Search results for "Mitogen-Activated Protein Kinase Kinases"

showing 10 items of 27 documents

AM fungal exudates activate MAP kinases in plant cells in dependence from cytosolic Ca2+ increase

2011

International audience; The molecular dialogue occurring prior to direct contact between the fungal and plant partners of arbuscular-mycorrhizal (AM) symbioses begins with the release of fungal elicitors, so far only partially identified chemically, which can activate specific signaling pathways in the host plant. We show here that the activation of MAPK is also induced by exudates of germinating spores of Gigaspora margarita in cultured cells of the non-leguminous species tobacco (Nicotiana tabacum), as well as in those of the model legume Lotus japonicus. MAPK activity peaked about 15 min after the exposure of the host cells to the fungal exudates (FE). FE were also responsible for a rapi…

0106 biological sciencesMAPK/ERK pathwayTime FactorsMAP Kinase Signaling SystemPhysiologyNicotiana tabacumLotus japonicusPlant ScienceComplex MixturesBiology01 natural sciences03 medical and health sciencesPlant CellsTobaccoBotanyGenetics[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyGlomeromycotaSymbiosisNicotiana plumbaginifoliaPlant Proteins030304 developmental biologyMitogen-Activated Protein Kinase Kinasesarbuscular-mycorrhizal fungi0303 health sciencesdiffusible factorcalciumKinasefungiArbuscular-mycorrhizal fungi; Signaling; Diffusible factor; MAPK; Calciumfood and beveragesSpores FungalPlant cellbiology.organism_classificationMAPKsym pathwayCell biologyCytosolCell cultureLotus[SDE.BE]Environmental Sciences/Biodiversity and Ecologysignaling010606 plant biology & botanyPlant Physiology and Biochemistry
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Cytosolic calcium rises and related events in ergosterol-treated Nicotiana cells

2011

International audience; The typical fungal membrane component ergosterol was previously shown to trigger defence responses and protect plants against pathogens. Most of the elicitors mobilize the second messenger calcium, to trigger plant defences. We checked the involvement of calcium in response to ergosterol using Nicotiana plumbaginifolia and Nicotiana tabacum cv Xanthi cells expressing apoaequorin in the cytosol. First, it was verified if ergosterol was efficient in these cells inducing modifications of proton fluxes and increased expression of defence-related genes. Then, it was shown that ergosterol induced a rapid and transient biphasic increase of free [Ca2þ]cyt which intensity dep…

0106 biological sciencesTime FactorsPhysiologyNicotiana tabacumPlant SciencesterolsSecond Messenger Systemstobacco01 natural scienceschemistry.chemical_compoundCytosolpolycyclic compoundsPhosphorylationCalcium signalingreactive oxygen species0303 health sciencesErgosterolelicitorbiologyergosterolHydrogen-Ion ConcentrationPlants Genetically ModifiedRecombinant ProteinsCell biologyBiochemistrySecond messenger systemReactive oxygen species; Calcium signature; Elicitor; Signal transduction; MAPKs; tobaccolipids (amino acids peptides and proteins)Protonssignal transductionCell Survivalnicotiana plumbaginifoliachemistry.chemical_elementnicotiana tabacumoxydantCalciumcalcium signature03 medical and health sciencesAequorinMAPKsBAPTAGenetics[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyCalcium Signaling030304 developmental biologyMitogen-Activated Protein Kinase KinasesCalcium metabolismHydrogen Peroxidebiochemical phenomena metabolism and nutritionbiology.organism_classificationCytosolchemistryCalciumApoproteins010606 plant biology & botany
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Noncanonical GLI1 signaling promotes stemness features and in vivo growth in lung adenocarcinoma

2016

Aberrant Hedgehog/GLI signaling has been implicated in a diverse spectrum of human cancers, but its role in lung adenocarcinoma (LAC) is still under debate. We show that the downstream effector of the Hedgehog pathway, GLI1, is expressed in 76% of LACs, but in roughly half of these tumors, the canonical pathway activator, Smoothened, is expressed at low levels, possibly owing to epigenetic silencing. In LAC cells including the cancer stem cell compartment, we show that GLI1 is activated noncanonically by MAPK/ERK signaling. Different mechanisms can trigger the MAPK/ERK/GLI1 cascade including KRAS mutation and stimulation of NRP2 by VEGF produced by the cancer cells themselves in an autocrin…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsPyridinesPyridineMitogen-Activated Protein Kinase KinaseMice SCIDMiceCarcinoma Non-Small-Cell LungRNA Small InterferingNon-Small-Cell LungMolecular Biology; Genetics; Cancer ResearchTumorbiologyintegumentary systemHedgehog signaling pathwayCell biologyNeoplastic Stem CellsFemaleRNA InterferenceOriginal ArticleHumanXenograft Model Antitumor AssayAdenocarcinomaSCIDSmall InterferingZinc Finger Protein GLI1Cell LineProto-Oncogene Proteins p21(ras)Adenocarcinoma; Animals; Carcinoma Non-Small-Cell Lung; Cell Line Tumor; Female; Humans; Lung Neoplasms; Mice; Mice SCID; Mitogen-Activated Protein Kinase Kinases; Neoplastic Stem Cells; Neuropilin-2; Proto-Oncogene Proteins p21(ras); Pyridines; Pyrimidines; RNA Interference; RNA Small Interfering; Xenograft Model Antitumor Assays; Zinc Finger Protein GLI1; Molecular Biology; Genetics; Cancer Research03 medical and health sciencesParacrine signallingGeneticSettore MED/04 - PATOLOGIA GENERALEstem cellsCancer stem cellGLI1Cell Line TumorGeneticsAnimalsHumansAutocrine signallingMolecular BiologyMitogen-Activated Protein Kinase KinasesSettore MED/06 - ONCOLOGIA MEDICAAnimalCarcinomaXenograft Model Antitumor AssaysNeuropilin-2Lung Neoplasmlung cancer030104 developmental biologyPyrimidinesPyrimidineCancer cellbiology.proteinRNANeoplastic Stem CellSmoothened
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PI3K-driven HER2 expression is a potential therapeutic target in colorectal cancer stem cells

2020

ObjectiveCancer stem cells are responsible for tumour spreading and relapse. Human epidermal growth factor receptor 2 (HER2) expression is a negative prognostic factor in colorectal cancer (CRC) and a potential target in tumours carrying the gene amplification. Our aim was to define the expression of HER2 in colorectal cancer stem cells (CR-CSCs) and its possible role as therapeutic target in CRC resistant to anti- epidermal growth factor receptor (EGFR) therapy.DesignA collection of primary sphere cell cultures obtained from 60 CRC specimens was used to generate CR-CSC mouse avatars to preclinically validate therapeutic options. We also made use of the ChIP-seq analysis for transcriptional…

0301 basic medicineReceptor ErbB-2Colorectal cancerCetuximabcolorectal cancermedicine.disease_cause03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellstem cellsTumor Cells CulturedmedicineAdjuvant therapyAnimalsHumansEpidermal growth factor receptorProtein kinase BPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase Kinasesdrug resistancebiologybusiness.industryGastroenterologyTrastuzumabmedicine.diseaseantibody targeted therapy030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisNeoplastic Stem CellsCancer researchbiology.proteinKRASPhosphatidylinositol 3-KinaseStem cellColorectal Neoplasmsbusiness
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A role for the MAP kinase gene MKC1 in cell wall construction and morphological transitions in Candida albicans.

1998

The Candida albicans MKC1 gene encodes a mitogen-activated protein (MAP) kinase, which has been cloned by complementation of the lytic phenotype associated with Saccharomyces cerevisiae slt2 (mpk1) mutants. In this work, the physiological role of this MAP kinase in the pathogenic fungus C. albicans was characterized and a role for MKC1 in the biogenesis of the cell wall suggested based on the following criteria. First, C. albicans mkc1Δ/mkc1Δ strains displayed alterations in their cell surfaces under specific conditions as evidenced by scanning electron microscopy. Second, an increase in specific cell wall epitopes (O-glycosylated mannoprotein) was shown by confocal microscopy in mkc1Δ/mkc1…

Antifungal AgentsTranscription GeneticSaccharomyces cerevisiaeMutantMAP Kinase Kinase 2MAP Kinase Kinase 1ChitinSaccharomyces cerevisiaeProtein Serine-Threonine KinasesMicrobiologyGene Expression Regulation EnzymologicFungal ProteinsPseudohyphal growthCell WallGene Expression Regulation FungalCandida albicansCandida albicansDNA FungalFluorescent Antibody Technique IndirectGlucansProtein Kinase CMitogen-Activated Protein Kinase KinasesRecombination GeneticMembrane GlycoproteinsMicroscopy ConfocalbiologyKinaseProtein-Tyrosine Kinasesbiology.organism_classificationFlow Cytometrybeta-GalactosidaseCorpus albicansComplementationMicroscopy ElectronBiochemistryMitogen-activated protein kinaseCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMicroscopy Electron ScanningMitogen-Activated Protein KinasesPlasmidsMicrobiology (Reading, England)
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Reciprocal regulation of human platelet function by endogenous prostanoids and through multiple prostanoid receptors

2014

Platelets are permanently exposed to a variety of prostanoids formed by blood cells or the vessel wall. The two major prostanoids, prostacyclin and thromboxane act through well established pathways mediated by their respective G-protein coupled receptors inhibiting or promoting platelet aggregation accordingly. Yet the role of other prostanoids and prostanoid receptors for platelet function regulation has not been thoroughly investigated. We aimed at a comprehensive analysis of prostanoid effects on platelets, the receptors and pathways involved and functional consequences. We analyzed cAMP formation and phosphorylation of proteins pivotal to platelet function as well as functional platelet…

Blood PlateletsSerotoninmedicine.medical_specialtyPlatelet AggregationProstaglandin E2 receptorReceptors ProstaglandinProstaglandinProstacyclinchemistry.chemical_compoundAdenosine TriphosphateP2Y12Internal medicineCyclic AMPmedicineHumansPlateletPlatelet activationReceptorMitogen-Activated Protein Kinase KinasesPharmacologyChemistryMicrofilament Proteinsrap1 GTP-Binding ProteinsProstanoidrespiratory systemPhosphoproteinsCell biologyAdenosine DiphosphateP-SelectinEndocrinologyProstaglandinscardiovascular systemCalciumlipids (amino acids peptides and proteins)Cell Adhesion Moleculesmedicine.drugEuropean Journal of Pharmacology
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Cardiotoxicity mechanisms of the combination of BRAF-inhibitors and MEK-inhibitors.

2018

Many new drugs have appeared in last years in the oncological treatment scenario. Each drug carries an important set of adverse events, not less, cardiovascular adverse events. This aspect is even more important considering the increasing use of combination therapies with two drugs, or three drugs as in some ongoing clinical trials. Besides it represents a growing problem for Cardiologists, that face it in every day clinical practice and that will face it probably more and more in the coming years. This work reviews the mechanism of action of BRAF-inhibitors and MEK-inhibitors used together, the pathophysiological mechanisms that lead to cardiovascular toxicity. Particularly, it focuses on …

DrugCardiovascular toxicityBRAF inhibitorProto-Oncogene Proteins B-rafmedicine.medical_specialtyCombination therapySettore MED/06 - Oncologia Medicamedia_common.quotation_subjectDecreased ejection fraction030204 cardiovascular system & hematologyCardiovascular System03 medical and health sciences0302 clinical medicineCardiovascular toxicityAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansPharmacology (medical)Intensive care medicineAdverse effectBRAF inhibitor; Cardio-oncology; Cardiovascular toxicity; Decreased ejection fraction; Hypertension; MEK inhibitor; Pharmacology; Pharmacology (medical)MelanomaProtein Kinase Inhibitorsmedia_commonPharmacologyMitogen-Activated Protein Kinase KinasesCardiotoxicityMEK inhibitorClinical Trials as Topicbusiness.industryMEK inhibitorCancermedicine.diseaseCardiotoxicityClinical trialCardio-oncology030220 oncology & carcinogenesisHypertensionbusinessPharmacologytherapeutics
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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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Inhibitory effects of cynaropicrin on human melanoma progression by targeting MAPK, NF-κB, and Nrf-2 signaling pathways in vitro

2021

Malignant melanoma is the deadliest skin cancer, due to its propensity to metastasize. MAPKs and NF-κB pathways are constitutively activated in melanoma and promote cell proliferation, cell invasion, metastasis formation, and resistance to therapeutic regimens. Thus, they represent potential targets for melanoma prevention and treatment. Phytochemicals are gaining considerable attention for the management of melanoma because of their several cellular and molecular targets. A screening of a small library of sesquiterpenes lactones selected cynaropicrin, isolated from the aerial parts of Centaurea drabifolia subsp. detonsa, for its potential anticancer effect against melanoma cells. Treatment…

MAPK/ERK pathwayApoptosisBiologymedicine.disease_causeLactones03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - Biochimicasesquiterpene lactonesmedicinemelanomaHumansoxidative stresschemopreventionTranscription factorCell ProliferationMitogen-Activated Protein Kinase KinasesPharmacology0303 health sciencesoxidative streCell growthMelanoma030302 biochemistry & molecular biologyNF-kappa BNF-κBmedicine.diseaseMAPKCynaropicrinchemistry030220 oncology & carcinogenesiscynaropicrinDisease ProgressionCancer researchSignal transductionCarcinogenesisSesquiterpenesSignal Transduction
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Potentiation of the antitumor effects of both selective cyclooxygenase-1 and cyclooxygenase-2 inhibitors in human hepatic cancer cells by inhibition …

2007

The molecular mechanisms behind the anti-neoplastic effects of non-steroidal anti-inflammatory drugs (NSAIDs) are not completely understood and cannot be explained by the inhibition of the cyclooxygenase (COX) enzymes COX-1 and COX-2 alone. We previously reported that both the selective COX-1 inhibitor SC-560 and the selective COX-2 inhibitor CAY10404 exhibit anti-tumor effects in human hepatoma cells. NSAID inhibitors have many COX-independent actions and, among others, the mitogen-activated protein kinase (MAPK) pathways are targets for NSAIDs. Here, we examined the role of MEK/ERK1/2 signaling in the anti-neoplastic effects of both selective COX-1 and COX-2 inhibitors in two human hepato…

MAPK/ERK pathwayCancer ResearchCarcinoma HepatocellularTime FactorsBlotting WesternApoptosisPharmacologyCOX-1 COX-2 NSAIDs MEK1/2 ERK1/2NitrilesButadienesTumor Cells CulturedHumansCyclooxygenase InhibitorsSulfonesEnzyme InhibitorsPhosphorylationProtein kinase ACell ProliferationPharmacologychemistry.chemical_classificationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinase 3biologyDose-Response Relationship DrugLiver NeoplasmsCytochromes cLong-term potentiationDrug SynergismIsoxazolesFlow CytometryEnzymeOncologychemistryCyclooxygenase 2CaspasesCancer cellbiology.proteinCyclooxygenase 1Molecular MedicineMEK-ERK PathwayPyrazolesDrug Therapy CombinationCyclooxygenaseHepatoma cellCancer biologytherapy
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