Search results for "Glycogen synthase"

showing 10 items of 61 documents

Diverse roles of GSK-3: tumor promoter-tumor suppressor, target in cancer therapy.

2013

Glycogen synthase kinase-3 (GSK-3) is a critical enzyme which participates in a complex array of important cellular processes and is often involved in various human diseases. It was first characterized in rat skeletal muscle as a serine/threonine (S/T) kinase that phosphorylated and inactivated glycogen synthase (GS). GS is the last enzyme in glycogen biosynthesis . Thus the initially identified role of GSK-3 was in metabolism. However, as we will soon see, GSK-3 has many diverse functions.

Cancer ResearchENZYMECarcinogenesisCancer therapymacromolecular substancesBiologymedicine.disease_causeGSK3law.inventionGlycogen Synthase Kinase 3GeneticlawGSK-3NeoplasmsGeneticsmedicineAnimalsHumansGenes Tumor SuppressorGenes tumor suppressorMolecular BiologyGeneCarcinogenesiAnimalNeoplasms therapyMolecular medicineMetabolismCancer researchNeoplasmMolecular MedicineSuppressorCarcinogenesisGlycogenHumanAdvances in biological regulation
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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Estrogen-induced cell signalling in a cellular model of Alzheimer's disease.

2003

Alzheimer's disease (AD) is characterised by deposition of a 4 kDa amyloid-beta peptide (Abeta) into senile plaques of the affected brain. Abeta is a proteolytic product of the membrane protein, amyloid precursor protein (APP). An alternative cleavage pathway involves alpha-secretase activity and results in secretion of a 100 kDa non-amyloidogenic APP (sAPPalpha) and therefore a potential reduction in Abeta secretion. We have shown that estrogen induces alpha-cleavage and therefore results in the secretion of sAPPalpha. This secretion is signalled via MAP-kinase and PI-3 kinase signal-transduction pathways. These pathways also have the potential to inhibit the activation of glycogen synthas…

Cell signalingMAP Kinase Signaling SystemEndocrinology Diabetes and MetabolismClinical BiochemistryBiologyBiochemistryModels BiologicalAmyloid beta-Protein PrecursorGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesEndocrinologyGSK-3Alzheimer DiseaseAmyloid precursor proteinAnimalsHumansSecretionSenile plaquesMolecular BiologyGSK3BAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaCell DeathKinaseBrainEstrogensCell BiologyCell biologybiology.proteinMolecular MedicineSignal transductionLithium ChloridePeptidesSignal TransductionThe Journal of steroid biochemistry and molecular biology
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Dual effects of increased glycogen synthase kinase-3β activity on adult neurogenesis

2013

Adult neurogenesis, the generation of new neurons during the adulthood, is a process controlled by several kinases and phosphatases among which GSK3β exerts important functions. This protein is particularly abundant in the central nervous system, and its activity deregulation is believed to play a key role in chronic disorders such as Alzheimer's disease. Previously, we reported that in vivo overexpression of GSK3β (Tet/GSK3β mice) causes alterations in adult neurogenesis, leading to a depletion of the neurogenic niches. Here, we have further characterized those alterations, finding a delay in the switching-off of doublecortin marker as well as changes in the survival and death rates of imm…

Chemokine CCL11Doublecortin Domain ProteinsCell SurvivalNeurogenesisTransgeneCentral nervous systemMice TransgenicNerve Tissue ProteinsBiologySubgranular zoneNestinGlycogen Synthase Kinase 3MiceIntermediate Filament ProteinsNeural Stem CellsGenes ReporterGlial Fibrillary Acidic ProteinGeneticsmedicineAnimalsStem Cell NicheMolecular BiologyGSK3BGenetics (clinical)NeuronsGlycogen Synthase Kinase 3 betaNeuropeptidesNeurogenesisNuclear ProteinsGeneral MedicineNestinbeta-GalactosidaseCell biologyDoublecortinDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureEnzyme InductionDentate GyrusImmunologybiology.proteinMicrotubule-Associated ProteinsNeural developmentBiomarkersHuman Molecular Genetics
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EFFECT OF THE IMPase INHIBITOR L690,330 ON SEA URCHIN DEVELOPMENT

1998

Abstract A variety of concentrations of the IMPase inhibitor L690,330 were added to sea urchin embryos. Immediate arrest of development was obtained for concentrations from 7.5 m m on. Concentrations lower than 3.5 m m permitted gastrulation but inhibited skeletogenesis and disturbed elongation along the animal–vegetal axis. The latter results are similar to those obtained by counteracting lithium effect with myoinositol, which are suggested to be due to partial relief of IMPase inhibition.

Embryo NonmammalianSea UrchinCalcium-Calmodulin-Dependent Protein KinaseLithiumMorulaGlycogen Synthase Kinase 3biology.animalMorphogenesisEnzyme InhibitorMorphogenesiAnimalsIMPaseEnzyme InhibitorsSea urchin embryo5'-NucleotidaseSea urchinDiphosphonatesbiologyAnimalAbnormalities Drug-InducedCell BiologyGeneral MedicineAnatomySea urchin embryoCell biologyGastrulationDiphosphonateSea UrchinsCalcium-Calmodulin-Dependent Protein KinasesElongationLithium ChlorideInositolCell Biology International
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Isolation and characterization of Wnt pathway-related genes from Porifera.

2006

The Wnt signal acts by binding to Frizzled receptors, with the subsequent activation of two different signal transduction cascades, the canonical and the non-canonical Wnt pathways, involved in cell growth, differentiation, migration and fate. The canonical pathway functions through the translocation of beta-catenin to the nucleus and the activation of TCF/LEF transcription factors; it plays an important role in developmental patterning and cell fate decisions during embryogenesis. The non-canonical Wnt pathway is responsible for the planar cell polarity process in invertebrates, and for the convergent-extension movements during vertebrate gastrulation. The final effect of the non-canonical…

FrizzledMyosin Light ChainsMolecular Sequence DataGTPaseCell fate determinationGlycogen Synthase Kinase 3AnimalsAmino Acid Sequencecdc42 GTP-Binding ProteinCells CulturedPhylogenybiologyGene Expression ProfilingWnt signaling pathwayIntracellular Signaling Peptides and ProteinsLRP6LRP5Cell BiologyGeneral Medicinebiology.organism_classificationFrizzled ReceptorsCell biologyPoriferaSuberites domunculaWnt ProteinsGene Expression RegulationSignal transductionTCF Transcription FactorsrhoA GTP-Binding ProteinCell biology international
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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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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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GSK3β overexpression induces neuronal death and a depletion of the neurogenic niches in the dentate gyrus

2010

Overexpression of GSK3β in transgenic mice induces learning deficits and some features associated with Alzheimer's disease (AD), including dentate gyrus (DG) atrophy. Here, we assessed whether these mice also recapitulate DG atrophy as well as impaired neurogenesis reported in AD. Ultrastructural analysis revealed that there were fewer and more disorganized neurogenic niches in these animals, coupled with an increase in the proportion of immature neurons. Indeed, the maturation of granule cells is delayed as witnessed by the alterations to the length and patterning of their dendritic trees and to the mossy fiber terminals. Together with an increase in neuronal death, these phenomena lead to…

Genetically modified mouseProgrammed cell deathOverexpressionNeurogenesisproliferationCognitive NeuroscienceCellular differentiationeducationProliferationMice TransgenicBiologyGlycogen Synthase Kinase 3MiceAtrophyAlzheimer DiseaseMaturationmedicineAnimalsHumanshippocampal stem cellsGSK3Bhealth care economics and organizationsCell ProliferationGlycogen Synthase Kinase 3 betaCell DeathMicrogliamaturationDentate gyrusNeurogenesisGSK3 betaCell DifferentiationAlzheimer's diseasemedicine.diseaseMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureHippocampal stem cellsDentate GyrusGSK3bMicrogliaAlzheimer’s diseaseNeuroscienceoverexpressionHippocampus
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Human SPG11 cerebral organoids reveal cortical neurogenesis impairment

2018

Abstract Spastic paraplegia gene 11(SPG11)-linked hereditary spastic paraplegia is a complex monogenic neurodegenerative disease that in addition to spastic paraplegia is characterized by childhood onset cognitive impairment, thin corpus callosum and enlarged ventricles. We have previously shown impaired proliferation of SPG11 neural progenitor cells (NPCs). For the delineation of potential defect in SPG11 brain development we employ 2D culture systems and 3D human brain organoids derived from SPG11 patients’ iPSC and controls. We reveal that an increased rate of asymmetric divisions of NPCs leads to proliferation defect, causing premature neurogenesis. Correspondingly, SPG11 organoids appe…

GenotypeHereditary spastic paraplegiaNeurogenesisFluorescent Antibody TechniqueBiology03 medical and health sciencesGlycogen Synthase Kinase 3GeneticsOrganoidmedicineSpasticHumansMolecular BiologyGenetics (clinical)Allelesbeta CateninCerebral Cortex0303 health sciences030305 genetics & heredityNeurogenesisProteinsGeneral MedicineHuman brainmedicine.diseaseNeural stem cellnervous system diseasesOrganoidsmedicine.anatomical_structurePhenotypeMutationGeneral ArticleDisease SusceptibilityParaplegiaCognition DisordersNeuroscienceNeural developmentBiomarkersHuman Molecular Genetics
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