Search results for "Glycogen synthase"

showing 10 items of 61 documents

Design, Synthesis and Biological Evaluation of 7-Chloro-9

2019

Glycogen synthase kinase-3β (GSK-3β) represents a relevant drug target for the treatment of neurodegenerative pathologies including Alzheimer’s disease. We herein report on the optimization of a novel class of GSK-3β inhibitors based on the tofacitinib-derived screen hit 3-((3R,4R)-3-((7-chloro-9H-pyrimido[4,5-b]indol-4-yl)(methyl)amino)-4-methylpiperidin-1-yl)-3-oxopropanenitrile (1). We synthesized a series of 19 novel 7-chloro-9H-pyrimido[4,5-b]indole-based derivatives and studied their structure–activity relationships with focus on the cyanoacetyl piperidine moiety. We unveiled the crucial role of the nitrile group and its importance for the activity of this compound series. A successfu…

Glycogen synthase kinase-3βBinding SitesGlycogen Synthase Kinase 3 betatofacitinibDose-Response Relationship DrugMolecular Structurekinase inhibitorMolecular Conformationprotein kinaseChemistry Techniques SyntheticMolecular Dynamics SimulationArticle7-chloro-9H-pyrimido[45-b]indoleEnzyme ActivationMolecular Docking SimulationStructure-Activity RelationshipAdenosine TriphosphateDrug DesignHumansEnzyme InhibitorsHydrophobic and Hydrophilic InteractionsProtein Kinase InhibitorsProtein BindingMolecules (Basel, Switzerland)
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Integrin alpha 2 beta 1 promotes activation of protein phosphatase 2A and dephosphorylation of Akt and glycogen synthase kinase 3 beta.

2002

The integrins are a large family of heterodimeric transmembrane receptors composed of α and β subunits (22). In addition to mediating cell-matrix interactions, integrins have been shown to activate intracellular signaling pathways which, in collaboration with growth factor-induced signals, regulate cellular functions (46). Some integrin signaling cascades are activated via the β subunit cytoplasmic domain, and they are therefore triggered by several integrin heterodimers. These signals include the activation of protein tyrosine kinases of the Src and focal adhesion kinase (FAK) families (9, 47). More-recent studies have revealed signaling events that are activated specifically by an α subun…

IntegrinsReceptors CollagenIntegrinProtein Serine-Threonine KinasesCD49cp38 Mitogen-Activated Protein KinasesCollagen receptorGlycogen Synthase Kinase 3Proto-Oncogene ProteinsCell AdhesionPhosphoprotein PhosphatasesHumansIntegrin-linked kinaseProtein Phosphatase 2cdc42 GTP-Binding ProteinMolecular BiologyCell Growth and DevelopmentCells CulturedbiologyAkt/PKB signaling pathwayCell adhesion moleculeGlycogen Synthase KinasesCell BiologyCell biologyEnzyme ActivationBiochemistryIntegrin alpha MCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinIntegrin beta 6CollagenMitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktProtein BindingSignal TransductionMolecular and cellular biology
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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
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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
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Ex Vivo Treatment with a Polyphenol-Enriched Cocoa Extract Ameliorates Myocardial Infarct and Postischemic Mitochondrial Injury in Normotensive and H…

2016

Our objective was to determine the effects of a polyphenol-enriched cocoa extract (PCE) on myocardial postischemic alterations in normotensive (Wistar rats, W) and spontaneously hypertensive rats (SHR). Isolated hearts were submitted to 110 min of perfusion or 20 min stabilization, 30 min global ischemia, and 60 min reperfusion (R). Other hearts were treated with PCE at the onset of R. Infarct size, the reduced glutathione (GSH), and the expression of phospho-Akt, P-GSK-3β, and P-eNOS were assessed. In isolated mitochondria, the Ca2+-mediated response of mitochondrial permeability transition pore (mPTP), membrane potential (δψm), and superoxide production were determined. PCE decreased infa…

Male0301 basic medicineMyocardial InfarctionWistarBlood Pressure030204 cardiovascular system & hematologyPharmacologyMitochondrial Membrane Transport ProteinsInfarct sizeSHRGlycogen Synthase Kinase 3chemistry.chemical_compound0302 clinical medicineMITOCHONDRIAIschemiaSuperoxidesEnosRats Inbred SHRbiologySuperoxideMPTPINFARCT SIZEHeart//purl.org/becyt/ford/3.1 [https]GlutathioneMitochondriaMedicina BásicaHypertension//purl.org/becyt/ford/3 [https]General Agricultural and Biological SciencesPerfusionCocaCardiotonic AgentsCIENCIAS MÉDICAS Y DE LA SALUDInmunologíaIschemiaIn Vitro Techniques03 medical and health sciencesPOLYPHENOLSWISTARmedicineAnimalsHumansRats WistarSHR; Wistar; infarct size; mitochondria; polyphenolsMitochondrial Permeability Transition PorePlant ExtractsMyocardiumCocoa ExtractPolyphenolsGeneral ChemistryGlutathionemedicine.diseasebiology.organism_classificationRats030104 developmental biologychemistryMitochondrial permeability transition poreCiencias MédicasJournal of Agricultural and Food Chemistry
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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Pterostilbene Prevents Early Diabetic Retinopathy Alterations in a Rabbit Experimental Model

2019

Oxidative stress generated by diabetes plays a key role in the development of diabetic retinopathy (DR), a common diabetic complication. DR remains asymptomatic until it reaches advanced stages, which complicate its treatment. Although it is known that good metabolic control is essential for preventing DR, knowledge of the disease is incomplete and an effective treatment with no side effects is lacking. Pterostilbene (Pter), a natural stilbene with good antioxidant activity, has proved to beneficially affect different pathologies, including diabetes. Therefore, our study aimed to analyse the protective and/or therapeutic capacity of Pter against oxidant damage by characterising early retina…

Male0301 basic medicinepterostilbenePterostilbeneretinal damageNF-E2-Related Factor 2lcsh:TX341-641Pharmacologymedicine.disease_causeAntioxidantsArticlePhosphatidylinositol 3-Kinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDiabetes mellitusStilbenesmedicineAnimalsoxidative stressProtein kinase BPI3K/AKT/mTOR pathwayType 1 diabetesGlycogen Synthase Kinase 3 betaNutrition and Dieteticsbusiness.industryDiabetic retinopathymedicine.diseaseEnzyme ActivationDisease Models Animaldiabetic retinopathypolyphenol030104 developmental biologychemistryHyperglycemia030220 oncology & carcinogenesisMetabolic control analysisRabbitsbusinesslcsh:Nutrition. Foods and food supplyProto-Oncogene Proteins c-aktOxidative stressSignal TransductionFood ScienceNutrients
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Enzyme histochemical and immunohistochemical characterization of oval and parenchymal cells proliferating in livers of rats fed a choline-deficient/D…

1991

Male outbred Sprague-Dawley rats were fed a choline-deficient diet containing 0.10% DL-ethionine for up to 30 weeks. Liver slices from rats killed 4, 6, 10, 14, 22 and 30 weeks after starting the treatment were histochemically analyzed for the following parameters: basophilia, expression of cytokeratin 19 (which in the liver is bile duct epithelial cell-specific), glycogen content and activities of glycogen synthetase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6PASE), glucose-6-phosphate dehydrogenase (G6PDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), glycerin-3-phosphate dehydrogenase (G3PDH), 'malic enzyme' (MDH), alkaline phosphatase (ALKPASE) and gamma-glutamyl…

MaleCancer Researchmedicine.medical_specialtyPhosphorylasesPopulationGlycerolphosphate DehydrogenaseBiologyGlucosephosphate DehydrogenaseGlycogen phosphorylasechemistry.chemical_compoundMalate DehydrogenaseInternal medicineParenchymamedicineAnimalsEthionineeducationGlycogen synthaseeducation.field_of_studyEthionineGlycogenGlyceraldehyde-3-Phosphate DehydrogenasesRats Inbred StrainsGeneral Medicinegamma-GlutamyltransferaseAlkaline PhosphataseAnimal FeedImmunohistochemistryCholine DeficiencyLiver GlycogenRatsmedicine.anatomical_structureEndocrinologyGlycogen SynthasechemistryLiverHepatocyteFood Fortifiedbiology.proteinGlucose-6-PhosphataseAlkaline phosphataseKeratinsCell DivisionCarcinogenesis
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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
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Chronic lithium salt treatment reduces CRE/CREB-directed gene transcription and reverses its upregulation by chronic psychosocial stress in transgeni…

2007

The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMP-responsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) sig…

MaleTranscriptional ActivationBipolar DisorderTransgeneDown-RegulationMice TransgenicCREBDrug Administration Schedule03 medical and health sciencesGlycogen Synthase Kinase 3Mice0302 clinical medicineGSK-3Transcription (biology)Antimanic AgentsGenes ReporterGene expressionAnimalsPhosphorylationProtein kinase ACyclic AMP Response Element-Binding ProteinSocial BehaviorTranscription factor030304 developmental biologyPharmacology0303 health sciencesReporter genebiologyBehavior AnimalBrainMolecular biologyUp-RegulationPsychiatry and Mental healthDisease Models AnimalGene Expression RegulationChronic Diseasebiology.proteinLithium Compounds030217 neurology & neurosurgeryStress PsychologicalAdenylyl CyclasesSignal TransductionNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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