Search results for "LY294002"

showing 7 items of 7 documents

Estrogen Receptor Signaling and the PI3K/Akt Pathway Are Involved in Betulinic Acid-Induced eNOS Activation

2016

Betulinic acid (BA) is a naturally occurring pentacyclic triterpenoid with anti-inflammatory, antiviral and anti-cancer properties. Beneficial cardiovascular effects such as increased nitric oxide (NO) production through enhancement of endothelial NO synthase (eNOS) activity and upregulation of eNOS expression have been demonstrated for this compound. In the present study, immortalized human EA.hy 926 endothelial cells were incubated for up to 1 h with 1–100 µM BA and with the phosphatidylinositol-3-kinase (PI3K) inhibitors LY294002 and wortmannin, or the estrogen receptor (ER) antagonist ICI 182,780. Phosphorylation status of eNOS and total eNOS protein were analyzed by Western blotting us…

0301 basic medicinePharmaceutical ScienceEstrogen receptorPI3KAnalytical ChemistryWortmanninchemistry.chemical_compound0302 clinical medicineEnosDrug DiscoveryLY294002PhosphorylationFulvestrantLungbiologyEstradiolendothelial cellsReceptors EstrogenChemistry (miscellaneous)030220 oncology & carcinogenesisMolecular MedicinePhosphorylationSignal transductionPentacyclic TriterpenesWortmanninSignal Transductionestrogen receptormedicine.medical_specialtyNitric Oxide Synthase Type IIIMorpholinesArticleCell Linelcsh:QD241-44103 medical and health sciencesbetulinic acidlcsh:Organic chemistryInternal medicinemedicineAnimalsHumansPhysical and Theoretical ChemistryProtein kinase BPI3K/AKT/mTOR pathwayendothelial nitric oxide synthaseAktOrganic ChemistryFibroblastsbiology.organism_classificationMolecular biologyTriterpenesbetulinic acid; endothelial nitric oxide synthase; endothelial cells; estrogen receptor; PI3K; AktRatsAndrostadienes030104 developmental biologyEndocrinologychemistryGene Expression RegulationChromonesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktMolecules
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Quercetin ameliorates dysregulation of lipid metabolism genes via the PI3K/AKT pathway in a diet-induced mouse model of nonalcoholic fatty liver dise…

2015

Scope Flavonoids and related compounds seem to have favorable effects on nonalcoholic fatty liver disease (NAFLD) progression, although the exact mechanisms implicated are poorly understood. In this study, we aimed to investigate the effect of the flanovol quercetin on gene expression deregulation involved in the development of NAFLD, as well as the possible implication of phosphatidylinositol 3-kinase (PI3K)/AKT pathway modulation. Methods and results We used an in vivo model based on methionine- and choline-deficient (MCD) diet-fed mice and an in vitro model consisting of Huh7 cells incubated with MCD medium. MCD-fed mice showed classical pathophysiological characteristics of nonalcoholic…

CD36 AntigensMalemedicine.medical_specialtyOxidative phosphorylationBiologyMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseaseGene expressionmedicineTranscriptional regulationAnimalsLY294002PhosphatidylinositolCells CulturedPI3K/AKT/mTOR pathwayLipid metabolismLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyGene Expression RegulationchemistryCancer researchQuercetinLipid PeroxidationProto-Oncogene Proteins c-aktSignal TransductionFood ScienceBiotechnologyMolecular Nutrition & Food Research
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Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
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Inducible NO synthase confers chemoresistance in head and neck cancer by modulating survivin

2009

The dual role of the inducible NO synthase (iNOS) and NO signaling in head and neck squamous cell carcinoma (HNSCC) is a complex and can both promote or inhibit tumor progression. However, the underlying molecular mechanisms are not yet resolved in detail. We show for the first time that conditions, favoring low NO levels conferred resistance against cisplatin/taxol-induced apoptosis in HNSCC cell lines. Cytoprotection was mediated by survivin, because we observed its upregulation subsequent to low doses of the NO donors S-nitroso-N-acetyl-penicillamine (SNAP) and sodium nitroprusside (SNP) or ectopic expression of physiologic amounts of iNOS. Also, RNAi-mediated depletion of survivin block…

MaleUmbilical VeinsCancer ResearchSurvivinFluorescent Antibody TechniqueNitric Oxide Synthase Type IIApoptosisp38 Mitogen-Activated Protein KinasesInhibitor of Apoptosis ProteinsImmunoenzyme TechniquesPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundLY294002Enzyme InhibitorsRNA Small InterferingAged 80 and overReverse Transcriptase Polymerase Chain ReactionCell CycleMiddle AgedCell cycleOncologyHead and Neck NeoplasmsCarcinoma Squamous CellFemaleMicrotubule-Associated ProteinsNitroprussidePaclitaxelImmunoblottingAntineoplastic AgentsS-Nitroso-N-AcetylpenicillamineBiologyCell LineDownregulation and upregulationSurvivinmedicineHumansNitric Oxide DonorsRNA MessengerneoplasmsProtein kinase BNitritesPI3K/AKT/mTOR pathwayAgedmedicine.diseaseAntineoplastic Agents PhytogenicHead and neck squamous-cell carcinomachemistryDrug Resistance NeoplasmTumor progressionImmunologyCancer researchEndothelium VascularCisplatinProto-Oncogene Proteins c-aktInternational Journal of Cancer
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Drug connectivity mapping and functional analysis reveal therapeutic small molecules that differentially modulate myelination

2022

Disruption or loss of oligodendrocytes (OLs) and myelin has devastating effects on CNS function and integrity, which occur in diverse neurological disorders, including Multiple Sclerosis (MS), Alzheimer’s disease and neuropsychiatric disorders. Hence, there is a need to develop new therapies that promote oligodendrocyte regeneration and myelin repair. A promising approach is drug repurposing, but most agents have potentially contrasting biological actions depending on the cellular context and their dose-dependent effects on intracellular pathways. Here, we have used a combined systems biology and neurobiological approach to identify compounds that exert positive and negative effects on olig…

MyelinMiceMyelin SheathNSC Neural stem cellSystems BiologyOPC Oligodendrocyte progenitor cellHigh-Throughput Nucleotide SequencingLINCS The Library of Integrated Network-based Cellular SignaturesCell DifferentiationGeneral MedicineCNS Central Nervous SystemOligodendrogliamedicine.anatomical_structureOligodendrogenesisNFOL Newly formed oligodendrocyteOL OligodendrocyteSignal TransductionSubventricular zoneOptic nerveIn silicoSystems biologyMorpholinesSVZ subventricular zoneContext (language use)RM1-950BiologyArticlemedicinePharmacogenomics The Library of Integrated Network-Based Cellular Signatures/LINCSAnimalsH-LY29 High concentration of LY294002Computer SimulationPI3K/AKT/mTOR pathwayL-LY29 Low concentration of LY294002PharmacologyPI3K/AktTCN TriciribineDose-Response Relationship DrugRegeneration (biology)Multiple sclerosismedicine.diseaseOligodendrocyteOligodendrocyteiNSCs iPSC-derived NSCsTAPs Transiently amplifying progenitorsMice Inbred C57BLMS Multiple SclerosisiPCS induced Pluripotent Stem CellChromonesPharmacogeneticsTherapeutics. PharmacologyMOL Myelinating oligodendrocyteNeuroscienceBiomedicine & Pharmacotherapy
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Effect of LIF-withdrawal on acetylcholine synthesis in the embryonic stem cell line CGR8 is not mediated by STAT3, PI3Ks or cAMP/PKA pathways.

2015

Acetylcholine (ACh) acts as a local cellular signaling molecule and is widely expressed in nature, including mammalian cells and embryonic stem cells. The murine embryonic stem cell line CGR8 synthesizes and releases substantial amounts of ACh. Particularly during early differentiation - a period associated with multiple alterations in geno-/phenotype functions - synthesis and release of ACh are increased by 10-fold. In murine stem cells second messengers of the STAT-3, PI3K and cAMP/PKA pathways are involved in maintaining self-renewal and pluripotency. The present experiments were designed to test whether blockers of these signaling pathways enhance ACh cell content in the presence of LIF…

STAT3 Transcription FactorCell signalingCurcuminMorpholinesImmunologyBiologyLeukemia Inhibitory FactorGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePhosphatidylinositol 3-KinasesCyclic AMPImmunology and AllergyAnimalsLY294002PI3K/AKT/mTOR pathwayEmbryonic Stem CellsPharmacologySulfonamidesForskolinColforsinIsoquinolinesEmbryonic stem cellCyclic AMP-Dependent Protein KinasesAcetylcholineCell biologychemistryChromonesSecond messenger systemSignal transductionStem cellSignal TransductionInternational immunopharmacology
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TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies

2009

AIM: To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors, in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL), on overcoming TRAIL resistance in hepatocellular carcinoma (HCC) and to study the efficacy of agonistic TRAIL antibodies, as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS: Surface expression of TRAIL receptors (TRAIL-R1-4) and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting, respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNA…

SorafenibCarcinoma Hepatocellularbcl-X ProteinBcl-xLAntineoplastic AgentsApoptosisTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundCell Line TumormedicineAnimalsHumansLY294002Viability assayEnzyme InhibitorsPI3K/AKT/mTOR pathwaybiologyKinaseLiver NeoplasmsGastroenterologyGeneral Medicinedigestive system diseasesReceptors TNF-Related Apoptosis-Inducing LigandchemistryProto-Oncogene Proteins c-bcl-2ApoptosisDoxorubicinCancer researchbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinTumor necrosis factor alphaOriginal ArticleFluorouracilmedicine.drug
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