Search results for "Signal Transduction"

showing 10 items of 2020 documents

Spatio-Temporal Analysis of Constitutive Exocytosis in Epithelial Cells

2006

Exocytosis is an essential cellular trafficking process integral to the proper distribution and function of a plethora of molecules, including transporters, receptors, and enzymes. Moreover, incorrect protein targeting can lead to pathological conditions. Recently, the application of evanescent wave microscopy has allowed us to image the final steps of exocytosis. However, spatio-temporal analysis of fusion of constitutive vesicular traffic with the plasma membrane has not been systematically performed. Also, the spatial sites and times of vesicle fusion have not yet been analyzed together. In addition, more formal tests are required in testing biological hypotheses, rather than visual insp…

FusionVesicle fusionApplied MathematicsCell MembraneSpatio-Temporal AnalysisMolecular biophysicsMembrane ProteinsEpithelial CellsBiologymedicine.disease_causeMembrane FusionModels BiologicalExocytosisExocytosisCell LineCell biologyConstitutive exocytosisProtein targetingGeneticsmedicineComputer SimulationBiological systemFunction (biology)Signal TransductionBiotechnologyIEEE/ACM Transactions on Computational Biology and Bioinformatics
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Metabolite Sensing GPCRs: Promising Therapeutic Targets for Cancer Treatment?

2020

G-protein-coupled receptors constitute the most diverse and largest receptor family in the human genome, with approximately 800 different members identified. Given the well-known metabolic alterations in cancer development, we will focus specifically in the 19 G-protein-coupled receptors (GPCRs), which can be selectively activated by metabolites. These metabolite sensing GPCRs control crucial processes, such as cell proliferation, differentiation, migration, and survival after their activation. In the present review, we will describe the main functions of these metabolite sensing GPCRs and shed light on the benefits of their potential use as possible pharmacological targets for cancer treat…

G-protein-coupled receptorMetaboliteReviewComputational biologyBiologyReceptors G-Protein-CoupledBile Acids and Saltschemistry.chemical_compoundNeoplasmsmetabolite sensing GPCRBiomarkers TumormedicinecancerAnimalsHumansMolecular Targeted TherapyAmino AcidsReceptorlcsh:QH301-705.5G protein-coupled receptorCell growthDisease ManagementCancerGeneral MedicineLipid Metabolismmedicine.diseaseCancer treatmentlcsh:Biology (General)Gene Expression RegulationchemistryHuman genomeDisease SusceptibilityCancer developmentEnergy MetabolismSignal TransductionCells
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Isomer-nonspecific action of dichlorodiphenyltrichloroethane on aryl hydrocarbon receptor and G-protein-coupled receptor 30 intracellular signaling i…

2014

Abstract Extended residual persistence of the pesticide dichlorodiphenyltrichloroethane (DDT) raises concerns about its long-term neurotoxic effects. Little is known, however, about DDT toxicity during the early stages of neural development. This study demonstrated that DDT-induced apoptosis of mouse embryonic neuronal cells is a caspase-9-, caspase-3-, and GSK-3β-dependent process, which involves p,p’ -DDT-specific impairment of classical ERs. It also provided evidence for DDT-isomer-nonspecific alterations of AhR- and GPR30-mediated intracellular signaling, including changes in the levels of the receptor and receptor-regulated mRNAs, and also changes in the protein levels of the receptors…

GPR30Time FactorsGSK-3 betaEstrogen receptorApoptosisStimulationBiochemistryReceptors G-Protein-CoupledGlycogen Synthase Kinase 3MiceEndocrinologyneurotoxicityestrogenReceptorCells CulturedNeuronsbiologyCaspase 3estrogen receptorsCaspase InhibitorsCell biologycaspasesReceptors EstrogenQuinolinesGPERNeural developmentSignal Transductionmedicine.medical_specialtyAryl hydrocarbon receptor nuclear translocatorneuronal cell culturesDDT17-beta-estradiolIsomerismbeta-NaphthoflavoneInternal medicineparasitic diseasesCytochrome P-450 CYP1A1medicineAnimalsBcl-2BenzodioxolesRNA MessengerMolecular BiologyG protein-coupled receptorBenzoflavonesGlycogen Synthase Kinase 3 betaL-Lactate DehydrogenaseAryl hydrocarbon receptorPyrimidinesEndocrinologyReceptors Aryl Hydrocarbonbiology.proteinPyrazolesMolecular and Cellular Endocrinology
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Roles for ELMOD2 and Rootletin in ciliogenesis.

2021

AbstractELMOD2 is a GTPase activating protein (GAP) with uniquely broad specificity for ARF family GTPases. We previously showed that it acts with ARL2 in mitochondrial fusion and microtubule stability and with ARF6 during cytokinesis. Mouse embryonic fibroblasts deleted for ELMOD2 also displayed changes in cilia related processes including increased ciliation, multiciliation, ciliary morphology, ciliary signaling, centrin accumulation inside cilia, and loss of rootlets at centrosomes with loss of centrosome cohesion. Increasing ARL2 activity or overexpressing Rootletin reversed these defects, revealing close functional links between the three proteins. This was further supported by the fin…

GTPase-activating proteinBiologyMicrotubulesMitochondrial DynamicsCell Line03 medical and health sciencesMice0302 clinical medicineMicrotubuleGTP-Binding ProteinsCiliogenesisAnimalsHumansCiliaMolecular Biology030304 developmental biologyCytokinesisCentrosome0303 health sciencesADP-Ribosylation FactorsCiliumGTPase-Activating ProteinsCell BiologyArticlesFibroblastsCell biologyMitochondriaCytoskeletal Proteinsmitochondrial fusionCentrosomeCentrinRootletin030217 neurology & neurosurgeryCytokinesisSignal TransductionMolecular biology of the cell
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Ras-pathway has a dual role in yeast galactose metabolism

2007

AbstractIn the yeast Saccharomyces cerevisiae the genes involved in galactose metabolism (GAL1,7,10) are transcriptionally activated more than a 1000-fold in the presence of galactose as the sole carbon source in the culture media. In the present work, we monitored the activity of the GAL10 gene promoter in different Ras-cAMP genetic backgrounds. We demonstrate that overexpression of C-terminus of the nucleotide exchange factor Cdc25p stimulates GAL10 transcription in yeast strains carrying the contemporary deletion of both RAS genes. Moreover, the deletion of the chromosomal CDC25 gene provokes impaired growth on galactose based media in yeast strain lacking both RAS genes and adenylate cy…

Galactose metabolismSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeBiophysicsGene ExpressionSaccharomyces cerevisiaeRas glucose and galactose metabolism cancerGTP-binding proteinSignal transductionBiochemistryLeloir pathwaychemistry.chemical_compoundRas-GRF1Protein kinase AStructural BiologyGenes ReporterGene Expression Regulation FungalGeneticsRNA MessengerProtein kinase APromoter Regions GeneticMolecular BiologyChromosomal DeletionAllelesbiologyras-GRF1GalactosePromoterCell Biologybiology.organism_classificationLeloir pathwayExchange factorPhenotypechemistryBiochemistryGalactoseras ProteinsSignal transductionGene DeletionAdenylyl CyclasesPlasmidsFEBS Letters
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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From non-excitable single-cell to multicellular bioelectrical states supported by ion channels and gap junction proteins: Electrical potentials as di…

2019

Endogenous bioelectric patterns within tissues are an important driver of morphogenesis and a tractable component of a number of disease states. Developing system-level understanding of the dynamics by which non-neural bioelectric circuits regulate complex downstream cascades is a key step towards both, an evolutionary understanding of ion channel genes, and novel strategies in regenerative medicine. An important capability gap is deriving rational modulation strategies targeting individual cells' bioelectric states to achieve global (tissue- or organ-level) outcomes. Here, we develop an ion channel-based model that describes multicellular states on the basis of spatio-temporal patterns of …

Gap Junction Proteins030303 biophysicsCellBiophysicsCell CommunicationRegenerative medicineModels BiologicalConnexinsIon ChannelsCell membrane03 medical and health sciencesmedicineMorphogenesisAnimalsHumansMolecular BiologyIon channelPhysics0303 health sciencesCell potentialElectrical potentialsGap JunctionsElectrophysiological PhenomenaMulticellular organismmedicine.anatomical_structureSingle-Cell AnalysisNeuroscienceSignal TransductionProgress in biophysics and molecular biology
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Influence ofKi-ras-driven oncogenic transformation on the protein network of murine fibroblasts

2007

Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordi…

Gel electrophoresismedicine.diagnostic_testWild typeFibroblastsBiologyGene mutationTransfectionmedicine.disease_causeProteomicsBiochemistryMolecular biologyMiceCell Transformation NeoplasticWestern blotHeat shock proteinNIH 3T3 Cellsras ProteinsmedicineAnimalsMitogen-Activated Protein KinasesCarcinogenesisMolecular BiologyGeneSignal TransductionPROTEOMICS
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Oxidative stress inhibits IFN-α-induced antiviral gene expression by blocking the JAK–STAT pathway

2006

Abstract BACKGROUND/AIMS: Unresponsiveness to IFN-alpha is common in chronic hepatitis C. Since conditions associated with an increased oxidative stress (advanced age, steatosis, fibrosis, iron overload, and alcohol consumption) reduce the likelihood of response, we hypothesized that oxidative stress may affect the antiviral actions of IFN-alpha. METHODS: We examined in a human hepatocellular carcinoma cell line (Huh-7) the effect of hydrogen peroxide (H2O2), as a generator of oxidative stress, on the IFN-alpha signaling pathway. RESULTS: Pretreatment of Huh-7 cells with 0.5-1 mM H2O2 resulted in the suppression of the IFN-alpha-induced antiviral protein MxA and of IRF-9 mRNA expression. Th…

Gene Expression Regulation ViralMyxovirus Resistance ProteinsCarcinoma HepatocellularBlotting WesternAntiviral proteinProtein tyrosine phosphataseInterferon alpha-2Biologymedicine.disease_causechemistry.chemical_compoundGTP-Binding ProteinsCell Line TumormedicineHumansRNA NeoplasmHepatologyTyk-2Reverse Transcriptase Polymerase Chain ReactionSTATLiver NeoplasmsInterferon-alphaJAK-STAT signaling pathwayTyrosine phosphorylationHydrogen PeroxideJanus Kinase 1Flow CytometryInterferon-Stimulated Gene Factor 3 gamma SubunitRecombinant ProteinsIFN-aJAK-1Oxidative StressSTAT Transcription FactorsHydrogen peroxide; IFN-a; STAT; JAK-1; Tyk-2chemistryImmunologySTAT proteinCancer researchSignal transductionTyrosine kinaseOxidative stressSignal TransductionJournal of Hepatology
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Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
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