Search results for "Protein kinases"

showing 10 items of 427 documents

Pentoxifylline Prevents Loss of PP2A Phosphatase Activity and Recruitment of Histone Acetyltransferases to Proinflammatory Genes in Acute Pancreatitis

2009

Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production. Our aim was to elucidate the mechanism of action of pentoxifylline as an anti-inflammatory agent in acute pancreatitis. Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied. Phosphorylation of ERK and ERK kinase (MEK1/2), as well as PP2A, PP2B, and PP2C serine/threonine phosphatase activiti…

MaleMAPK/ERK pathwayChromatin ImmunoprecipitationPhosphodiesterase InhibitorsBlotting WesternPhosphataseAnti-Inflammatory AgentsPharmacologyBiologyCell LinePentoxifyllineProinflammatory cytokineCyclic AMPPhosphoprotein PhosphatasesmedicineAnimalsPentoxifyllineRats WistarExtracellular Signal-Regulated MAP KinasesHistone AcetyltransferasesInflammationPharmacologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaProtein phosphatase 2medicine.diseaseCyclic Nucleotide Phosphodiesterases Type 2RatsEnzyme ActivationPancreatitisBiochemistryAcute DiseaseRNAMolecular MedicinePhosphorylationPancreatitisMitogen-Activated Protein KinasesChromatin immunoprecipitationmedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Differential modulation of CYP2E1 activity by cAMP-dependent protein kinase upon Ser129 replacement.

1998

Many toxic compounds are activated by cytochrome P450 (CYP) 2E1 to reactive metabolites, which represents a potential hazard for cellular homeostasis. Therefore knowledge about CYP2E1 regulation could be of great biological importance. It has been shown that CYP2E1 is controlled transcriptionally and post-translationally by phosphorylation. In the present study we investigated the role of serine-129 (Ser129) in the protein kinase A (PKA) recognition sequence motif Arg-Arg-Phe-Ser129. To gain further insights into the possible relevance of Ser129 for CYP2E1 function, Ser129 was replaced by alanine (Ala) or glycine (Gly) by site-directed mutations of the cDNA coding for CYP2E1. The mutant cDN…

MaleMutantCellular homeostasisTransfectionDimethylnitrosamineSubstrate SpecificityRats Sprague-DawleyMiceCricetulusCricetinaeIsoniazidSerineAnimalsEnzyme inducerPhosphorylationProtein kinase ALungCells Culturedchemistry.chemical_classificationMice Inbred BALB CbiologyCytochrome P-450 CYP2E1Cell BiologyFibroblastsMolecular biologyCyclic AMP-Dependent Protein KinasesAmino acidRatsEnzymechemistryBiochemistryAmino Acid SubstitutionBucladesineEnzyme InductionInactivation MetabolicMutationbiology.proteinMicrosomes LiverPhosphorylationDemethylaseMutagensExperimental cell research
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Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle

2005

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 µmol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 µmol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 µmol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1…

MaleNitroprussideThapsigarginCharybdotoxinPhysiologyMouse ileumIn Vitro TechniquesPharmacologyApaminSettore BIO/09 - FisiologiaPotassium channelsMicePotassium Channels Calcium-Activatedchemistry.chemical_compoundIleumPhysiology (medical)Cyclic GMP-Dependent Protein KinasesPotassium Channel BlockersmedicineAnimalsNitric Oxide DonorsChannel blockerCyclic GMPPharmacologyRyanodineRyanodine receptorCalcium storeMuscle SmoothPotassium channel blockerNitric oxideGeneral MedicineTetraethylammonium chlorideMice Inbred C57BLchemistryCalciumSodium nitroprussideMuscle ContractionSignal Transductionmedicine.drug
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Proteins from rat liver cytosol which stimulate mRNA transport. Purification and interactions with the nuclear envelope mRNA translocation system.

1986

Two polysome-associated proteins with particular affinities for poly(A) have been purified from rat liver. These proteins stimulate the efflux of mRNA from isolated nuclei in conditions under which such efflux closely stimulates mRNA transport in vivo, and they are therefore considered as mRNA-transport-stimulatory proteins. Their interaction with the mRNA-translocation system in isolated nuclear envelopes has been studied. The results are generally consistent with the most recently proposed kinetic model of mRNA translocation. One protein, P58, has not been described previously. It inhibits the protein kinase that down-regulates the NTPase, it enhances the NTPase activity in both the prese…

MaleNucleocytoplasmic Transport ProteinsNuclear EnvelopeRNA-binding proteinBiologyBiochemistryCytosolPhosphoprotein PhosphatasesMRNA transportAnimalsRNA MessengerProtein kinase AMessenger RNANucleocytoplasmic Transport ProteinsRNARNA-Binding ProteinsBiological TransportRats Inbred StrainsNucleoside-TriphosphatasePhosphoric Monoester HydrolasesCell biologyRatsCytosolBiochemistryLiverPolyribosomesPhosphorylationCarrier ProteinsPoly AProtein KinasesEuropean journal of biochemistry
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Identification of the novel D297fsX318 PINK1 mutation and phenotype variation in a family with early-onset Parkinson's disease

2008

Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which results in a loss of kinase domain on the PINK1 protein (D297fsX318). This mutation was identified in two brothers with early-onset Parkinson disease (EOPD) from a Sicilian consanguineous family. Of note, while one of the two patients developed mental deterioration and psychiatric problems, the other showed no cognitive decline. The present study supports the view that PINK1 is a pathogenic gene in some Italian families with EOPD and contributes to define the PINK1-associated phenotype. Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which r…

MaleParkinson's diseaseGenotypeParkinson's diseaseMolecular Sequence DataPINK1DiseaseBiologyAntiparkinson AgentsLevodopaExonmedicineHumansAmino Acid SequenceAge of OnsetCognitive declineGeneAgedGeneticsGenotype–phenotype correlationPINK1Parkinson DiseaseExonsFamilial formmedicine.diseasePhenotypePedigreeSettore BIO/18 - GeneticaPhenotypeNeurologyMutationMutation (genetic algorithm)Settore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyCognition DisordersProtein KinasesGene DeletionParkinsonism & Related Disorders
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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Human periodontal fibroblast response to a nanostructured hydroxyapatite bone replacement graft in vitro

2007

Abstract Objective The efficacy of nanostructured hydroxyapatite (NHA) for the treatment of osseous defects has been demonstrated in recent studies, even though the underlining biological mechanism is still poorly known. This study examined the alterations in cellular adhesion and mitogenic responses in human periodontal ligament (PDL) cells treated with a novel nanostructured hydroxyapatite bone graft substitute and characterized associated changes in cellular signalling pathways. Methods Cultured PDL cells were stimulated with NHA in a surface coated form. Proliferation was determined by bromodeoxyuridine (BrdU) incorporation and cell adhesion was analysed by a colorimetric assay. In orde…

MalePeriodontal LigamentIntegrinBiocompatible MaterialsFocal adhesionstomatognathic systemCell AdhesionHumansEpidermal growth factor receptorCell adhesionProtein kinase AGeneral DentistryProtein kinase BCells CulturedCell ProliferationbiologyChemistryCell BiologyGeneral MedicineAnatomyFibroblastsNanostructuresCell biologyErbB ReceptorsDurapatiteOtorhinolaryngologyFocal Adhesion Kinase 1Mitogen-activated protein kinasebiology.proteinPhosphorylationFemaleMitogen-Activated Protein KinasesSignal TransductionArchives of Oral Biology
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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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PINK1 displays tissue-specific subcellular location and regulates apoptosis and cell growth in breast cancer cells.

2010

The PINK1 gene is mutated in the germ line of patients with hereditary early-onset Parkinson disease, and PINK1 prosurvival function at neuronal mitochondria has been related with the etiology of this disease. However, the expression and function of PINK1 protein in nonneuronal tissues has not been determined yet. Here, we have analyzed PINK1 protein expression and subcellular distribution in normal and neoplastic human tissues and investigated the function of PINK1 in breast carcinoma cells. PINK1 protein, as stained by a specific anti-PINK1 monoclonal antibody, was widely expressed in human tissues, displaying high expression in epithelial tissues and in the central nervous system and low…

MaleProgrammed cell deathLung NeoplasmsApoptosisBreast NeoplasmsBiologymedicine.disease_causePathology and Forensic MedicineMiceCell Line TumormedicineAnimalsHumansTissue DistributionCell ProliferationCell growthCancermedicine.diseaseSquamous carcinomaCancer researchCarcinoma Squamous CellEctopic expressionFemaleBreast diseaseCarcinogenesisBreast carcinomaProtein KinasesHuman pathology
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Mutations in the RAS-MAPK, PI(3)K (phosphatidylinositol-3-OH kinase) signaling network correlate with poor survival in a population-based series of c…

2008

The RAS-MAPK, PI (3)K signaling pathways form a network that play a central role in tumorigenesis. The BRAF, KRAS and PI3KCA genes code 3 partners of this network and have been found to be activated by mutation in colorectal cancer; these mutations lead to unrestricted cell growth. We evaluated the clinicopathological features and the prognosis of patients with activated-network colon cancers in a population-based study. A total of 586 colon adenocarcinomas were evaluated using sequencing for mutations of KRAS and PI3KCA, and allelic discrimination for mutation of BRAF. Clinicopathological characteristics were correlated to the risk of bearing a mutation of the network using logistic regres…

MaleProto-Oncogene Proteins B-rafCancer Researchmedicine.medical_specialtyClass I Phosphatidylinositol 3-KinasesColorectal cancerPopulationAdenocarcinomaBiologymedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesProto-Oncogene ProteinsInternal medicineBiomarkers TumormedicineHumanseducationSurvival rateAgedMutationeducation.field_of_studyMicrosatellite instabilityCancermedicine.diseaseSurvival RateEndocrinologyOncologyColonic NeoplasmsMutationras ProteinsCancer researchFemaleMicrosatellite InstabilityFranceKRASMitogen-Activated Protein KinasesCarcinogenesisSignal TransductionInternational Journal of Cancer
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