding to its receptor, the uPAR. Since PON2 is regulated by both OS and cholesterol content, we hypothesized that uPA elicits a cascade of signal transduction events shared by NADPH oxidase and cholesterol biosynthesis that culminates in PON2 gene expression. Here, we investigated the signalling pathway that leads to the expression of PON2 in macrophages in response to uPA. Methods and results The increase in macrophage PON2 mRNA levels in response to uPA was shown to depend on PON2 gene promoter activation…

Transcription GeneticPhysiologyReceptor Platelet-Derived Growth Factor betaPhosphatidylinositol 3-KinasesPhysiology (medical)Gene expressionHumansExtracellular Signal-Regulated MAP KinasesTranscription factorCells CulturedMitogen-Activated Protein Kinase KinasesRegulation of gene expressionNADPH oxidasebiologyAryldialkylphosphataseKinaseMacrophagesNADPH OxidasesUrokinase-Type Plasminogen ActivatorCell biologySterol regulatory element-binding proteinUrokinase receptorGene Expression RegulationBiochemistryTissue Plasminogen Activatorbiology.proteinSignal transductionReactive Oxygen SpeciesCardiology and Cardiovascular MedicineSignal TransductionSterol Regulatory Element Binding Protein 2Cardiovascular Research
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Cross-talk between Different Enhancer Elements during Mitogenic Induction of the Human Stromelysin-1 Gene

1996

Platelet-derived growth factor (PDGF) induces the expression of human stromelysin-1, a matrix metalloproteinase involved in tumor invasion and metastasis. Here it is shown that stromelysin-1 gene induction by PDGF depends on Ras and involves three previously identified promoter elements (the stromelysin-1 PDGF-responsive element (SPRE) site, the two head-to-head polyomavirus enhancer A-binding protein-3 (PEA3) sites, and the activator protein-1 (AP-1) binding site). During mitogenic induction, these responsive elements appear to be organized in two independent transcriptional units, SPRE-AP-1 and PEA3-AP-1, which result from specific element cross-talking. Interestingly, expression of a dom…

Transcription GeneticProto-Oncogene Proteins c-junMolecular Sequence DataProtein Serine-Threonine KinasesBiologyTransfectionBiochemistryStromelysin 1Proto-Oncogene Proteins p21(ras)MiceProto-Oncogene ProteinsAnimalsHumansBinding siteEnhancerMolecular BiologyTranscription factorGeneProtein Kinase CProtein kinase CPlatelet-Derived Growth FactorBase SequenceActivator (genetics)Metalloendopeptidases3T3 CellsCell BiologyMolecular biologyRecombinant ProteinsDNA-Binding ProteinsProto-Oncogene Proteins c-rafTranscription Factor AP-1Enhancer Elements GeneticEnzyme Inductionbiology.proteinMatrix Metalloproteinase 3MitogensPlatelet-derived growth factor receptorJournal of Biological Chemistry
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Nerve growth factor and epidermal growth factor stimulate clusterin gene expression in PC12 cells

1999

Clusterin (apolipoprotein J) is an extracellular glycoprotein that might exert functions in development, cell death and lipid transport. Clusterin gene expression is elevated at sites of tissue remodelling, such as differentiation and apoptosis; however, the signals responsible for this regulation have not been identified. We use here the clusterin gene as a model system to examine expression in PC12 cells under the control of differentiation and proliferation signals produced by nerve growth factor (NGF) and by epidermal growth factor (EGF) respectively. NGF induced clusterin mRNA, which preceded neurite outgrowth typical of neuronal differentiation. EGF also activated the clusterin mRNA, …

Transcriptional ActivationProgrammed cell deathNeuriteMolecular Sequence DataResponse ElementsTransfectionBinding CompetitivePC12 CellsBiochemistryEpidermal growth factorConsensus SequenceNeuritesAnimalsNerve Growth FactorsRNA MessengerCloning MolecularPromoter Regions GeneticMolecular BiologyGlycoproteinsSequence DeletionNeuronsRegulation of gene expressionMessenger RNABase SequenceEpidermal Growth FactorClusterinbiologyKinaseCell DifferentiationDNACell BiologyMolecular biologyeye diseasesRatsTranscription Factor AP-1ClusterinNerve growth factorbiology.proteinsense organsCell DivisionMolecular ChaperonesSignal TransductionResearch ArticleBiochemical Journal
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TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
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Hypoxia-inducible factor 1Α may regulate the commitment of mesenchymal stromal cells toward angio-osteogenesis by mirna-675-5P

2017

Abstract Background aims During bone formation, angiogenesis and osteogenesis are regulated by hypoxia, which is able to induce blood vessel formation, as well as recruit and differentiate human mesenchymal stromal cells (hMSCs). The molecular mechanisms involved in HIF-1α response and hMSC differentiation during bone formation are still unclear. This study aimed to investigate the synergistic role of hypoxia and hypoxia-mimetic microRNA miR-675-5p in angiogenesis response and osteo-chondroblast commitment of hMSCs. Methods By using a suitable in vitro cell model of hMSCs (maintained in hypoxia or normoxia), the role of HIF-1α and miR-675-5p in angiogenesis and osteogenesis coupling was inv…

Transcriptional ActivationVascular Endothelial Growth Factor A0301 basic medicineCancer ResearchAngiogenesisCellular differentiationImmunologyNeovascularization PhysiologicBiology03 medical and health scienceschemistry.chemical_compoundOsteogenesisMiR-675-5pmedicineHumansImmunology and AllergyHypoxiaCells Culturedbeta CateninGenetics (clinical)TransplantationOsteoblastsMesenchymal stromal cellMesenchymal stem cellWnt signaling pathwayCell DifferentiationMesenchymal Stem CellsOsteoblastCell BiologyHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaUp-RegulationCell biologyVascular endothelial growth factorMicroRNAsVascular endothelial growth factor A030104 developmental biologymedicine.anatomical_structureGene Expression RegulationOncologyHypoxia-inducible factorschemistryRegenerative medicineImmunologyOsteoblast commitmentCytotherapy
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Interactions between cholinergic and fibroblast growth factor receptors in brain trophism and plasticity

2014

Acetylcholine, acting on both nicotinic receptors (nAChRs) and muscarinic receptors (mAChRs), plays a role in the regulation of synaptic plasticity, being involved in the regulation of cellular processes and cognitive functions, such as learning, memory and attention. Recently, G protein coupled receptors (GPCRs), including mAChRs, have been reported to transactivate tyrosine-kinase receptors (RTK), such as epidermal growth factor receptor (EGFR), and initiate their intracellular signaling. In this minireview we have first analysed the RTK transactivation mechanisms, involving cholinergic receptors, and thereafter the interplay between AChR and neurotrophic factor systems built up by FGF2 a…

Transcriptional Activationmedicine.medical_specialtyClass C GPCRG protein coupled receptorBiologyCholinergic AgonistsBiochemistrySynaptic plasticityTransactivationNicotinic receptorNeurotrophic factorsInternal medicinemedicineAnimalsHumansReceptors CholinergicProtein Interaction MapsReceptorMolecular BiologyG protein-coupled receptorTransactivationNeuronal PlasticityFibroblast growth factor receptor 1Muscarinic receptorBrainReceptor Protein-Tyrosine KinasesCell BiologyGeneral MedicineReceptors Fibroblast Growth FactorErbB ReceptorsEndocrinologyFGFR1Fibroblast growth factor receptorFGFR1; G protein coupled receptor; Muscarinic receptors; Nicotinic receptors; Receptor-receptor interaction; Synaptic plasticity; Transactivation; Tyrosine-kinase receptorsSignal transductionTyrosine-kinase receptorsNeuroscienceReceptor-receptor interactionSignal Transduction
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