Search results for " Mitogen"

showing 10 items of 202 documents

DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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Different muscarinic receptor subtypes modulate proliferation of primary human detrusor smooth muscle cells via Akt/PI3K and map kinases.

2013

While acetylcholine (ACh) and muscarinic receptors in the bladder are mainly known for their role in the regulation of smooth muscle contractility, in other tissues they are involved in tissue remodelling and promote cell growth and proliferation. In the present study we have used primary cultures of human detrusor smooth muscle cells (HDSMCs), in order to investigate the role of muscarinic receptors in HDSMC proliferation. Samples were obtained as discarded tissue from men >65 years undergoing radical cystectomy for bladder cancer and cut in pieces that were either immediately frozen or placed in culture medium for the cell culture establishment. HDSMCs were isolated from samples, propagat…

AtropineMalePyrrolidinesMessenger030232 urology & nephrologyGene ExpressionPhosphatidylinositol 3-Kinases0302 clinical medicineAged Atropine; pharmacology Benzofurans; pharmacology Carbachol; pharmacology Cell Proliferation Cells; Cultured Cholinergic Agonists; pharmacology Gene Expression Humans Male Mitogen-Activated Protein Kinases; metabolism Muscarinic Antagonists; pharmacology Myocytes; Smooth Muscle; metabolism Phosphatidylinositol 3-Kinases; metabolism Piperidines; pharmacology Pirenzepine; analogs /&/ derivatives/pharmacology Proto-Oncogene Proteins c-akt; metabolism Pyrrolidines; pharmacology RNA; Messenger; metabolism Receptors; Muscarinic; physiology Urinary Bladder; cytologyPiperidinesSmooth MuscleReceptorsMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptorCells CulturedCulturedMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Smooth muscle contractionMuscarinic acetylcholine receptor M1Receptors Muscarinic030220 oncology & carcinogenesisMitogen-Activated Protein KinasesAcetylcholinemedicine.drugmedicine.medical_specialtyCarbacholCellsMyocytes Smooth MuscleUrinary BladderMuscarinic AntagonistsBiologyCholinergic Agonists03 medical and health sciencesInternal medicineMuscarinicmedicineHumansRNA MessengerAgedBenzofuransCell ProliferationPharmacologyMyocytesPirenzepineEndocrinologyphysiologycytologyRNACarbacholanalogs /&/ derivatives/pharmacologymetabolismProto-Oncogene Proteins c-aktPharmacological research
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Determination of lectin-cell-binding parameters by a new agglutination technique.

1992

We applied a recently described technique which is based on a light transmission/scattering method to determine the association characteristics of the Geodia lectin to sheep erythrocytes. The agglutination assays were performed in a total volume of 3 ml with 5.4 x 10(6) erythrocytes/ml. At a concentration of 360 ng/ml 50% of the lectin molecules were bound to the cells within the first 10 s of incubation. Scatchard analyses revealed an association constant (K(a)) of 0.9 +/- 0.1 x 10(8) M-1 and a number of 3.8 +/- 0.6 x 10(6) lectin binding sites on one erythrocyte. The method was also successfully applied to determine quantitatively the inhibitory potential of sugars competing with cell sur…

BiochemistryAgglutination techniquechemistry.chemical_compoundLectinsmedicineAnimalsLactoseIncubationchemistry.chemical_classificationScatchard plotChromatographySheepbiologyChemistryLectinHemagglutination TestsHemagglutination Inhibition TestsPoriferaRed blood cellAgglutination (biology)Kineticsmedicine.anatomical_structureReceptors MitogenImmunologyCalibrationbiology.proteinGlycoproteinProtein BindingBiological chemistry Hoppe-Seyler
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N-acetyl-L-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A…

2011

64% of chronic obstructive pulmonary disease (COPD) exacerbations are caused by respiratory infections including influenza (strains A and B) and respiratory syncytial virus (RSV). They affect the airway epithelium increasing inflammatory and apoptosis events through mechanisms involving ROS generation, and induce the release of mucins from epithelial cells that are involved in the deterioration of the patient's health during the course of the disease. The antioxidant NAC has proved useful in the management of COPD reducing symptoms, exacerbations and accelerated lung function decline. It has been shown to inhibit influenza virus replication and to diminish the release of inflammatory and ap…

BiologyMucin 5ACmedicine.disease_causeVirus ReplicationBiochemistryp38 Mitogen-Activated Protein KinasesVirusCell LinePulmonary Disease Chronic ObstructivemedicineHumansInterleukin 8PhosphorylationPharmacologyA549 cellMucinNF-kappa BAcetylcysteineRespiratory Syncytial VirusesPulmonary AlveoliInfluenza B virusRespiratory syncytial virus (RSV)Viral replicationApoptosisInfluenza A virusImmunologyRespiratory epitheliumInflammation MediatorsBiochemical pharmacology
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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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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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