Search results for "Cyclic AMP-Dependent Protein Kinases"

showing 10 items of 42 documents

Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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Fasting regulates EGR1 and protects from glucose- and dexamethasone-dependent sensitization to chemotherapy

2017

Fasting reduces glucose levels and protects mice against chemotoxicity, yet drugs that promote hyperglycemia are widely used in cancer treatment. Here, we show that dexamethasone (Dexa) and rapamycin (Rapa), commonly administered to cancer patients, elevate glucose and sensitize cardiomyocytes and mice to the cancer drug doxorubicin (DXR). Such toxicity can be reversed by reducing circulating glucose levels by fasting or insulin. Furthermore, glucose injections alone reversed the fasting-dependent protection against DXR in mice, indicating that elevated glucose mediates, at least in part, the sensitizing effects of rapamycin and dexamethasone. In yeast, glucose activates protein kinase A (P…

0301 basic medicineTime FactorsImmunology and Microbiology (all)Peptide Hormonesmedicine.medical_treatmentAMP-Activated Protein KinasesToxicologyPathology and Laboratory MedicineBiochemistryDexamethasoneMiceEndocrinologyAMP-activated protein kinaseAtrial natriuretic peptideNatriuretic Peptide BrainMedicine and Health SciencesNatriuretic peptideInsulinSmall interfering RNAsBiology (General)Statistical DatabiologyOrganic CompoundsGeneral NeuroscienceMonosaccharidesHeartFastingMetformin3. Good healthMetforminNucleic acidsChemistryPhysical SciencesFemaleAnatomyGeneral Agricultural and Biological SciencesStatistics (Mathematics)Atrial Natriuretic FactorResearch Articlemedicine.drugmedicine.medical_specialtyQH301-705.5medicine.drug_classCarbohydratesEGR1Antineoplastic AgentsCardiotoxinsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesNatriuretic PeptideStress PhysiologicalInternal medicineGeneticsmedicineAnimalsNon-coding RNAProtein kinase AEarly Growth Response Protein 1Diabetic EndocrinologyNeuroscience (all)Biochemistry Genetics and Molecular Biology (all)Biology and life sciencesToxicityGeneral Immunology and MicrobiologyInsulinOrganic ChemistryChemical CompoundsCorrectionAMPKCyclic AMP-Dependent Protein KinasesHormonesGene regulationDietAtrial Natriuretic PeptideMice Inbred C57BLNeuroscience (all); Immunology and Microbiology (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Glucose030104 developmental biologyEndocrinologyAgricultural and Biological Sciences (all)CytoprotectionMetabolic DisordersHyperglycemiaCardiovascular Anatomybiology.proteinRNAGene expressionMathematicsPLOS Biology
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Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression

2016

SummaryImmune system defects are at the center of aging and a range of diseases. Here, we show that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells (LT-HSCs) and niche cells that promote stress resistance, self-renewal, and lineage-balanced regeneration. Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients. The proregenerative effects of fasting on stem cells were recapitula…

0301 basic medicinemedicine.medical_specialtyhematopoietic regenerationfastingmedicine.medical_treatmentCellBiologyMice03 medical and health sciences0302 clinical medicineImmune systemSettore BIO/13 - Biologia ApplicataInternal medicinemedicineGeneticsAnimalsRegenerationInsulin-Like Growth Factor I030304 developmental biologyImmunosuppression Therapy0303 health sciencesstem cells; fasting; nutrition; hematopoietic regenerationRegeneration (biology)Hematopoietic stem cellImmunosuppressionCell BiologyHematopoietic Stem CellsCyclic AMP-Dependent Protein Kinases3. Good healthCell biologyMice Inbred C57BLstem cellHaematopoiesisEndocrinologynutrition030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMolecular MedicineSignal transductionStem cellCell Stem Cell
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Increased protein kinase A regulatory subunit content and cGMP binding in erythrocyte membranes in liver cirrhosis

2003

Abstract Background/Aims : Patients with liver disease show increased plasma cGMP and decreased intracellular cGMP in lymphocytes. The initial aim of this work was to assess whether decreased intracellular cGMP and increased plasma cGMP may be due to increased ATP-dependent release of cGMP from cells. The results obtained led to a new aim: to identify and quantify a protein responsible for the increased cGMP binding found in erythrocyte membranes from patients with liver disease. Methods : ATP-dependent cGMP transport was determined in inside-out vesicles from erythrocyte membranes. cGMP-binding proteins were isolated from the membranes and identified by MALDI-TOF peptide mass fingerprint. …

AdultLiver CirrhosisMalemedicine.medical_specialtyProtein subunitPhosphodiesterase 3Biological Transport ActiveIn Vitro TechniquesBiologyInternal medicinemedicineHumansProtein kinase ACyclic GMPAgedCGMP bindingHepatologyErythrocyte MembraneMiddle AgedCyclic AMP-Dependent Protein KinasesMolecular WeightKineticsProtein SubunitsEndocrinologyCase-Control StudiesSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCGMP transportbiology.proteinFemaleProtein AcGMP-dependent protein kinaseIntracellularJournal of Hepatology
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A Highly Decreased Binding of Cyclic Adenosine Monophosphate to Protein Kinase A in Erythrocyte Membranes is Specific for Active Psoriasis

2002

A cyclic adenosine monophosphate binding abnormality in psoriatic erythrocytes that could be corrected by retinoid treatment has been reported. It was tested whether this binding abnormality is specific for psoriasis and the effects of treatment were compared with etretinate, cyclosporine A, or anthralin on 2-(3)H-8-N(3)-cyclic adenosine monophosphate binding to the regulatory subunit of protein kinase A in erythrocyte membranes. One hundred and fifteen individuals were evaluated, including: (i) 34 healthy persons; (ii) 15 patients with nonatopic inflammatory skin diseases (eczema, erythroderma, tinea, Grover's disease, erysipelas, urticaria); (iii) eight with other dermatoses mediated by i…

AdultMaleAzidesmedicine.medical_specialtyAdolescentmedicine.drug_classAdministration TopicalAnti-Inflammatory AgentsErythrodermaEtretinateDermatologySeverity of Illness IndexBiochemistryRetinoidschemistry.chemical_compoundPsoriasis Area and Severity IndexKeratolytic AgentsPsoriasis Area and Severity IndexPsoriasisInternal medicineCyclic AMPmedicineHumansPsoriasisCyclic adenosine monophosphateRetinoidMolecular BiologydermatitisAgedErythema nodosumbusiness.industryErythrocyte MembraneAffinity LabelsCell BiologyAtopic dermatitisAnthralinMiddle Agedmedicine.diseaseCyclic AMP-Dependent Protein KinasesEndocrinologychemistryEtretinateCyclosporineFemaleDermatologic Agentsbusinesscyclosporine AProtein Bindingmedicine.drugJournal of Investigative Dermatology
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Structure-activity relationship of staurosporine analogs in regulating expression of endothelial nitric-oxide synthase gene.

2000

In human umbilical vein endothelial cells and in human umbilical vein endothelial cell-derived EA.hy 926 cells, staurosporine (Stsp) and its glycosidic indolocarbazole analogs 7-hydroxystaurosporine (UCN-01) and 4'-N-benzoyl staurosporine (CGP 41251) enhanced nitric-oxide synthase (NOS) III mRNA expression (analyzed by RNase protection assay), protein expression (determined by Western blot), and activity [measured by rat fetal lung fibroblast (RFL-6) reporter cell assay] in a concentration- and time-dependent manner. In contrast, the bisindolylmaleimide analogs GF 109203X, Ro 31-8220 and Go 6983 had no effect on NOS III expression, and Go 6976, a methyl- and cyanoalkyl-substituted nonglycos…

BisindolylmaleimideNitric Oxide Synthase Type IIIBiologyEndothelial NOSNitric OxideGene Expression Regulation Enzymologicchemistry.chemical_compoundStructure-Activity RelationshipAlkaloidsmedicineCyclic GMP-Dependent Protein KinasesStaurosporineAnimalsHumansDrug InteractionsRNA MessengerEnzyme InhibitorsProtein kinase APromoter Regions GeneticProtein Kinase InhibitorsProtein kinase CCells CulturedProtein Kinase CPharmacologyKinaseTumor Necrosis Factor-alphaNitric Oxide Synthase Type IIIProtein-Tyrosine KinasesStaurosporineMolecular biologyCyclic AMP-Dependent Protein KinasesRatschemistryMolecular MedicineEndothelium VascularNitric Oxide SynthaseTyrosine kinaseProtein Kinasesmedicine.drugMolecular pharmacology
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Differential roles of cAMP and cGMP in megakaryocyte maturation and platelet biogenesis

2012

The cyclic nucleotides cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) regulate the activity of protein kinase A (PKA) and protein kinase G (PKG), respectively. This process helps maintain circulating platelets in a resting state. Here we studied the role of cAMP and cGMP in the regulation of megakaryocyte (MK) differentiation and platelet formation. Cultured, platelet-producing MKs were differentiated from fetal livers harvested from 13.5 days postcoital mouse embryos. MK development was accompanied by a dramatic increase in cAMP production and expression of soluble guanylate cyclase, PKG, and PKA as well as their downstream targets vasodilator-stimulated ph…

Blood PlateletsCancer Researchmegakaryocytes; cAMP; cGMP; plateletsPhosphodiesterase 3BiologyArticleAdenylyl cyclaseMicechemistry.chemical_compoundPregnancyCyclic AMPGeneticsAnimalsCyclic adenosine monophosphatePhosphorylationProtein kinase ACyclic GMPMolecular BiologyCyclic guanosine monophosphateMicrofilament ProteinsCell DifferentiationCell BiologyHematologyPhosphoproteinsCyclic AMP-Dependent Protein KinasesCell biologyMice Inbred C57BLCytoskeletal ProteinsThrombopoietinchemistrycAMP-dependent pathwayFemalePDE10ASignal transductionCell Adhesion MoleculesMegakaryocytesExperimental Hematology
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Time-resolved characterization of cAMP/PKA-dependent signaling reveals that platelet inhibition is a concerted process involving multiple signaling p…

2014

One of the most important physiological platelet inhibitors is endothelium-derived prostacyclin which stimulates the platelet cyclic adenosine monophosphate/protein kinase A (cAMP/PKA)-signaling cascade and inhibits virtually all platelet-activating key mechanisms. Using quantitative mass spectrometry, we analyzed time-resolved phosphorylation patterns in human platelets after treatment with iloprost, a stable prostacyclin analog, for 0, 10, 30, and 60 seconds to characterize key mediators of platelet inhibition and activation in 3 independent biological replicates. We quantified over 2700 different phosphorylated peptides of which 360 were significantly regulated upon stimulation. This com…

Blood PlateletsImmunologyProstacyclinBiologyBiochemistrychemistry.chemical_compoundCyclic AMPmedicineHumansCyclic adenosine monophosphateIloprostProtein Interaction MapsPlatelet activationPhosphorylationProtein kinase AKinaseCell BiologyHematologyPlatelet ActivationCyclic AMP-Dependent Protein KinaseschemistryBiochemistryPlatelet aggregation inhibitorPhosphorylationSignal transductionPlatelet Aggregation InhibitorsSignal Transductionmedicine.drugBlood
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Potential and limitations of PKA/ PKG inhibitors for platelet studies

2021

Cyclic nucleotides (cAMP and cGMP) and corresponding protein kinases, protein kinase A (PKA) and protein kinase G (PKG), are the main intracellular mediators of endothelium-derived platelet inhibitors. Pharmacological PKA/PKG inhibitors are often used to discriminate between these two kinase activities and to analyze their underlying mechanisms. Previously we showed that all widely used PKG inhibitors (KT5823, DT3, RP isomers) either did not inhibit PKG or inhibited and even activated platelets independently from PKG. In this study, we examined several PKA inhibitors as well as inhibitors of adenylate and guanylate cyclases to reveal their effects on platelets and establish whether they are…

Blood PlateletsKinaseIntracellular Signaling Peptides and ProteinsAdenylate kinaseHematologyGeneral MedicineKT5720Cyclic AMP-Dependent Protein Kinaseschemistry.chemical_compoundchemistryBiochemistryCyclic AMPCyclic GMP-Dependent Protein Kinasescardiovascular systemHumansPlateletPlatelet activationProtein kinase ACyclic GMPcGMP-dependent protein kinaseIntracellularPlatelets
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Phosphorylation of CalDAG-GEFI by protein kinase A prevents Rap1b activation.

2013

Summary Background Signaling via protein kinase A (PKA) and protein kinase G (PKG) is critical for maintaining platelets in the resting state. Both kinases down-regulate the activity of the small GTPase Rap1b, a critical signaling switch for integrin activation and platelet aggregation. However, the mechanism of Rap1b regulation by PKA and PKG is largely unknown. Objective To identify the PKA phosphorylation sites in calcium and diacylglycerol-regulated guanine nucleotide exchange factor I (CalDAG-GEFI), the main GEF for Rap1b in platelets, and the effect of CalDAG-GEFI phosphorylation in Rap1b activation. Methods The phosphorylation sites in CalDAG-GEFI were identified by radio-active phos…

Blood PlateletsPlatelet AggregationMolecular Sequence DataBiologyMass SpectrometryPhosphorylation cascadeCyclic AMPGuanine Nucleotide Exchange FactorsHumansImmunoprecipitationProtein phosphorylationAmino Acid SequenceCalcium SignalingPhosphorylationProtein kinase ACalcium signalingAlanineSequence Homology Amino AcidKinaseHematologyCyclic AMP-Dependent Protein KinasesEnzyme Activationrab1 GTP-Binding ProteinsHEK293 CellsBiochemistryMutationPhosphorylationGuanine nucleotide exchange factorGuanosine TriphosphatecGMP-dependent protein kinasePlasmidsSignal TransductionJournal of thrombosis and haemostasis : JTH
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