Search results for "Mitogen-Activated Protein Kinases"

showing 10 items of 246 documents

TORC1 controls G1–S cell cycle transition in yeast via Mpk1 and the greatwall kinase pathway

2015

The target of rapamycin complex 1 (TORC1) pathway couples nutrient, energy and hormonal signals with eukaryotic cell growth and division. In yeast, TORC1 coordinates growth with G1–S cell cycle progression, also coined as START, by favouring the expression of G1 cyclins that activate cyclin-dependent protein kinases (CDKs) and by destabilizing the CDK inhibitor Sic1. Following TORC1 downregulation by rapamycin treatment or nutrient limitation, clearance of G1 cyclins and C-terminal phosphorylation of Sic1 by unknown protein kinases are both required for Sic1 to escape ubiquitin-dependent proteolysis prompted by its flagging via the SCFCdc4 (Skp1/Cul1/F-box protein) ubiquitin ligase complex.…

BioquímicaBiologiaSaccharomyces cerevisiae ProteinsImmunoblottingGeneral Physics and AstronomyCell Cycle ProteinsSaccharomyces cerevisiaeMechanistic Target of Rapamycin Complex 1ArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineCyclin-dependent kinaseCyclinsImmunoprecipitationProtein Phosphatase 2Cell division control protein 4PhosphorylationProtein kinase ACyclin-Dependent Kinase Inhibitor Proteins030304 developmental biology0303 health sciencesMultidisciplinarybiologyTOR Serine-Threonine KinasesUbiquitin-Protein Ligase ComplexesGeneral ChemistryBlotting NorthernFlow CytometryG1 Phase Cell Cycle CheckpointsSic1Cyclin-Dependent KinasesCell biologyBiochemistryMultiprotein Complexes030220 oncology & carcinogenesisUbiquitin ligase complexbiology.proteinIntercellular Signaling Peptides and ProteinsPhosphorylationTOR Serine-Threonine KinasesMitogen-Activated Protein KinasesPeptidesProtein KinasesCyclin-dependent kinase inhibitor proteinNature Communications
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Specific and global regulation of mRNA stability during osmotic stress in Saccharomyces cerevisiae.

2009

Hyperosmotic stress yields reprogramming of gene expression in Saccharomyces cerevisiae cells. Most of this response is orchestrated by Hog1, a stress-activated, mitogen-activated protein kinase (MAPK) homologous to human p38. We investigated, on a genomic scale, the contribution of changes in transcription rates and mRNA stabilities to the modulation of mRNA amounts during the response to osmotic stress in wild-type and hog1 mutant cells. Mild osmotic shock induces a broad mRNA destabilization; however, osmo-mRNAs are up-regulated by increasing both transcription rates and mRNA half-lives. In contrast, mild or severe osmotic stress in hog1 mutants, or severe osmotic stress in wild-type cel…

BioquímicaMessenger RNASaccharomyces cerevisiae ProteinsTranscription GeneticOsmotic shockMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesSaccharomyces cerevisiaeMRNA stabilizationSaccharomyces cerevisiaeBiologybiology.organism_classificationMolecular biologyArticleGenètica molecularCell biologyOsmotic PressureGene Expression Regulation FungalGene expressionOsmotic pressureRNA MessengerMitogen-Activated Protein KinasesMolecular Biology
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Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.

2013

p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influ…

Blood PlateletsCancer ResearchcPLA2p38 mitogen-activated protein kinasesImmunologyBlotting Westernp38 Mitogen-Activated Protein KinasesPiperazinesNitrophenolsCellular and Molecular NeurosciencePhospholipase A2Crotalid VenomsHumansLectins C-Typeddc:610Cells CulturedMembrane Potential MitochondrialplateletSulfonamidesbiologyKinaseGroup IV Phospholipases A2Biphenyl CompoundsapoptosisConvulxinCell BiologyFlow Cytometryp38 MAP kinaseCell biologyApoptosisMitogen-activated protein kinasebiology.proteinPhosphorylationOriginal ArticleSignal transductionReactive Oxygen SpeciesSignal TransductionCell deathdisease
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Activation of cGMP-dependent Protein Kinase Iβ Inhibits Interleukin 2 Release and Proliferation of T Cell Receptor-stimulated Human Peripheral T Cells

2000

Several major functions of type I cGMP-dependent protein kinase (cGK I) have been established in smooth muscle cells, platelets, endothelial cells, and cardiac myocytes. Here we demonstrate that cGK Ibeta is endogenously expressed in freshly purified human peripheral blood T lymphocytes and inhibits their proliferation and interleukin 2 release. Incubation of human T cells with the NO donor, sodium nitroprusside, or the membrane-permeant cGMP analogs PET-cGMP and 8-pCPT-cGMP, activated cGK I and produced (i) a distinct pattern of phosphorylation of vasodilator-stimulated phosphoprotein, (ii) stimulation of the mitogen-activated protein kinases ERK1/2 and p38 kinase, and, upon anti-CD3 stimu…

Blood PlateletsNitroprussideInterleukin 2Cell Membrane PermeabilityCD3 ComplexT-Lymphocytesp38 mitogen-activated protein kinasesT cellReceptors Antigen T-CellCell SeparationBiologyLymphocyte ActivationBiochemistryJurkat cellsJurkat CellsCyclic AMPCyclic GMP-Dependent Protein KinasesmedicineHumansProtein kinase ACyclic GMPMolecular BiologyCyclic GMP-Dependent Protein Kinase Type IKinaseCell growthMicrofilament ProteinsCell BiologyPhosphoproteinsMolecular biologyCell biologyEnzyme ActivationAlternative Splicingmedicine.anatomical_structureInterleukin-2Mitogen-Activated Protein KinasesCell Adhesion MoleculescGMP-dependent protein kinasemedicine.drugJournal of Biological Chemistry
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Induction of CD36 and thrombospondin-1 in macrophages by hypoxia-inducible factor 1 and its relevance in the inflammatory process.

2012

Inflammation is part of a complex biological response of vascular tissue to pathogens or damaged cells. First inflammatory cells attempt to remove the injurious stimuli and this is followed by a healing process mediated principally by phagocytosis of senescent cells. Hypoxia and p38-MAPK are associated with inflammation, and hypoxia inducible factor 1 (HIF-1) has been detected in inflamed tissues. We aimed to analyse the role of p38-MAPK and HIF-1 in the transcriptional regulation of CD36, a class B scavenger receptor, and its ligand thrombospondin (TSP-1) in macrophages and to evaluate the involvement of this pathway in phagocytosis of apoptotic neutrophils. We have also assessed HIF-1α, p…

CD36 AntigensMaleAnatomy and PhysiologyNeutrophilsCD36Digestive Physiologylcsh:MedicineApoptosisp38 Mitogen-Activated Protein KinasesBiochemistryMonocytesThrombospondin 1Intestinal mucosaCrohn DiseaseIntestinal Mucosalcsh:ScienceHypoxiaPromoter Regions GeneticMultidisciplinaryProtein StabilityMiddle AgedOxygen Metabolismmedicine.anatomical_structureMedicineFemaleHypoxia-Inducible Factor 1medicine.symptomProtein BindingSignal TransductionResearch ArticleAdultCell PhysiologyAdolescentPhagocytosisImmune CellsImmunologyInflammationGastroenterology and HepatologyBiologyCell LineYoung AdultPhagocytosismedicineHumansUlcerative ColitisScavenger receptorBiologyInflammationLamina propriaDigestive RegulationMacrophageslcsh:RInflammatory Bowel DiseaseHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMetabolismApoptosisImmunologyCancer researchbiology.proteinlcsh:QColitis UlcerativeDigestive SystemPloS one
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CD8+ cytotoxic T lymphocytes isolated from allogeneic healthy donors recognize HLA class Ia/Ib–associated renal carcinoma antigens with ubiquitous or…

2004

AbstractAllogeneic hematopoietic stem cell transplantation can induce considerable tumor remissions in metastatic renal-cell carcinoma (RCC) patients. The precise effector mechanisms mediating these graft-versus-tumor reactions are unknown. We studied RCC-directed CD8+ T-cell responses in blood lymphocytes of healthy individuals matched with established RCC cell lines for HLA-class I. In 21 of 22 allogeneic mixed lymphocyte/tumor-cell cultures (MLTCs), RCC-reactive cytotoxic T-lymphocytes (CTLs) were readily obtained. From MLTCs, 121 CD8+ CTL clones with memory phenotype were isolated. Their anti–RCC reactivity was restricted by multiple classical HLA-Ia molecules, in particular by HLA-A2, …

CD4-Positive T-LymphocytesCytotoxicity ImmunologicGenotypemedicine.medical_treatmentMolecular Sequence DataImmunologyCell SeparationHuman leukocyte antigenHematopoietic stem cell transplantationCross ReactionsBiologyurologic and male genital diseasesBiochemistryEpitheliumCell therapyEpitopesAntigenAntigens NeoplasmmedicineHumansTransplantation HomologousCytotoxic T cellAmino Acid SequenceCarcinoma Renal CellHistocompatibility Antigens Class ICell BiologyHematologyImmunotherapyFlow CytometryHematopoietic Stem CellsTissue DonorsCTL*HealthSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationColonic NeoplasmsImmunologyMitogen-Activated Protein KinasesPeptidesCD8T-Lymphocytes CytotoxicBlood
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Docosahexaenoic acid modulates the expression of T-bet and GATA-3 transcription factors, independently of PPARα, through suppression of MAP kinase ac…

2009

The present study was conducted on CD4(+) T cells, isolated from wild type (WT) and PPARalpha(null) mice, in order to assess the mechanism of action of docosahexaenoic acid (DHA), an n-3 fatty acid, in the modulation of two transcription factors, i.e., T-bet and GATA-3, implicated in T-cell differentiation towards, respectively, T(H)1 and T(H)2 phenotype. The T-cells from PPARalpha(null) mice secreted higher IFN-gamma and lower IL-4 concentrations than WT T-cells. Furthermore, the deletion of PPARalpha gene in T-cells resulted in the upregulation of T-bet and downregulation of GATA-3 both at mRNA and protein levels. DHA exerted not only an inhibitory effect on T-cell proliferation, but also…

CD4-Positive T-LymphocytesTranscriptional ActivationDocosahexaenoic AcidsMAP Kinase Signaling SystemT-LymphocytesCellular differentiationp38 mitogen-activated protein kinasesDown-RegulationPeroxisome proliferator-activated receptorGATA3 Transcription FactorBiologyMitogen-activated protein kinase kinaseBiochemistryInterferon-gammaMiceAnimalsPPAR alphaRNA MessengerPhosphorylationTranscription factorMice Knockoutchemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionKinaseCell DifferentiationGeneral MedicineTh1 CellsUp-RegulationCell biologychemistryDocosahexaenoic acidMitogen-activated protein kinaseCancer researchbiology.proteinlipids (amino acids peptides and proteins)Bronchial HyperreactivityMitogen-Activated Protein KinasesT-Box Domain ProteinsSignal TransductionTranscription FactorsBiochimie
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Midregion PTHrP regulates Rip1 and caspase expression in MDA-MB231 breast cancer cells.

2007

It was previously reported that the midregion PTHrP domain (38-94)-amide restrains growth and invasion "in vitro", causes striking toxicity and accelerates death of some breast cancer cell lines, the most responsive being MDA-MB231 whose tumorigenesis was also attenuated "in vivo". In addition, we have demonstrated that midregion PTHrP is imported in the nucleoplasm of cultured MDA-MB231 cells, and that "in vitro" it can bind chromatin of metaphase spread preparations and also an isolated 20-mer oligonucleotide, thereby appearing endowed with a putative transcription factor-like DNA-binding ability. Here, we examined whether PTHrP (38-94)-amide was able to modulate the expression of genes e…

Cancer ResearchProgrammed cell deathbcl-X ProteinApoptosisBreast NeoplasmsPTHrP Rip1 caspase breast cancer cellsmedicine.disease_causeTransfectionCell MovementCell Line TumorGene expressionmedicineTranscriptional regulationHumansNeoplasm InvasivenessSettore BIO/06 - Anatomia Comparata E Citologiaskin and connective tissue diseasesCaspaseCell ProliferationNucleoplasmbiologyJNK Mitogen-Activated Protein KinasesParathyroid Hormone-Related ProteinRNA-Binding ProteinsOligonucleotides AntisenseMolecular biologyPeptide FragmentsChromatinCell biologyNuclear Pore Complex ProteinsSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaOncologyApoptosisCaspasesbiology.proteinFemalebcl-Associated Death ProteinCarcinogenesisSignal TransductionBreast cancer research and treatment
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The role of oxidative stress in apoptosis induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid in human colon adenocarcinoma …

2008

Histone deacetylase inhibitors (HDACIs) activate genes that promote cell cycle arrest and apoptosis in a number of tumor cells. This study showed that suberoylanilide hydroxamic acid (SAHA), a potent and commonly used HDACI, induced apoptosis in human colon adenocarcinoma HT-29 cells in a time- and dose-dependent manner. This effect was accompanied by the induction of oxidative stress, dissipation of mitochondrial transmembrane potential and activation of executioner caspases. Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK. The addition of either the antioxidant N-acetylcysteine or the specific inhibitor of NADPH oxidase diphenylene iodonium chloride reduc…

Cancer ResearchProgrammed cell deathmedicine.drug_classCell Survivalp38 mitogen-activated protein kinasesBlotting WesternApoptosisAdenocarcinomamedicine.disease_causeHydroxamic AcidsAntioxidantsSettore BIO/10 - BiochimicamedicineHumansEnzyme InhibitorsProtein kinase BCaspaseMembrane Potential MitochondrialVorinostatbiologyHistone deacetylase inhibitorEnzyme ActivationHistone Deacetylase InhibitorsOxidative StressOncologyBiochemistryApoptosisCaspasesColonic NeoplasmsCancer researchbiology.proteinHistone deacetylaseReactive Oxygen Speciescolon adenomacarcinoma cells histone deacetylase inhibitors apoptosisHT29 CellsOxidative stressSignal TransductionInternational journal of oncology
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Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: involvement of the transcription factor PPARgamma.

2008

It has recently been shown that cannabinoids induce growth inhibition and apoptosis in different tumour cell lines. In the current study, the effects of WIN 55,212-2 (WIN), a synthetic and potent cannabinoid receptor agonist, are investigated in hepatoma HepG2 cells and a possible signal transduction pathway is proposed. In these cells, WIN induces a clear apoptotic effect which was accompanied by up-regulation of the death-signalling factors Bax, Bcl-X(S), t-Bid and down-regulation of the survival factors survivin, phospho-AKT, Hsp72 and Bcl-2. Moreover, WIN-induced apoptosis is associated with JNK/p38 MAPK pathway activation and mitochondrial depolarisation demonstrated by a cytofluorimet…

Cannabinoid receptorCarcinoma HepatocellularCell SurvivalPyridinesmedicine.medical_treatmentp38 mitogen-activated protein kinasesMorpholinesApoptosisBiologyNaphthalenesBiochemistryReceptor Cannabinoid CB2Membrane Microdomainscannabinoids PPARgamma factor apoptosis cancer cellsSettore BIO/10 - BiochimicaCell Line TumorSurvivinmedicineHumansAnilidesViability assayCannabinoidsLiver NeoplasmsGeneral MedicineCell biologyBenzoxazinesPPAR gammaApoptosisCancer cellBenzamidesCannabinoidSignal transductionApoptosis Regulatory ProteinsProtein KinasesSignal TransductionBiochimie
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