Search results for "Protein kinases"

showing 10 items of 427 documents

AMP-activated protein kinase (AMPK) signaling pathway: A potential mechanism involved in PAFIYAMA syndrome?

2016

medicine.medical_specialtyLeft atriumAMP-Activated Protein KinasesProtein Serine-Threonine Kinases030204 cardiovascular system & hematologyleft atrium03 medical and health sciences0302 clinical medicineAMP-activated protein kinaseFibrosisInternal medicinemedicineHumansAmpk signalingPhosphorylationPotential mechanismremodelingendurancebiologyexercisebusiness.industryfibrosismedicine.diseaseCell biologyEnzyme Activationmedicine.anatomical_structureEndocrinologybiology.proteinexercise; endurance; arrhythmias; fibrosis; remodeling; left atriumCardiology and Cardiovascular Medicinebusinessarrhythmias030217 neurology & neurosurgerySignal Transduction
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Neuroendocrine Regulation Of The IL-27-Dependent Immune Response In Macrophages

2013

Abstract The central nervous system has the ability for modulating immune responses, but the molecular mechanisms of such interactions are only partly understood. Interleukin-27 (IL-27) is a heterodimeric protein and structurally related to the IL-12 family of cytokines. IL-27 is composed of the subunits EBI3 and p28. The biological functions of IL-27 have been described as either anti-inflammatory or pro-inflammatory depending on the experimental models studied. In the current study, we investigated how production of Interleukin-27 (IL-27) is regulated by neuroendocrine hormones. We focused our work on the subunit p28, since EBI3 is also present in IL-35 and therefore is not a specific com…

medicine.medical_specialtyLipopolysaccharidebiologyp38 mitogen-activated protein kinasesmedicine.medical_treatmentImmunologyInflammationCell BiologyHematologyBiochemistrychemistry.chemical_compoundEndocrinologyCytokineImmune systemchemistryIntegrin alpha MInternal medicinemedicinebiology.proteinmedicine.symptomReceptorHormoneBlood
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Mechanisms of C-reactive protein-induced blood-brain barrier disruption.

2009

Background and Purpose— Increased mortality after stroke is associated with brain edema formation and high plasma levels of the acute phase reactant C-reactive protein (CRP). The aim of this study was to examine whether CRP directly affects blood–brain barrier stability and to analyze the underlying signaling pathways. Methods— We used a cell coculture model of the blood–brain barrier and the guinea pig isolated whole brain preparation. Results— We could show that CRP at clinically relevant concentrations (10 to 20 μg/mL) causes a disruption of the blood–brain barrier in both approaches. The results of our study further demonstrate CRP-induced activation of surface Fcγ receptors CD16/32 fo…

medicine.medical_specialtyMyosin light-chain kinaseMyosin Light ChainsGuinea PigsBrain Edemamedicine.disease_causeBlood–brain barrierp38 Mitogen-Activated Protein KinasesMyosin light chain kinase activityTight JunctionsInternal medicineMyosinmedicineAnimalsPhosphorylationReceptorCells CulturedAdvanced and Specialized Nursingbusiness.industryReceptors IgGCoculture TechniquesCell biologyRatsStrokeEndocrinologymedicine.anatomical_structureC-Reactive ProteinBlood-Brain BarrierPhosphorylationNeurology (clinical)Endothelium VascularSignal transductionCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressSignal TransductionStroke
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NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Angiotensin-Converting Enzyme Inhibitor Ramiprilat Interferes With the Sequestration of the B 2 Kinin Receptor Within the Plasma Membrane of Native E…

1999

Background —ACE (kininase II) inhibitors have been shown to exert their beneficial cardiovascular effects via the inhibition of both angiotensin II formation and bradykinin breakdown. Because recent evidence suggests that ACE inhibitors may also interfere with B 2 kinin receptor signaling and thus enhance the vascular response to bradykinin, we examined whether the distribution of B 2 kinin receptors within the plasma membrane of native endothelial cells is affected by an ACE inhibitor. Methods and Results —Localization of the B 2 kinin receptor in membranes prepared from native porcine aortic endothelial cells was evaluated by means of specific [ 3 H]bradykinin binding and immunoprecipita…

medicine.medical_specialtyReceptor Bradykinin B2SwineBradykininAngiotensin-Converting Enzyme InhibitorsPharmacologyBradykininchemistry.chemical_compoundRamiprilPhysiology (medical)Internal medicinemedicineAnimalsCalcium SignalingBradykinin receptorReceptorAortaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyReceptors BradykininMembrane ProteinsBiological TransportAngiotensin-converting enzymeKininAngiotensin IIEndothelial stem cellEndocrinologychemistryCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinEndothelium VascularMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineRamiprilatSignal TransductionCirculation
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POLYPHENOLS FROM RED WINE MODULATE IMMUNE RESPONSIVENESS: BIOLOGICAL AND CLINICAL SIGNIFICANCE.

2008

Many studies have been conducted on the effects of red wine polyphenols on certain diseases, primarily, coronary heart disease (CHD) and, in this respect, evidence has been demonstrated that intake of red wine is associated with a reduction of CHD symptomatology. In this framework, the purpose of this review is to illustrate the effects of polyphenols on immune cells from human healthy peripheral blood. Data will show that polyphenols are able to stimulate both innate and adaptive immune responses. In particular, the release of cytokines such as interleukin (IL)-12, interferon (IFN)-gamma, and IL-10 as well as immunoglobulins may be important for host protection in different immune related …

medicine.medical_treatmentImmunoglobulinsCoronary DiseaseWineImmunoglobulin ENitric OxidePeripheral blood mononuclear cellp38 Mitogen-Activated Protein KinasesNitric oxidePOLYPHENOLSIMMUNE SYSTEMCYTOKINESIMMUNOGLOBULINSNITRIC OXIDEATHEROSCLEROSISRED WINEchemistry.chemical_compoundImmune systemPhenolsInterferonDrug DiscoverymedicineAnimalsHumansPharmacologyFlavonoidsSettore MED/04 - Patologia Generalebiologybusiness.industryImmunityfood and beveragesInterleukinPolyphenolsCytokinechemistryImmunologyChronic Diseasebiology.proteinLeukocytes MononuclearCytokinesAntibodybusinessmedicine.drug
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Myeloperoxidase mediates neutrophil activation by association with CD11b/CD18 integrins.

2004

Recruitment and activation of polymorphonuclear neutrophils (PMNs) reflects a primary immunological response to invading pathogens and has also emerged as a hallmark of vascular inflammation. One of the principal enzymes released upon PMN activation is myeloperoxidase (MPO), a heme protein that not only generates cytotoxic oxidants but also impacts deleteriously on nitric oxide-dependent signaling cascades within the vasculature. Because MPO also associates with the membrane of PMN, we evaluated whether MPO could also function as an autocrine modulator of PMN activation. The extent of PMN membrane-associated MPO was elevated in patients with acute inflammatory vascular disease compared with…

medicine.medical_treatmentanimal diseasesCD18p38 Mitogen-Activated Protein KinasesCell DegranulationNeutrophil ActivationProinflammatory cytokinechemistry.chemical_compoundSuperoxidesmedicineHumansPhosphorylationPeroxidaseMultidisciplinaryCD11b AntigenbiologySuperoxideElastaseDegranulationNF-kappa Bhemic and immune systemsBiological SciencesMolecular biologyCytokineIntegrin alpha MchemistryMyeloperoxidaseCD18 AntigensImmunologybiology.proteinProceedings of the National Academy of Sciences of the United States of America
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Protein Phosphorylation by Peroxisome Proliferators: Species-specific Stimulation of Protein Kinases and Its Role in PP-induced Transcriptional Activ…

1996

p38 mitogen-activated protein kinasesMicrobodiesGene Expression Regulation EnzymologicGeneral Biochemistry Genetics and Molecular BiologyMAP2K7Retinoblastoma-like protein 1History and Philosophy of ScienceAnimalsHumansProtein phosphorylationClofibrateRNA MessengerAcetyl-CoA C-AcetyltransferaseProtein kinase ACells CulturedProtein Kinase CHypolipidemic AgentsbiologyChemistryKinaseGeneral NeuroscienceGRB10Autophagy-related protein 13PhosphoproteinsStaurosporineRats Inbred F344RatsCell biologybiology.proteinProtein KinasesAnnals of the New York Academy of Sciences
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Activation of NF-kappaB and IL-8 by yersinia enterocolitica invasin protein is conferred by engagement of rac1 and MAP kinase cascades.

2003

International audience; Yersinia enterocolitica triggers activation of the nuclear factor (NF)-kappaB and production of the proinflammatory chemokine interleukin (IL)-8 in intestinal epithelial cells. This activation is due to adhesion of the bacteria via their outer membrane protein invasin to the host cells. Using Clostridium difficile toxins that specifically inactivate small GTPases, and transfection of inhibitory proteins of the Rho-GTPases, we demonstrate that Rac1, but not Cdc42 or Rho, is required for activation of NF-kappaB by invasin. Invasin activated the mitogen activated protein kinases (MAPK) p38 and c-Jun N-terminal protein kinase (JNK) but not extracellular signal regulated …

rac1 GTP-Binding ProteinMAP Kinase Kinase 4MAP Kinase Signaling SystemRNA Stability[SDV]Life Sciences [q-bio]ImmunologyMitogen-activated protein kinase kinasep38 Mitogen-Activated Protein KinasesMicrobiologyBacterial AdhesionMAP2K703 medical and health sciencesBacterial ProteinsVirologyHumansASK1RNA Messengerc-RafAdhesins Bacterialcdc42 GTP-Binding ProteinrhoB GTP-Binding ProteinYersinia enterocolitica030304 developmental biologyMitogen-Activated Protein Kinase Kinases0303 health sciencesbiologyMAP kinase kinase kinase030306 microbiologyInterleukin-8Cyclin-dependent kinase 2JNK Mitogen-Activated Protein KinasesNF-kappa BProtein kinase RMolecular biologyCell biologybiology.proteinCyclin-dependent kinase 9Mitogen-Activated Protein KinasesrhoA GTP-Binding ProteinHeLa CellsSignal Transduction
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