Search results for "Protein kinase B"

showing 10 items of 191 documents

mGluR2/3 agonist LY379268, by enhancing the production of GDNF, induces a time-related phosphorylation of RET receptor and intracellular signaling Er…

2011

In the present study we aimed to verify if the enhancement of glial cell line-derived neurotrophic factor (GDNF) production in mouse striatum following treatment with LY379268 may also induce in the nigrostriatal system a time-related activation of RET receptor and its specific intracellular signaling. For this purpose, we have investigated the effects of LY379268 treatment on RET phosphorylation at the Tyr1062 and on downstream signaling Erk1/2, Akt and PLCγ1 pathway activation. The results showed that treatment with LY379268 (3 mg/kg) induces a significant increase of GDNF levels and time-related RET and Erk1/2 phosphorylation in the striatum. These increases were detected at 24 h and 48 …

Intracellular FluidMalemedicine.medical_specialtyTime FactorsMAP Kinase Signaling SystemSubstantia nigraStriatumReceptors Metabotropic GlutamateSettore BIO/09 - FisiologiaCellular and Molecular NeuroscienceMiceErk1/2Neurotrophic factorsInternal medicinemedicineGlial cell line-derived neurotrophic factorAnimalsGlial Cell Line-Derived Neurotrophic FactorAmino AcidsPhosphorylationReceptormGluR2/3Protein kinase BPharmacologyMitogen-Activated Protein Kinase 3biologyChemistryProto-Oncogene Proteins c-retLY379268Bridged Bicyclo Compounds HeterocyclicGDNFCorpus StriatumUp-RegulationMice Inbred C57BLEndocrinologynervous systembiology.proteinPhosphorylationTrK phosphorylationRETGDNF family of ligandsNeuropharmacology
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Sirolimus treatment of severe PTEN hamartoma tumor syndrome: case report and in vitro studies

2013

Background: Phosphatase and tensin homolog (PTEN) hamartoma tumor syndrome (PHTS) is caused by germ line mutations in the PTEN gene. Symptoms include cancer pre- disposition, immune deviations, and lipomas/lipomatosis. No causal standard therapy is available. We describe a therapeutic attempt with the mammalian target of rapamycin (mTOR) inhibitor sirolimus for a PHTS patient suffering from thymus hyperplasia and lipomatosis. We furthermore assessed the in vitro effects of sirolimus and other inhibitors on lipoma cells of the patient. Methods: The patient underwent clinical and blood examinations and whole-body magnetic resonance imaging to assess tumor sizes. Lipoma cells of the patient we…

LipomatosisIn Vitro TechniquesDrug therapy Hamartoma Paediatrics PTEN PHTS PI3K AKT mTORmedicineHumansTensinPTENddc:610Protein kinase BPI3K/AKT/mTOR pathwaySirolimusbiologybusiness.industryInfant NewbornPTEN PhosphohydrolaseInfantLipomamedicine.diseaseChild PreschoolSirolimusPediatrics Perinatology and Child HealthCancer researchbiology.proteinThymus hyperplasiaHamartoma Syndrome Multiplebusinessmedicine.drugPediatric Research
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Anti-inflammatory effects of cinnamon extract and identification of active compounds influencing the TLR2 and TLR4 signaling pathways

2018

Purpose: Inflammatory processes are involved in many diseases. The bark of Cinnamomum verum and its extracts are well known for anti-inflammatory effects, but the underlying active compounds and chemical mechanisms are not yet fully identified. The objective of this study was to elucidate how cinnamon extract, specifically active compounds, and their combinations influence the signaling pathways of inflammation, especially through toll-like receptors TLR2 and TLR4. Methods: Bioassay-guided fractionation was performed for standard ethanolic cinnamon extract using high performance liquid chromatography followed by compound identification in the determined active fractions by high-resolution m…

Lipopolysaccharides0301 basic medicineCinnamomum zeylanicumCell SurvivalTHP-1 Cellsmedicine.drug_classAnti-Inflammatory AgentsPharmacologyMonocytesCinnamic acidAnti-inflammatory03 medical and health scienceschemistry.chemical_compoundNF-KappaB Inhibitor alphamedicineHumansAcroleinPhosphorylationProtein kinase BCinnamyl alcoholbiologyPlant ExtractsChemistryInterleukin-8Cinnamomum verumNF-kappa BDrug SynergismGeneral Medicinebiology.organism_classificationToll-Like Receptor 2Toll-Like Receptor 4IκBα030104 developmental biologyMonoterpenesCymenesPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionFood ScienceFood & Function
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New agents and approaches for targeting the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR cell survival pathways.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Targeting these pathways is often complex and can result in pathway activation depending on the presence of upstream mutations (e.g., Raf inhibitors induce Raf activation in cells with wild type (WT) RAF in the presence of mutant, activated RAS) and rapamycin can induce Akt activation. Targeting with inhibitors directed at two constituents of the same pathway or two different signaling pathways may be a more effective approach. This review will first evaluate potential uses of Raf, MEK, PI3K, Akt and mTOR inhibitors that have…

MAPK/ERK pathway0303 health sciencesCell signalingbiologyChemistryAKTApoptosisGrowth factorRafOncogens: Signaling pathway3. Good healthMalignant transformation03 medical and health sciences0302 clinical medicineApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinEpidermal growth factor receptorSignal transductionpi3kProtein kinase BRaPI3K/AKT/mTOR pathway030304 developmental biology
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BRAFV600E mutation, TIMP-1 upregulation, and NF-κB activation: closing the loop on the papillary thyroid cancer trilogy.

2011

BRAFV600E is the most common mutation found in papillary thyroid carcinoma (PTC). Tissue inhibitor of metalloproteinases (TIMP-1) and nuclear factor (NF)-κB have been shown to play an important role in thyroid cancer. In particular, TIMP-1 binds its receptor CD63 on cell surface membrane and activates Akt signaling pathway, which is eventually responsible for its anti-apoptotic activity. The aim of our study was to evaluate whether interplay among these three factors exists and exerts a functional role in PTCs. To this purpose, 56 PTC specimens were analyzed for BRAFV600E mutation, TIMP-1 expression, and NF-κB activation. We found that BRAFV600E mutation occurs selectively in PTC nodules an…

MAPK/ERK pathwayAdultMaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismThyroid cancer TIMP-1 papillary thyroid cancerMutation MissenseGlutamic AcidGene Expression Regulation EnzymologicSettore MED/13 - EndocrinologiaPapillary thyroid cancerEndocrinologyDownregulation and upregulationInternal medicinemedicineTumor Cells CulturedGene silencingHumansGene Regulatory NetworksNeoplasm InvasivenessThyroid NeoplasmsProtein kinase BThyroid cancerTissue Inhibitor of Metalloproteinase-1ChemistryAkt/PKB signaling pathwayCarcinomaNF-kappa BValineMiddle Agedmedicine.diseaseCarcinoma PapillaryUp-RegulationGene Expression Regulation NeoplasticEndocrinologyCell Transformation NeoplasticOncologyAmino Acid SubstitutionThyroid Cancer PapillaryCancer researchDisease ProgressionFemaleV600ESignal TransductionEndocrine-related cancer
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR inhibitors: Rationale and importance to inhibiting these pathways in human health

2011

William H. Chappell 1 , Linda S. Steelman 1,2 , Jacquelyn M. Long 2 , Ruth C. Kempf 2 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Jorg Basecke 3 , Franca Stivala 4 , Marco Donia 4 , Paolo Fagone 4 , Graziella Malaponte 4 , Maria C. Mazzarino 4 , Ferdinando Nicoletti 4 , Massimo Libra 4 , Danijela Maksimovic-Ivanic 5 , Sanja Mijatovic 5 , Giuseppe Montalto 6 , Melchiorre Cervello 7 , Piotr Laidler 8 , Michele Milella 9 , Agostino Tafuri 10 , Antonio Bonati 11 , Camilla Evangelisti 12 , Lucio Cocco 12 , Alberto M. Martelli 12,13 , and James A. McCubrey 1 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University 2 Department of Physics, Greenville, N…

MAPK/ERK pathwayAgingmedicine.medical_treatmentDrug ResistancerafPI3KTargeted therapycombination therapyPhosphatidylinositol 3-Kinases0302 clinical medicineTARGETED THERAPYCANCER STEM CELLSNeoplasmsCancer Stem CellsMedicineExtracellular Signal-Regulated MAP Kinases0303 health sciencesCombination TherapybiologyTOR Serine-Threonine KinasesMTORHuman health Ras inhibitors MEK ERKTargeted TherapyDiscovery and development of mTOR inhibitors3. Good healthDRUG RESISTANCECell Transformation NeoplasticOncology030220 oncology & carcinogenesismTORraf KinasesPremature agingMAP Kinase Signaling SystemReviewsSenescence03 medical and health sciencesCell Line TumorHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyMitogen-Activated Protein Kinase Kinasesbusiness.industryAKTAktagingPTEN PhosphohydrolaseRafTransplantationSENESCENCEImmunologyras Proteinsbiology.proteinCancer researchaging; akt; cancer stem cells; combination therapy; drug resistance; mtor; pi3k; raf; senescence; targeted therapybusinessProto-Oncogene Proteins c-akt
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Cajaninstilbene acid (CSA) exerts cytoprotective effects against oxidative stress through the Nrf2-dependent antioxidant pathway.

2013

Cajaninstilbene acid (CSA), an active compound separated from pigeon pea leaves, possesses the highly efficient antioxidant activities. Transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) is an important regulator of cellular oxidative stress. This study examined the role of Nrf2 in CSA-mediated antioxidant effects on human hepatocarcinoma (HepG2) cell line. The generation of reactive oxygen species (ROS) upon H2O2 and CSA treatment was lower than that of H2O2 alone. CSA activated Nrf2 as evaluated by Western blotting. A luciferase reporter assay also demonstrated that CSA-activated signaling resulted in the increased transcriptional activity of Nrf2 through binding to t…

MAPK/ERK pathwayAntioxidantNF-E2-Related Factor 2medicine.medical_treatmentBlotting WesternBiologyToxicologymedicine.disease_causeenvironment and public healthAntioxidantsStilbenesmedicineNAD(P)H Dehydrogenase (Quinone)HumansProtein kinase BTranscription factorPI3K/AKT/mTOR pathwaychemistry.chemical_classificationReactive oxygen speciesGeneral MedicineHep G2 Cellsrespiratory systemAntioxidant Response ElementsSalicylatesOxidative StressBiochemistrychemistryCytoprotectionNAD+ kinaseOxidative stressHeme Oxygenase-1Signal TransductionToxicology letters
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Evaluation and clinical analyses of downstream targets of the Akt inhibitor GDC-0068.

2013

Abstract Purpose: The oncogenic PI3K/Akt/mTOR pathway is an attractive therapeutic target in cancer. However, it is unknown whether the pathway blockade required for tumor growth inhibition is clinically achievable. Therefore, we conducted pharmacodynamic studies with GDC-0068, an ATP competitive, selective Akt1/2/3 inhibitor, in preclinical models and in patients treated with this compound. Experimental Design: We used a reverse phase protein array (RPPA) platform to identify a biomarker set indicative of Akt inhibition in cell lines and human-tumor xenografts, and correlated the degree of pathway inhibition with antitumor activity. Akt pathway activity was measured using this biomarker se…

MAPK/ERK pathwayCancer ResearchAKT1PharmacologyPiperazines03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineIn vivoMedicineAnimalsHumansProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbusiness.industryTOR Serine-Threonine KinasesCancerReverse phase protein lysate microarraymedicine.diseaseXenograft Model Antitumor Assays3. Good healthOncogene Protein v-aktPyrimidinesOncology030220 oncology & carcinogenesisBiomarker (medicine)businessSignal TransductionClinical cancer research : an official journal of the American Association for Cancer Research
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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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The novel dual PI3K/mTOR inhibitor GDC-0941 synergizes with the MEK inhibitor U0126 in non-small cell lung cancer cells.

2011

Lung cancer is a malignant disease with poor outcome, which has led to a search for new therapeutics. The PI3K/Akt/mTOR and Ras/raf/Erk pathways are key regulators of tumor growth and survival. In the present study, their roles were evaluated by MTT assay, flow cytometry and Western blotting in lung cancer cells. We found that a high efficacy of antitumor activity was shown with GDC-0941 treatment in two gefitinib-resistant non-small cell lung cancer (NSCLC) cell lines, A549 and H460. In addition, H460 cells with activating mutations of PIK3CA were relatively more sensitive to GDC-0941 than A549 cells with wild-type PIK3CA. Furthermore, GDC-0941 was highly efficacious in combination with U0…

MAPK/ERK pathwayCancer ResearchIndazolesLung NeoplasmsApoptosisBiologyBiochemistryPhosphatidylinositol 3-KinasesCarcinoma Non-Small-Cell LungCell Line TumorNitrilesGeneticsmedicineButadienesHumansMolecular BiologyProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsSulfonamidesOncogeneCell growthMEK inhibitorTOR Serine-Threonine KinasesCancerDrug SynergismCell cyclemedicine.diseaseG1 Phase Cell Cycle Checkpointsrespiratory tract diseasesEnzyme ActivationOncologyCancer researchMolecular MedicineMitogen-Activated Protein KinasesSignal TransductionMolecular medicine reports
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