Search results for "3-KINASE"

showing 10 items of 120 documents

Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases.

2017

Natural products or nutraceuticals promote anti-aging, anti-cancer and other health-enhancing effects. A key target of the effects of natural products may be the regulation of the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway. This review will focus on the effects of curcumin (CUR), berberine (BBR) and resveratrol (RES), on the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway, with a special focus on GSK-3. These natural products may regulate the pathway by multiple mechanisms including: reactive oxygen species (ROS), cytokine receptors, mirco-RNAs (miRs) and many others. CUR is present the root of turmeric (Curcuma longa). CUR is used in the treatment of many disorders, especially in those involving inflammatory p…

0301 basic medicineCancer ResearchCurcuminBerberinemTORC1PharmacologyResveratrolMechanistic Target of Rapamycin Complex 1Protective AgentsNatural product03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesBerberineGeneticNeoplasmsOsteoarthritisStilbenesGeneticsPTENHumansCurcumaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInflammationNatural productsbiologyBerberine; Curcumin; Natural products; ResveratrolPTEN PhosphohydrolaseNeurodegenerative Diseasesbiology.organism_classification030104 developmental biologyBiochemistrychemistryGene Expression RegulationCardiovascular DiseasesResveratrolbiology.proteinCurcuminMolecular MedicineProto-Oncogene Proteins c-aktSignal Transduction
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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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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

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). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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PIK3R1 Mutations Cause Syndromic Insulin Resistance with Lipoatrophy

2013

International audience; Short stature, hyperextensibility of joints and/or inguinal hernia, ocular depression, Rieger anomaly, and teething delay (SHORT) syndrome is a developmental disorder with an unknown genetic cause and hallmarks that include insulin resistance and lack of subcutaneous fat. We ascertained two unrelated individuals with SHORT syndrome, hypothesized that the observed phenotype was most likely due to de novo mutations in the same gene, and performed whole-exome sequencing in the two probands and their unaffected parents. We then confirmed our initial observations in four other subjects with SHORT syndrome from three families, as well as 14 unrelated subjects presenting wi…

ProbandEXPRESSIONmedicine.medical_specialty030209 endocrinology & metabolismBiologymedicine.disease_causeMICE LACKINGShort stature03 medical and health sciencesHYPOGLYCEMIA0302 clinical medicineInsulin resistancePIK3R1Internal medicineReportmedicineGeneticsKINASEGenetics(clinical)LipoatrophyGenetics (clinical)030304 developmental biology0303 health sciencesMutationAKT2[SDV.GEN]Life Sciences [q-bio]/GeneticsRECEPTORmedicine.disease3-KINASE3. Good healthInsulin receptorEndocrinologyAUTOPHOSPHORYLATIONSHORT syndromebiology.proteinSKELETAL-MUSCLEGROWTHmedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Endothelial Nitric Oxide Synthase Regulates T Cell Receptor Signaling at the Immunological Synapse

2006

The role of nitric oxide (NO) in T cells remains controversial, and the origin and localization of endogenous NO and whether it regulates lymphocyte activation are unclear. We show here that, within minutes of binding to antigen, T cells produce NO via endothelial nitric oxide synthase (eNOS). This process required increased intracellular Ca2+ and phosphoinositide3-kinase activity. By using an eNOS-green fluorescent fusion protein and fluorescent probes to detect NO, we show that eNOS translocates with the Golgi apparatus to the immune synapse of T helper cells engaged with antigen-presenting cells (APC), where it was fully activated. Overexpression of eNOS prevented the central coalescence…

Interleukin 2CD3 ComplexNitric Oxide Synthase Type IIIT-LymphocytesImmunologyReceptors Antigen T-CellAntigen-Presenting CellsGolgi ApparatusBiologyLymphocyte ActivationNitric OxideNitric oxideImmunological synapseInterferon-gammaMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAntigenmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellAntigensMOLIMMUNOAntigen-presenting cellNitric Oxide Synthase Type IIIMice Mutant StrainsCell biologyInfectious DiseaseschemistryInterleukin-2CalciumSignal transductionSignal Transductionmedicine.drugImmunity
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Inhibition of FcεRI-mediated Activation of Rat Basophilic Leukemia Cells by Clostridium difficile Toxin B (Monoglucosyltransferase)

1996

Abstract Treatment of rat basophilic leukemia (RBL) 2H3-hm1 cells with Clostridium difficile toxin B (2 ng/ml), which reportedly depolymerizes the actin cytoskeleton, blocked [3H]serotonin release induced by 2,4-dinitrophenyl-bovine serum albumin, carbachol, mastoparan, and reduced ionophore A23187-stimulated degranulation by about 55-60%. In lysates of RBL cells, toxin B 14C-glucosylated two major and one minor protein. By using two-dimensional gel electrophoresis and immunoblotting, RhoA and Cdc42 were identified as protein substrates of toxin B. In contrast to toxin B, Clostridium botulinum transferase C3 that selectively inactivates RhoA by ADP-ribosylation did not inhibit degranulation…

SerotoninRHOABacterial ToxinsClostridium difficile toxin AWasp VenomsClostridium difficile toxin BBiologyCytoplasmic GranulesTritiummedicine.disease_causeBiochemistryCell LinePhosphatidylinositol 3-KinasesBacterial ProteinsTumor Cells CulturedmedicineAnimalsEnzyme InhibitorsMolecular BiologyCalcimycinAdenosine Diphosphate RiboseClostridioides difficileReceptors IgEToxinDegranulationSerum Albumin BovineCell BiologyActin cytoskeletonMolecular biologyRatsAndrostadienesKineticsPhosphotransferases (Alcohol Group Acceptor)Leukemia Basophilic AcuteBiochemistryGlucosyltransferasesMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsClostridium botulinumCarbacholCattle24-DinitrophenolPeptidesWortmanninDinitrophenolsJournal of Biological Chemistry
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Distinct Signaling Cascades of TREM-1, TLR and NLR in Neutrophils and Monocytic Cells

2013

Triggering receptor expressed on myeloid cells 1 (TREM-1) is an important mediator of innate inflammatory responses in microbial infections and sepsis. TREM-1 ligation on neutrophils (PMN) or monocytes results in the production of proinflammatory cytokines. Engagement of TREM-1 induces the activation of MAP kinases as well as rapid Ca<sup>2+</sup> mobilization. However, a detailed understanding of TREM-1 signaling pathways is currently lacking. We evaluated the TREM-1 signaling hierarchy in monocytic cells and found that the acute myeloid leukemia cell line MUTZ-3 expresses TREM-1 in a natural and functional manner. We compared essential signaling molecules of the TREM-1, TLR an…

Cell signalingMyeloidNeutrophilsp38 Mitogen-Activated Protein KinasesMonocytesProinflammatory cytokinePhosphatidylinositol 3-KinasesCell Line TumormedicineHumansImmunology and AllergyCalcium SignalingReceptors ImmunologicExtracellular Signal-Regulated MAP KinasesPI3K/AKT/mTOR pathwayCalcium signalingMembrane GlycoproteinsChemistryToll-Like ReceptorsMyeloid leukemiaImmunity InnateTriggering Receptor Expressed on Myeloid Cells-1Cell biologyLeukemia Myeloid Acutemedicine.anatomical_structureOrgan SpecificityCell cultureImmunologyCytokinesInflammation MediatorsSignal transductionResearch ArticleJournal of Innate Immunity
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Variation in genomic landscape of clear cell renal cell carcinoma across Europe

2014

The incidence of renal cell carcinoma (RCC) is increasing worldwide, and its prevalence is particularly high in some parts of Central Europe. Here we undertake whole-genome and transcriptome sequencing of clear cell RCC (ccRCC), the most common form of the disease, in patients from four different European countries with contrasting disease incidence to explore the underlying genomic architecture of RCC. Our findings support previous reports on frequent aberrations in the epigenetic machinery and PI3K/mTOR signalling, and uncover novel pathways and genes affected by recurrent mutations and abnormal transcriptome patterns including focal adhesion, components of extracellular matrix (ECM) and …

AdultMaleOncogene Proteins FusionRNA SplicingGeneral Physics and AstronomyBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCohort StudiesTranscriptomePhosphatidylinositol 3-KinasesMutation RatemedicineHumansEpigeneticsCarcinoma Renal CellAgedAged 80 and overGeneticsFocal AdhesionsMutationMultidisciplinaryGenome HumanGene Expression ProfilingGenetic VariationGenomicsSequence Analysis DNAGeneral ChemistryMiddle Agedmedicine.diseaseHuman genetics3. Good healthEuropeGene Expression Regulation NeoplasticGene expression profilingClear cell renal cell carcinomaMutationFemaleCarcinogenesisClear cellSignal TransductionNature Communications
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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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The dark side of the moon: The PI3K/PTEN/AKT pathway in colorectal carcinoma

2009

Wild-type KRAS status is required but not sufficient to confer sensitivity to anti-epidermal growth factor receptor (EGFR) monoclonal antibodies (mAbs) in colorectal cancer patients. As a consequence, one of the major challenges is to identify, in non-mutant KRAS patients, other markers that can predict lack of response to this therapy. Small series have investigated the clinical effect of PIK3CA mutations on resistance to anti-EGFR mAbs and discrepant results have been observed. Furthermore, PTEN loss in metastases may be predictive of resistance to anti-EGFR mAbs, even if PTEN determination is far from an immediate clinical application. The introduction of modulators of the PI3K/AKT/mTOR …

PTENCancer ResearchClass I Phosphatidylinositol 3-KinasesPrognosiSettore MED/06 - Oncologia MedicaColorectal cancerCetuximabColorectal NeoplasmPhosphoinositide 3-kinasemedicine.disease_causePhosphatidylinositol 3-KinasesAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineHumansPTENPanitumumabEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayClass I Phosphatidylinositol 3-KinaseAntineoplastic Combined Chemotherapy ProtocolbiologyCetuximabAKTMTORPanitumumabPTEN PhosphohydrolaseAntibodies MonoclonalGeneral MedicinePrognosismedicine.diseaseErbB ReceptorsOncologyMutationbiology.proteinCancer researchReceptor Epidermal Growth FactorKRASPhosphatidylinositol 3-KinaseColorectal NeoplasmsProto-Oncogene Proteins c-aktHumanSignal Transductionmedicine.drug
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