Search results for "PROTEIN KINASES"

showing 10 items of 427 documents

EFFECT OF THE IMPase INHIBITOR L690,330 ON SEA URCHIN DEVELOPMENT

1998

Abstract A variety of concentrations of the IMPase inhibitor L690,330 were added to sea urchin embryos. Immediate arrest of development was obtained for concentrations from 7.5 m m on. Concentrations lower than 3.5 m m permitted gastrulation but inhibited skeletogenesis and disturbed elongation along the animal–vegetal axis. The latter results are similar to those obtained by counteracting lithium effect with myoinositol, which are suggested to be due to partial relief of IMPase inhibition.

Embryo NonmammalianSea UrchinCalcium-Calmodulin-Dependent Protein KinaseLithiumMorulaGlycogen Synthase Kinase 3biology.animalMorphogenesisEnzyme InhibitorMorphogenesiAnimalsIMPaseEnzyme InhibitorsSea urchin embryo5'-NucleotidaseSea urchinDiphosphonatesbiologyAnimalAbnormalities Drug-InducedCell BiologyGeneral MedicineAnatomySea urchin embryoCell biologyGastrulationDiphosphonateSea UrchinsCalcium-Calmodulin-Dependent Protein KinasesElongationLithium ChlorideInositolCell Biology International
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Early asymmetric cues triggering the dorsal/ventral gene regulatory network of the sea urchin embryo

2014

Dorsal/ventral (DV) patterning of the sea urchin embryo relies on a ventrally-localized organizer expressing Nodal, a pivotal regulator of the DV gene regulatory network. However, the inceptive mechanisms imposing the symmetry-breaking are incompletely understood. In Paracentrotus lividus, the Hbox12 homeodomain-containing repressor is expressed by prospective dorsal cells, spatially facing and preceding the onset of nodal transcription. We report that Hbox12 misexpression provokes DV abnormalities, attenuating nodal and nodal-dependent transcription. Reciprocally, impairing hbox12 function disrupts DV polarity by allowing ectopic expression of nodal. Clonal loss-of-function, inflicted by b…

Embryo NonmammalianTranscription GeneticEctodermp38 Mitogen-Activated Protein Kinasessymmetry breakingdorsal ventral axis sea urchin embryo nodal homeodomain repressor p38 MAPKAnimals Genetically ModifiedCell polarityMorphogenesisGene Regulatory NetworksBiology (General)ZebrafishSea urchinsea urchin embryoGeneticsbiologyGeneral NeuroscienceQRdorsal/ventral polarityCell PolarityGene Expression Regulation DevelopmentalEmbryoGeneral MedicineCell biologymedicine.anatomical_structureGene Knockdown Techniquesembryonic structuresParacentrotusMedicineCuesResearch Articleanimal structuresQH301-705.5Nodal ProteinScienceEmbryonic DevelopmentSettore BIO/11 - Biologia Molecolarep38 MAPKModels BiologicalGeneral Biochemistry Genetics and Molecular Biologybiology.animalEctodermmedicineAnimalsBody PatterningHomeodomain ProteinsGeneral Immunology and MicrobiologyotherCell Biologybiology.organism_classificationEmbryonic stem cellhomeodomain repressorRepressor ProteinsDevelopmental Biology and Stem CellsnodalNODALDevelopmental biologyeLife
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The p21-activated kinase Mbt is a component of the apical protein complex in central brain neuroblasts and controls cell proliferation

2013

The final size of the central nervous system is determined by precisely controlled generation, proliferation and death of neural stem cells. We show here that the Drosophila PAK protein Mushroom bodies tiny (Mbt) is expressed in central brain progenitor cells (neuroblasts) and becomes enriched to the apical cortex of neuroblasts in a cell cycle- and Cdc42-dependent manner. Using mushroom body neuroblasts as a model system, we demonstrate that in the absence of Mbt function, neuroblasts and their progeny are correctly specified and are able to generate different neuron subclasses as in the wild type, but are impaired in their proliferation activity throughout development. In general, loss of…

Embryo Nonmammaliananimal structuresMitosisApoptosisCell CountSpindle ApparatusBiologyNeural Stem CellsNeuroblastGTP-Binding ProteinsTubulinCell polarityAnimalsDrosophila ProteinsProgenitor cellMolecular BiologyMitosisCell ProliferationCell SizeBinding SitesApical cortexAsymmetric Cell DivisionfungiBrainCell PolarityGene Expression Regulation DevelopmentalNeural stem cellCell biologyEnzyme ActivationActin CytoskeletonPhenotypenervous systemLarvaMultiprotein Complexesembryonic structuresMushroom bodiesDrosophilaProtein KinasesGanglion mother cellDevelopmental BiologyDevelopment
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Adverse events associated with encorafenib plus binimetinib in the COLUMBUS study: incidence, course and management.

2019

Abstract Background Dual inhibition of the mitogen-activated protein kinase pathway with BRAF/MEK inhibitor (BRAFi/MEKi) therapy is a standard treatment for BRAFV600-mutant metastatic melanoma and has historically been associated with grade III pyrexia or photosensitivity depending on the combination used. The objective of this study was to fully describe adverse events from the COLUMBUS study evaluating the most recent BRAF/MEK inhibitor combination encorafenib+binimetinib. Patients and methods Patients with locally advanced, unresectable or metastatic BRAFV600-mutant melanoma were randomised to receive encorafenib 450 mg once daily plus binimetinib 45 mg twice daily, encorafenib 300 mg on…

Encorafenib0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBinimetinib; Encorafenib; Melanoma; Safety; Vemurafenib;MedizinBinimetinibchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy Protocols1306 Cancer ResearchVemurafenibMelanomaFatigueeducation.field_of_studySulfonamidesMEK inhibitorMelanomaStandard treatmentIncidence10177 Dermatology ClinicBinimetinibNauseaMiddle AgedOncology030220 oncology & carcinogenesis2730 OncologyFemaleSafetyMitogen-Activated Protein Kinasesmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomitingPopulation610 Medicine & health03 medical and health sciencesInternal medicinemedicineHumanseducationAdverse effectProtein Kinase Inhibitorsbusiness.industrymedicine.diseaseDiscontinuation030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesbusinessEuropean journal of cancer (Oxford, England : 1990)
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Gcn5p is involved in the acetylation of histone H3 in nucleosomes.

1997

Abstract Enzymatic extracts from a gcn5 mutant and wild-type strains of Saccharomyces cerevisiae were chromatographically fractionated and the histone acetyltransferase activities compared. When free histones were used as substrate, extracts from wild-type cells showed two peaks of activity on histone H3 but extracts from gcn5 mutant cells showed only one. With nucleosomes as substrate, the histone acetyltransferase activities present in extracts from the gcn5 mutant strain were not able to modify H3 whereas wild-type cell extracts acetylated intensely this histone. The activity that acetylated nucleosome-bound H3 behaved as a 170-kDa complex. We suggest that Gcn5p represents a catalytic su…

ErythrocytesSaccharomyces cerevisiae ProteinsBiophysicsSaccharomyces cerevisiaeBiochemistryFungal ProteinsHistonesHistone H3Histone H1Structural BiologyHistone H2AHistone methylationGeneticsHistone codeAnimalsHistone octamerMolecular BiologyHistone AcetyltransferasesHistone acetyltransferase GCN5biologyAcetylationCell BiologyHistone acetyltransferaseChromatinNucleosomesDNA-Binding ProteinsMolecular WeightBiochemistryNucleosomeHistone methyltransferasebiology.proteinChickensProtein KinasesFEBS letters
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Oligomeric Sensor Kinase DcuS in the Membrane of Escherichia coli and in Proteoliposomes: Chemical Cross-linking and FRET Spectroscopy

2010

The DcuSR (dicarboxylate uptake sensor and regulator) system of Escherichia coli is a typical two-component system consisting of a membranous sensor kinase (DcuS) and a cytoplasmic response regulator (DcuR) (11, 26, 48). DcuS responds to C4-dicarboxylates like fumarate, malate, or succinate (19). In the presence of the C4-dicarboxlates, the expression of the genes of anaerobic fumarate respiration (dcuB, fumB, and frdABCD) and of aerobic C4-dicarboxylate uptake (dctA) is activated. DcuS is a histidine protein kinase composed of two transmembrane helices with an intermittent sensory PAS domain in the periplasm (PASP) that was also termed the PDC domain (for PhoQ/DcuS/DctB/CitA domain or fold…

Escherichia coli ProteinsProteolipidsCell MembraneGreen Fluorescent ProteinsHistidine kinaseAutophosphorylationBiologyMicrobiologyLuminescent ProteinsResponse regulatorTransmembrane domainSpectrometry FluorescenceProtein kinase domainBiochemistryPAS domainEscherichia coliFluorescence Resonance Energy TransferKinase activityProtein kinase AProtein KinasesMolecular BiologySignal TransductionJournal of Bacteriology
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Influence ofKi-ras-driven oncogenic transformation on the protein network of murine fibroblasts

2007

Ki-ras gene mutations that specifically occur in codons 12, 13 and 61 are involved in the carcinogenesis of acute myeloid leukemia, melanoma and different carcinomas. In order to define potential mutation-specific therapeutic targets, stable transfectants of NIH3T3 cells carrying different Ki-ras4B gene mutations were generated. Wild type Ki-ras transformants, mock transfectants and parental cells served as controls. These in vitro model systems were systematically analyzed for their protein expression pattern using two-dimensional gel electrophoresis followed by mass spectrometry and/or protein sequencing. Using this approach, a number of target molecules that are differentially but coordi…

Gel electrophoresismedicine.diagnostic_testWild typeFibroblastsBiologyGene mutationTransfectionmedicine.disease_causeProteomicsBiochemistryMolecular biologyMiceCell Transformation NeoplasticWestern blotHeat shock proteinNIH 3T3 Cellsras ProteinsmedicineAnimalsMitogen-Activated Protein KinasesCarcinogenesisMolecular BiologyGeneSignal TransductionPROTEOMICS
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Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice

2002

The serine-threonine kinase Akt seems to be central in mediating stimuli from different classes of receptors. In fact, both IGF-1 and IL6-like cytokines induce hypertrophic and antiapoptotic signals in cardiomyocytes through PI3K-dependent Akt activation. More recently, it was shown that Akt is involved also in the hypertrophic and antiapoptotic effects of β-adrenergic stimulation. Thus, to determine the effects of Akt on cardiac function in vivo, we generated a model of cardiac-specific Akt overexpression in mice. Transgenic mice were generated by using the E40K, constitutively active mutant of Akt linked to the rat α-myosin heavy chain promoter. The effects of cardiac-selective Akt overex…

Gene ExpressionTransgenicGlycogen Synthase Kinase 3MiceGSK-3Receptorsgenetics/physiologycytology/metabolismMultidisciplinaryBiological SciencesProtein-Serine-Threonine KinasesDNA-Binding Proteinsenzymology/genetics/pathologyAdrenergicPhosphorylationSignal transductionMitogen-Activated Protein KinasesSignal Transductionmedicine.medical_specialtyCardiomyopathyAnimals; Calcium-Calmodulin-Dependent Protein Kinases; metabolism; Cardiomyopathy; Hypertrophic; enzymology/genetics/pathology; Cell Size; physiology; DNA-Binding Proteins; GATA4 Transcription Factor; Gene Expression; Glycogen Synthase Kinase 3; Mice; Transgenic; Mitogen-Activated Protein Kinases; Myocardial Contraction; Myocardium; cytology/metabolism; Point Mutation; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins; genetics/physiology; Rats; Receptors; Adrenergic; beta; Signal Transduction; Transcription FactorsMice TransgenicBiologyProtein Serine-Threonine KinasesContractilityIn vivoInternal medicineProto-Oncogene ProteinsReceptors Adrenergic betamedicineAnimalsPoint MutationGlycogen synthaseProtein kinase BPI3K/AKT/mTOR pathwayCell SizeMyocardiumCardiomyopathy HypertrophicMyocardial ContractionGATA4 Transcription FactorRatsEndocrinologyHypertrophicphysiologyCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinbetametabolismProto-Oncogene Proteins c-aktTranscription Factors
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Role of Gadd45a in Wip1-dependent regulation of intestinal tumorigenesis.

2012

Conversion of intestinal stem cells into tumor-initiating cells is an early step in Apc(Min)-induced polyposis. Wild-type p53-induced phosphatase 1 (Wip1)-dependent activation of a DNA damage response and p53 has a permanent role in suppression of stem cell conversion, and deletion of Wip1 lowers the tumor burden in Apc(Min) mice. Here we show that cyclin-dependent kinase inhibitor 2a, checkpoint kinase 2, and growth arrest and DNA damage gene 45a (Gadd45a) exert critical functions in the tumor-resistant phenotype of Wip1-deficient mice. We further identified Gadd45a as a haploinsufficient gene in the regulation of Wip1-dependent tumor resistance in mice. Gadd45a appears to function through…

Genes APCDNA RepairDNA repairDNA damageApoptosisCell Cycle ProteinsBiologyProtein Serine-Threonine KinasesReceptors G-Protein-CoupledMicePhosphoprotein PhosphatasesGene silencingAnimalsMolecular BiologyCheckpoint Kinase 2Cyclin-Dependent Kinase Inhibitor p16beta CateninMice KnockoutOriginal PaperKinaseIntestinal PolyposisStem CellsJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyCell biologyProtein Phosphatase 2CCheckpoint Kinase 2Cell Transformation NeoplasticCancer researchSignal transductionStem cellTumor Suppressor Protein p53GADD45ASignal TransductionCell death and differentiation
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Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
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