Search results for "Protein Kinases"

showing 10 items of 427 documents

Apremilast, a novel phosphodiesterase 4 (PDE4) inhibitor, regulates inflammation through multiple cAMP downstream effectors

2015

Introduction This work was undertaken to delineate intracellular signaling pathways for the PDE4 inhibitor apremilast and to examine interactions between apremilast, methotrexate and adenosine A2A receptors (A2AR). Methods After apremilast and LPS incubation, intracellular cAMP, TNF-α, IL-10, IL-6 and IL-1α were measured in the Raw264.7 monocytic murine cell line. PKA, Epac1/2 (signaling intermediates for cAMP) and A2AR knockdowns were performed by shRNA transfection and interactions with A2AR and A2BR, as well as with methotrexate were tested in vitro and in the murine air pouch model. Statistical differences were determined using one or two-way ANOVA or Student’s t test. The alpha nominal…

MaleAdenosineReceptor Adenosine A2AImmunologyBlotting WesternAdenosine A2A receptorGene ExpressionPharmacologyBiologyCell LineMiceRheumatologyPhenethylaminesmedicineCyclic AMPImmunology and AllergyAnimalsGuanine Nucleotide Exchange FactorsReceptorIC50ArtritisReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaMacrophagesAdenosineMolecular biologyCyclic AMP-Dependent Protein KinasesThalidomideMethotrexateMechanism of actionAntirheumatic AgentsCytokinesTumor necrosis factor alphaRNA InterferenceApremilastPhosphodiesterase 4 Inhibitorsmedicine.symptomInflammation MediatorsIntracellularMedicamentsmedicine.drugResearch Article
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Activation of p38, p21, and NRF-2 Mediates Decreased Proliferation of Human Dental Pulp Stem Cells Cultured under 21% O2

2014

Summary High rates of stem cell proliferation are important in regenerative medicine and in stem cell banking for clinical use. Ambient oxygen tensions (21% O2) are normally used for in vitro culture, but physiological levels in vivo range between 3% and 6% O2. We compared proliferation of human dental pulp stem cells (hDPSCs) cultured under 21% versus 3% O2. The rate of hDPSC proliferation is significantly lower at 21% O2 compared to physiological oxygen levels due to enhanced oxidative stress. Under 21% O2, increased p38 phosphorylation led to activation of p21. Increased generation of reactive oxygen species and p21 led to activation of the NRF-2 signaling pathway. The upregulation of NR…

MaleAdolescentNF-E2-Related Factor 2Biologymedicine.disease_causep38 Mitogen-Activated Protein KinasesBiochemistryYoung AdultDownregulation and upregulationReportDental pulp stem cellsGeneticsmedicineHumanslcsh:QH301-705.5Cells CulturedDental PulpCell Proliferationchemistry.chemical_classificationReactive oxygen specieslcsh:R5-920Cell growthCell BiologyCell biologyOxygenAdult Stem CellsOxidative Stressp21-Activated Kinaseschemistrylcsh:Biology (General)ImmunologySignal transductionStem celllcsh:Medicine (General)Oxidative stressDevelopmental BiologyAdult stem cellStem Cell Reports
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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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Differential expression of PGC-1α and metabolic sensors suggest age-dependent induction of mitochondrial biogenesis in Friedreich ataxia fibroblasts.

2011

11 pages, 6 figures. PMID:21687738[PubMed] PMCID: PMC3110204

MaleAgingMitochondrial DiseasesMitochondrial MyopathyUbiquinoneCardiomyopathylcsh:MedicineMitochondrionAMP-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesAntioxidantsAdenosine TriphosphateAMP-activated protein kinaseTrinucleotide RepeatsFibrosisMolecular Cell BiologyChildlcsh:ScienceHeat-Shock ProteinsRegulation of gene expressionMultidisciplinaryMovement DisordersbiologyNeuromuscular DiseasesMiddle AgedCatalasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCell biologyMitochondriaDNA-Binding ProteinsNeurologyDisease ProgressionMedicineFemalemedicine.symptomSignal TransductionResearch ArticleAdultcongenital hereditary and neonatal diseases and abnormalitiesAtaxiaAdolescentMitochondrial ProteinsmedicineGeneticsHumansBiologyAllelesGlutathione PeroxidaseSuperoxide Dismutaselcsh:RHuman GeneticsFibroblastsmedicine.diseaseMolecular biologyOxidative StressMitochondrial biogenesisGene Expression RegulationFriedreich Ataxiabiology.proteinFrataxinlcsh:QEnergy MetabolismReactive Oxygen SpeciesTranscription FactorsPLoS ONE
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Effect of gender on mitochondrial toxicity of Alzheimer's Abeta peptide.

2007

The aim of this article is to review the role of mitochondria in the pathogenesis of Alzheimer's disease. Additionally, the effect of gender on the incidence of Alzheimer's disease and the pathophysiological mechanisms involved will be discussed. Mitochondria, in the presence of Alzheimer's amyloid-beta peptide, increase the formation of reactive oxygen species which act both as damaging agents and also as signaling molecules. These radicals, in fact, unleash a mechanism involving the liberation of cytochrome c that leads to neuronal apoptosis. Notably, young females appear protected against the mitochondrial toxicity of amyloid-beta, likely due to the upregulation of antioxidant enzymes wh…

MaleAntioxidantPhysiologymedicine.medical_treatmentClinical BiochemistryPharmacologyMitochondrionBiologymedicine.disease_causeBiochemistryp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundDownregulation and upregulationAlzheimer DiseasemedicineHumansMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesAmyloid beta-PeptidesEstrogensCell Biologymedicine.diseaseOxidantsMitochondriaEnzyme ActivationMitochondrial toxicitychemistryBiochemistryToxicityGeneral Earth and Planetary SciencesPhytoestrogensFemaleOxidative stressAntioxidantsredox signaling
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cAMP-dependent phosphorylation of CYP2B1 as a functional switch for cyclophosphamide activation and its hormonal controlin vitro andin vivo

2001

An important feature of cytochrome P450 (CYP) 2B1 is its high ability to convert the prodrug cyclophosphamide (CPA) to therapeutically cytotoxic metabolites, resulting in interstrand DNA-cross-linking and cell death. We have examined whether and how the phosphorylation of CYP2B1 influences CPA metabolic activation in vitro and in vivo. We found first that only part of the total CYP2B1 pool undergoes phosphorylation. This part is fully inactivated. Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic…

MaleCancer ResearchProgrammed cell deathTime FactorsCellRats Sprague-DawleyStructure-Activity RelationshipSex FactorsIn vivoCyclic AMPPhosphoprotein PhosphatasesSerinemedicineAnimalsCytotoxic T cellheterocyclic compoundsPhosphorylationProtein kinase AAntineoplastic Agents AlkylatingCyclophosphamideBiotransformationbiologyCytochrome P450GlucagonCyclic AMP-Dependent Protein KinasesIn vitroRatsCell biologymedicine.anatomical_structureOncologyBiochemistryCytochrome P-450 CYP2B1Hepatocytescardiovascular systembiology.proteinPhosphorylationFemaleMutagensInternational Journal of Cancer
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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Cannabinoid modulation of hippocampal long-term memory is mediated by mTOR signaling.

2009

Cognitive impairment is one of the most important negative consequences associated with cannabis consumption. We found that CB1 cannabinoid receptor (CB1R) activation transiently modulated the mammalian target of rapamycin (mTOR)/p70S6K pathway and the protein synthesis machinery in the mouse hippocampus, which correlated with the amnesic properties of delta9-tetrahydrocannabinol (THC). In addition, non-amnesic doses of either the mTOR blocker rapamycin or the protein synthesis inhibitor anisomycin abrogated the amnesic-like effects of THC, pointing to a mechanism involving new protein synthesis. Moreover, using pharmacological and genetic tools, we found that THC long-term memory deficits …

MaleCannabinoid receptormedicine.medical_treatmentGlutamic AcidHippocampusReceptors N-Methyl-D-AspartateGlutamatergicchemistry.chemical_compoundMiceCognitionReceptor Cannabinoid CB1Memorymental disordersmedicineAnimalsDronabinolPI3K/AKT/mTOR pathwayAnisomycingamma-Aminobutyric AcidMice KnockoutNeuronsProtein Synthesis InhibitorsSirolimusMemory DisordersChemistryGeneral NeuroscienceTOR Serine-Threonine KinasesRibosomal Protein S6 Kinases 70-kDanervous systemKnockout mouseNMDA receptorPhosphorylationCannabinoidNeuroscienceProtein KinasesAnisomycinCentral Nervous System AgentsSignal TransductionNature neuroscience
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p38 MAP kinase drives the expression of mast cell-derived IL-9 via activation of the transcription factor GATA-1.

2007

Mast cells are able to produce a huge panel of mediators including the Th2-type cytokine IL-9, which is considered to be a key mediator for the pathogenesis of allergic asthma, but detailed information on the regulation of IL-9 transcription in mast cells has been scarce. Herein we provide evidence that the erythroid/myeloid transcription factor GATA-1, which is not expressed in Th2 cells, is a potent activator of IL-9 expression in murine bone marrow-derived mast cells (BMMC). Furthermore, in mast cells, but not in Th2 cells, production of IL-9 is sensitive to inhibition of p38 MAP kinase. As transactivation mediated by GATA-1 is also sensitive to inhibition of p38 MAP kinase, and GATA-1 i…

MaleCell signalingmedicine.medical_treatmentImmunologyBone Marrow CellsGATA3 Transcription FactorBiologyp38 Mitogen-Activated Protein KinasesTransactivationMiceTh2 CellsmedicineAnimalsGATA1 Transcription FactorMast CellsRNA MessengerPhosphorylationPromoter Regions GeneticMolecular BiologyInterleukin 5Mice Inbred BALB CGATA2Interleukin-9Mast cellCell biologyInterleukin 33GATA2 Transcription FactorCytokinemedicine.anatomical_structureGene Expression RegulationInterleukin 15MutationFemaleMolecular immunology
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