Search results for "GSK-3"

showing 10 items of 35 documents

Amyloid-β toxicity and tau hyperphosphorylation are linked via RCAN1 in Alzheimer's disease.

2011

Amyloid-β peptide (Aβ) toxicity and tau hyperphosphorylation are hallmarks of Alzheimer’s disease (AD). How their molecular relationships may affect the etiology, progression, and severity of the disease, however, has not been elucidated. We now report that incubation of foetal rat cortical neurons with Aβ up-regulates expression of the Regulator of Calcineurin gene RCAN1, and this is mediated by Aβ-induced oxidative stress. Calcineurin (PPP3CA) is a serine-threonine phosphatase that dephosphorylates tau. RCAN1 proteins inhibit this phosphatase activity of calcineurin. Increased expression of RCAN1 also causes up-regulation of glycogen synthase kinase-3beta (GSK3β), a tau kinase. Thus, incr…

Apolipoprotein EAdultMuscle Proteinstau ProteinsBiologymedicine.disease_causeTransfectionArticleDephosphorylationGlycogen Synthase Kinase 3GSK-3Alzheimer DiseasemedicineAnimalsHumansLymphocytesPhosphorylationRNA Small InterferingGSK3BCells CulturedChromatography High Pressure LiquidRegulation of gene expressionCerebral CortexNeuronsAmyloid beta-PeptidesGlycogen Synthase Kinase 3 betaGeneral NeuroscienceCalcineurinIntracellular Signaling Peptides and ProteinsGeneral MedicineMiddle Agedmedicine.diseaseEmbryo MammalianMolecular biologyGlutathionePeptide FragmentsCell biologyRatsCalcineurinDNA-Binding ProteinsPsychiatry and Mental healthClinical PsychologyOxidative StressGene Expression RegulationFemaleGeriatrics and GerontologyAlzheimer's diseaseOxidative stressJournal of Alzheimer's disease : JAD
researchProduct

GSK-3? Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutra…

2021

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed wi…

Berberineendocrine system diseasesmedicine.medical_treatmentRegulatormedicine.disease_causeDeoxycytidinePiperazinesTargeted therapychemotherapeutic drugsTargeted therapyNitrophenolsBreast cancerGSK-3BGlycolysisMolecular Targeted TherapyNeoplasm Metastasistargeted therapy;lcsh:QH301-705.5Tumor Stem Cell AssaySulfonamidesTumorbiologyChemistryGeneral MedicineTransfectionMetforminDisease ProgressionMCF-7 CellsFemaleKRASNutraceuticalsFluorouracilSignal transductionGlycolysisSignal TransductionBCL2bcl-X ProteinAntineoplastic AgentsBreast Neoplasmsmacromolecular substancesAdenocarcinomaArticleCell LineInhibitory Concentration 50Cell Line TumorThiadiazolesmedicineDiabetes MellitusKRasHumansGlycogen synthaseProtein Kinase InhibitorsCell ProliferationChemotherapeu-tic drugsGlycogen Synthase Kinase 3 betaGSK-3βAdenylate KinaseBiphenyl Compoundsnutraceuticals;PDACβ-cateninGemcitabine?-cateninMalariaPancreatic Neoplasmslcsh:Biology (General)MCF-7DoxorubicinDietary SupplementsCancer researchbiology.protein
researchProduct

Downregulation of wild-type β-catenin expression by interleukin 6 in human hepatocarcinoma HepG2 cells: a possible role in the growth-regulatory effe…

2001

We investigated the antitumour effects of interleukin 6 (IL-6) on hepatocarcinoma HepG2 cells, endowed with high levels of a mutated, non-degradable, beta-catenin. IL-6 produced minimal growth-inhibitory effects and no apoptosis or gross changes in cell adhesion. Interestingly, however, it caused a consistent decrease in the cytoplasmic levels of wild-type, but not of mutated, beta-catenin protein. There was no effect on E-cadherin or gamma-catenin and a reduction in alpha-catenin occurred only at high concentrations. IL-4, a non-related cytokine, did not modify the content of beta-catenin. IL-6 did not influence beta-catenin mRNA levels. LiCl, a potent inhibitor of Glycogen Synthase Kinase…

Cancer ResearchCarcinoma Hepatocellularmedicine.medical_treatmentBlotting WesternDown-RegulationApoptosisEnzyme-Linked Immunosorbent AssayBiologyDownregulation and upregulationGSK-3Tumor Cells CulturedmedicineHumansRNA MessengerInterleukin 6beta CateninInterleukin 4Interleukin-6Cell growthLiver NeoplasmsWild typeCell biologyCytoskeletal ProteinsCytokineOncologyCateninTrans-ActivatorsCancer researchbiology.proteinEuropean Journal of Cancer
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct

Multifaceted roles of GSK-3 and Wnt/beta-catenin in hematopoiesis and leukemogenesis: opportunities for therapeutic intervention

2013

Glycogen synthase kinase-3 (GSK-3) is well documented to participate in a complex array of critical cellular processes. It was initially identified in rat skeletal muscle as a serine/threonine kinase that phosphorylated and inactivated glycogen synthase. This versatile protein is involved in numerous signaling pathways that influence metabolism, embryogenesis, differentiation, migration, cell cycle progression and survival. Recently, GSK-3 has been implicated in leukemia stem cell pathophysiology and may be an appropriate target for its eradication. In this review, we will discuss the roles that GSK-3 plays in hematopoiesis and leukemogenesis as how this pivotal kinase can interact with mul…

MAPK/ERK pathwayCancer ResearchBeta-catenintherapy resistanceCarcinogenesisWnt ProteinReviewmacromolecular substancesAkt; GSK-3; leukemia stem cells; targeted therapy; therapy resistance; Wnt/b-cateninWNTGlycogen Synthase Kinase 3GSK-3PTENAnimalsHumansHematopoiesiProtein kinase BCarcinogenesiPI3K/AKT/mTOR pathwaybeta CateninWnt/β-cateninGSK-3LeukemiabiologyAnimalKinaseAktleukemia stem cellWnt signaling pathwayHematologyleukemia stem cellstargeted therapy3. Good healthHematopoiesisWnt ProteinsAnesthesiology and Pain MedicineOncologyCancer researchbiology.proteinWnt/b-cateninHuman
researchProduct

Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells

2015

Pancreatic cancer is currently the fourth most common cancer, is increasing in incidence and soon will be the second leading cause of cancer death in the USA. This is a deadly malignancy with an incidence that approximates the mortality with 44,000 new cases and 36,000 deaths each year. Surgery, although only modestly successful, is the only curative option. However, due the locally aggressive nature and early metastasis, surgery can be performed on less than 20% of patients. Cytotoxic chemotherapy is palliative, has significant toxicity and improves survival very little. Thus new treatment paradigms are needed desperately. Due to the extremely high frequency of KRAS gene mutations (>90%) d…

MAPK/ERK pathwayCancer ResearchmiRsEGFRmedicine.disease_causeMetastasisProto-Oncogene Proteins p21(ras)Glycogen Synthase Kinase 3GeneticCancer stem cellKRaPancreatic cancerKRasGeneticsmedicineAnimalsHumansPTENEpidermal growth factor receptorMolecular BiologyPI3K/AKT/mTOR pathwayGSK-3biologyCancer stem cellsCancer stem cellmiRCancer stem cells; Drug resistance; EGFR; GSK-3; KRas; Metformin; miRsmedicine.diseaseMetforminErbB ReceptorsPancreatic NeoplasmsDrug resistanceNeoplastic Stem Cellsbiology.proteinCancer researchMolecular MedicineKRASSignal TransductionAdvances in Biological Regulation
researchProduct

Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
researchProduct