Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Synergistic Growth Inhibitory Activity of Combined Mek/Mtor Pathway Blockade in Pten-Null Cancers

2014

ABSTRACT Aim: We have recently shown that induction of PTEN expression plays an integral role in MEK inhibitors' antitumor activity. Here we hypothesize that PTEN status critically influences the functional outcome of combined MEK and PI3K/mTOR inhibition. Methods: Single and combined MEK (trametinib, T) and mTOR (everolimus, E) blockade were assessed in a panel of cancer cell lines and in patient-derived lung and colon cancer stem cells (L- or C-CSC). Pharmacologic interactions were analyzed by conservative isobologram analysis. PTEN role was assessed by shRNA-mediated silencing or overexpression by stable transfection. Treatment-induced changes in the phosphoproteome were analyzed by anti…

MEK/MTORMAPK/ERK pathwayTrametinibPhosphoinositide 3-kinasebiologyKinaseRPTORHematologyOncologySettore MED/04 - PATOLOGIA GENERALEbiology.proteinCancer researchPTENProtein kinase BPI3K/AKT/mTOR pathwayAnnals of Oncology
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A phosphorylation cycle shapes gradients of the DYRK family kinase Pom1 at the plasma membrane.

2011

http://linkinghub.elsevier.com/; International audience; Concentration gradients regulate many cell biological and developmental processes. In rod-shaped fission yeast cells, polar cortical gradients of the DYRK family kinase Pom1 couple cell length with mitotic commitment by inhibiting a mitotic inducer positioned at midcell. However, how Pom1 gradients are established is unknown. Here, we show that Tea4, which is normally deposited at cell tips by microtubules, is both necessary and, upon ectopic cortical localization, sufficient to recruit Pom1 to the cell cortex. Pom1 then moves laterally at the plasma membrane, which it binds through a basic region exhibiting direct lipid interaction. …

MESH : Molecular Sequence Data[SDV]Life Sciences [q-bio]CellMESH: Cell CycleMESH: Amino Acid SequenceAmino Acid Sequence; Cell Cycle; Cell Membrane/metabolism; Microtubule-Associated Proteins/metabolism; Molecular Sequence Data; Phosphorylation; Protein Kinases/chemistry; Protein Kinases/metabolism; Schizosaccharomyces/cytology; Schizosaccharomyces/metabolism; Schizosaccharomyces pombe Proteins/metabolism; Sequence AlignmentMESH : Phosphorylation0302 clinical medicinePhosphorylation0303 health sciencesKinaseMESH : Amino Acid SequenceMESH : Sequence AlignmentCell CycleCortical gradientMESH : Schizosaccharomyces pombe ProteinsFission yeastCell biologymedicine.anatomical_structureMESH: SchizosaccharomycesPom1PhosphorylationMicrotubule-Associated ProteinsMESH : Cell MembraneMolecular Sequence DataMESH: Sequence AlignmentMESH : Protein KinasesBiologyGeneral Biochemistry Genetics and Molecular BiologyPom1Dephosphorylation03 medical and health sciencesMicrotubuleMESH : Cell CycleSchizosaccharomycesCell cortexmedicineAmino Acid SequenceMitosisMESH: Protein Kinases030304 developmental biologyMESH: Molecular Sequence Data[ SDV ] Life Sciences [q-bio]Phosphorylation cycleMESH: PhosphorylationBiochemistry Genetics and Molecular Biology(all)Cell MembraneMESH: Schizosaccharomyces pombe ProteinsMESH: Microtubule-Associated ProteinsMESH : SchizosaccharomycesMESH : Microtubule-Associated ProteinsSchizosaccharomyces pombe ProteinsDYRK family kinaseProtein KinasesSequence Alignment030217 neurology & neurosurgeryMESH: Cell Membrane
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Use of CDC2 from etoposide-treated cells as substrate to assay CDC25 phosphatase activity

1999

International audience; Cyclin-dependent kinases (CDKs) regulate the key transition of the cell cycle in all organisms. In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Here we report that upon Etoposide treatment CDC2 is phosphorylated on tyrosine 15 and is dephosphorylated and activated in vitro by recombinant CDC25 phosphatase. We also show that inactive CDC2 kinase from Etoposide-treated cells can be used as a substrate in a sensitive two-step assay of CDC25 phosphatase. This assay, which is very simple to set-up, is based on the monitoring of CDC2 kinase activity after CDC25-depe…

MESH: HumansMESH: Phosphorylation[SDV]Life Sciences [q-bio]Cell Cycle Proteins[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]MESH: CDC2 Protein KinaseMESH: Tyrosine[SDV] Life Sciences [q-bio]AGENT ANTITUMORALenzymes and coenzymes (carbohydrates)MESH: Cell Cycle ProteinsMESH: cdc25 PhosphatasesCDC2 Protein KinaseMESH: HeLa CellsMESH: Phosphoprotein PhosphatasesPhosphoprotein PhosphatasesHumansTyrosinecdc25 PhosphatasesPhosphorylationbiological phenomena cell phenomena and immunityEtoposideHeLa CellsMESH: Etoposide
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Apelin treatment increases complete Fatty Acid oxidation, mitochondrial oxidative capacity, and biogenesis in muscle of insulin-resistant mice.

2012

Both acute and chronic apelin treatment have been shown to improve insulin sensitivity in mice. However, the effects of apelin on fatty acid oxidation (FAO) during obesity-related insulin resistance have not yet been addressed. Thus, the aim of the current study was to determine the impact of chronic treatment on lipid use, especially in skeletal muscles. High-fat diet (HFD)-induced obese and insulin-resistant mice treated by an apelin injection (0.1 μmol/kg/day i.p.) during 4 weeks had decreased fat mass, glycemia, and plasma levels of triglycerides and were protected from hyperinsulinemia compared with HFD PBS-treated mice. Indirect calorimetry experiments showed that apelin-treated mice…

MESH: Oxidation-Reduction[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionEndocrinology Diabetes and MetabolismGlucose uptakeAMP-Activated Protein KinasesInbred C57BLMice0302 clinical medicineAMP-activated protein kinaseMESH : Lipid MetabolismHyperinsulinemiaMESH: AnimalsMESH: AMP-Activated Protein KinasesMESH : Muscle SkeletalMESH : Fatty AcidsBeta oxidationMESH: Lipid Metabolism0303 health sciencesMESH: Muscle SkeletalbiologyMESH : Diet High-FatFatty AcidsMESH: Energy MetabolismMESH : AMP-Activated Protein KinasesMESH: Mitochondria MuscleSkeletal3. Good healthApelinMitochondriaMESH: Fatty AcidsMESH : Cyclic AMP-Dependent Protein KinasesMESH: Insulin ResistanceAlimentation et NutritionApelinIntercellular Signaling Peptides and ProteinsMuscleMESH : Insulin ResistanceOxidation-Reductionmedicine.medical_specialtyMESH : Mitochondria Muscle030209 endocrinology & metabolismMESH : Mice Inbred C57BLMESH: Cyclic AMP-Dependent Protein KinasesDiet High-Fat03 medical and health sciencesInsulin resistanceAdipokinesMESH: Mice Inbred C57BLInternal medicineMESH : MiceInternal MedicinemedicineFood and NutritionAnimalsMuscle SkeletalMESH: Intercellular Signaling Peptides and ProteinsMESH: MiceMESH : Intercellular Signaling Peptides and Proteins030304 developmental biologyMESH : Oxidation-ReductionAMPKmedicine.diseaseLipid MetabolismCyclic AMP-Dependent Protein KinasesMitochondria MuscleDietMice Inbred C57BLMESH : Energy Metabolism[SDV.AEN] Life Sciences [q-bio]/Food and NutritionAMP-Activated Protein Kinases;Animals;Cyclic AMP-Dependent Protein Kinases;Diet;High-Fat;Energy Metabolism;Fatty Acids;Insulin Resistance;Intercellular Signaling Peptides and Proteins;Lipid Metabolism;Mice;Inbred C57BL;Mitochondria;Muscle;Skeletal;Oxidation-ReductionHigh-FatMESH: Diet High-FatMetabolismEndocrinologyMitochondrial biogenesisbiology.proteinMESH : AnimalsInsulin ResistanceEnergy Metabolism[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
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Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
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Histidine kinases mediate differentiation, stress response, and pathogenicity in Magnaporthe oryzae.

2014

The aim of this study is a functional characterization of 10 putative histidine kinases (HIKs)-encoding genes in the phytopathogenic fungus Magnaporthe oryzae. Two HIKs were found to be required for pathogenicity in the fungus. It was found that the mutant strains ΔMohik5 and ΔMohik8 show abnormal conidial morphology and furthermore ΔMohik5 is unable to form appressoria. Both HIKs MoHik5p and MoHik8p appear to be essential for pathogenicity since the mutants fail to infect rice plants. MoSln1p and MoHik1p were previously reported to be components of the HOG pathway in M. oryzae. The ΔMosln1 mutant is more susceptible to salt stress compared to ΔMohik1, whereas ΔMohik1 appears to be stronger…

MagnaportheHistidine KinaseMutantVirulenceconidiaBiologyMicrobiologyMicrobiologyFungal Proteinshypoxia signalingGene Expression Regulation FungalpathogenicityAppressoriaPlant DiseasesOriginal ResearchAppressoriumFungal proteinVirulenceHistidine kinaseHOG pathwayOryzadifferentiationMagnaporthe oryzaeSpores Fungalbiology.organism_classificationYeastMagnaportheMultigene FamilyPhosphorylationProtein KinasesMicrobiologyOpen
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The nucleotide excision repair protein XPC is essential for bulky DNA adducts to promote interleukin-6 expression via the activation of p38-SAPK

2016

Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants, and many are potent carcinogens. Benzo[a]pyrene (B[a]P), one of the best-studied PAHs, is metabolized ultimately to the genotoxin anti-B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE). BPDE triggers stress responses linked to gene expression, cell death and survival. So far, the underlying mechanisms that initiate these signal transduction cascades are unknown. Here we show that BPDE-induced DNA damage is recognized by DNA damage sensor proteins to induce activation of the stress-activated protein kinase (SAPK) p38. Surprisingly, the classical DNA damage response, which involves the kinases ATM and ATR, is not involved in p38-SA…

Male0301 basic medicineCancer ResearchDNA RepairCarcinogenesisDNA damagep38 mitogen-activated protein kinases78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyReal-Time Polymerase Chain ReactionTransfectionp38 Mitogen-Activated Protein KinasesDNA AdductsMice03 medical and health scienceschemistry.chemical_compoundGeneticsmedicinepolycyclic compoundsAnimalsHumansRNA Small InterferingMolecular BiologyCarcinogenMice KnockoutCisplatinInterleukin-6KinaseFibroblastsCell biologyDNA-Binding ProteinsMice Inbred C57BL030104 developmental biologychemistryCarcinogensNIH 3T3 CellsCancer researchComet AssaySignal transductionDNADNA DamageHeLa CellsMutagensSignal Transductionmedicine.drugNucleotide excision repairOncogene
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Serine/threonine-kinase 33 (Stk33) – Component of the neuroendocrine network?

2016

The present study was conducted to investigate the expression of serine/threonine-kinase 33 (Stk33) in neuronal structures of the central nervous system in rat and hamster as well as the presence of the protein in the brain of higher mammals, using a polyclonal antibody on cryosections of fixed brains. We found a distinct immunostaining pattern that included intense fluorescence of the ependymal lining of cerebral ventricles, and of hypothalamic tanycytes and their processes. We further observed intense staining of magnocellular neurons in the hypothalamic paraventricular, supraoptic and accessory neurosecretory nuclei, in particular the circular nuclei, and less intense stained neurons in …

Male0301 basic medicineEpendymal CellBlotting WesternCentral nervous systemProtein Serine-Threonine KinasesBiologyRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCricetinaemedicineAnimalsHumansMolecular BiologyAgedNeuronsSerine/threonine-specific protein kinaseMice Inbred BALB CGeneral NeuroscienceTupaiidaeBrainColocalizationHuman brainImmunohistochemistryNeurosecretory SystemsCell biology030104 developmental biologymedicine.anatomical_structurenervous systemHypothalamusMagnocellular cellFemaleNeurology (clinical)Neuroscience030217 neurology & neurosurgeryImmunostainingPapioDevelopmental BiologyBrain Research
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Fibroblast Growth Factor 21 (FGF21) Protects against High Fat Diet Induced Inflammation and Islet Hyperplasia in Pancreas

2015

Fibroblast growth factor 21 (FGF21) is an important endocrine metabolic regulator expressed in multiple tissues including liver and adipose tissue. Although highest levels of expression are in pancreas, little is known about the function of FGF21 in this tissue. In order to understand the physiology of FGF21 in the pancreas, we analyzed its expression and regulation in both acinar and islet tissues. We found that acinar tissue express 20-fold higher levels than that observed in islets. We also observed that pancreatic FGF21 is nutritionally regulated; a marked reduction in FGF21 expression was noted with fasting while obesity is associated with 3–4 fold higher expression. Acinar and islet c…

Male0301 basic medicineFGF21Fibroblast Growth FactorPhysiologyReceptors Antigen T-Cell alpha-betaPeptide Hormoneslcsh:MedicineAdipose tissueAcinar CellsPathology and Laboratory MedicineBiochemistryFatsMiceEndocrinologyMedicine and Health SciencesInsulinlcsh:ScienceImmune ResponseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Multidisciplinarygeography.geographical_feature_categoryFOXP3Forkhead Transcription FactorsFastingHyperplasiaIsletLipidsmedicine.anatomical_structurePhysiological ParametersOrgan SpecificityTumor necrosis factor alphaAnatomymedicine.symptomPancreasSignal TransductionResearch Articlemedicine.medical_specialtyImmunologyEndocrine SystemInflammationBiologyDiet High-FatInterferon-gammaIslets of Langerhans03 medical and health sciencesExocrine GlandsSigns and SymptomsGrowth FactorsInternal medicinemedicineAnimalsObesityPancreasNutritionInflammationDiabetic EndocrinologygeographyHyperplasiaEndocrine PhysiologyTumor Necrosis Factor-alphaBody Weightlcsh:RBiology and Life SciencesGlucagonmedicine.diseaseDietary FatsHormonesDietFibroblast Growth FactorsMice Inbred C57BL030104 developmental biologyEndocrinologyGene Expression RegulationPancreatitisThy-1 Antigenslcsh:QPLOS ONE
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Muscle follistatin gene delivery increases muscle protein synthesis independent of periodical physical inactivity and fasting

2020

Blocking of myostatin and activins effectively counteracts muscle atrophy. However, the potential interaction with physical inactivity and fasting in the regulation of muscle protein synthesis is poorly understood. We used blockade of myostatin and activins by recombinant adeno-associated virus (rAAV)-mediated follistatin (FS288) overexpression in mouse tibialis anterior muscle. To investigate the effects on muscle protein synthesis, muscles were collected 7 days after rAAV-injection in the nighttime or in the daytime representing high and low levels of activity and feeding, respectively, or after overnight fasting, refeeding, or ad libitum feeding. Muscle protein synthesis was increased by…

Male0301 basic medicineFollistatinMuscle Proteinsphysical activitylihaksetMyostatinBiochemistryMice0302 clinical medicineTibialis anterior musclemedia_common2. Zero hungerbiologyChemistryactivinsFastingDependovirusMuscle atrophyCircadian RhythmMuscular Atrophymyostatinmedicine.symptomfyysinen aktiivisuusBiotechnologymedicine.medical_specialtyfastingmedia_common.quotation_subjectMechanistic Target of Rapamycin Complex 1Gene delivery03 medical and health sciencesPhysical Conditioning AnimalInternal medicineGeneticsmedicineAnimalsMolecular BiologypaastoPI3K/AKT/mTOR pathwaysolufysiologiaSarcolemmaJNK Mitogen-Activated Protein Kinasesmechanistic target of rapamycin proteinAppetiteGenetic TherapyMice Inbred C57BL030104 developmental biologyEndocrinologybiology.protein1182 Biochemistry cell and molecular biology3111 BiomedicineproteiinitEnergy Metabolismlihassurkastumasairaudet030217 neurology & neurosurgeryFollistatin
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