Search results for "Phosphorylation"

showing 10 items of 975 documents

Phosphorylation of Elp1 by Hrr25 is required for elongator-dependent tRNA modification in yeast.

2014

Elongator is a conserved protein complex comprising six different polypeptides that has been ascribed a wide range of functions, but which is now known to be required for modification of uridine residues in the wobble position of a subset of tRNAs in yeast, plants, worms and mammals. In previous work, we showed that Elongator's largest subunit (Elp1; also known as Iki3) was phosphorylated and implicated the yeast casein kinase I Hrr25 in Elongator function. Here we report identification of nine in vivo phosphorylation sites within Elp1 and show that four of these, clustered close to the Elp1 C-terminus and adjacent to a region that binds tRNA, are important for Elongator's tRNA modification…

ProteomicsSaccharomyces cerevisiae Proteinslcsh:QH426-470Saccharomyces cerevisiaeBiochemistryMolecular GeneticsRNA TransferGene Expression Regulation FungalMolecular Cell BiologyGeneticsFungal GeneticsPhosphorylationPost-Translational ModificationUridineMolecular BiologyAdaptor Proteins Signal TransducingHistone AcetyltransferasesAlanineSpectrometric Identification of ProteinsBiology and life sciencesCasein Kinase INucleotidesMicrobial GeneticsProteinsCell BiologyPeptide Elongation Factorslcsh:GeneticsPhenotypeMultiprotein ComplexesRNAMolecular ComplexesTransfer RNAAnticodonsResearch ArticlePLoS genetics
researchProduct

SIK2 orchestrates actin-dependent host response upon Salmonella infection

2021

Significance Through conducting quantitative proteomics upon Salmonella infection, we identified a SIK2 signaling network, implementing the kinase into a so far concealed biological function. Our data exposed SIK2 as a central orchestrator of an actin regulatory network, coordinating the stability of Salmonella-containing vacuole (SCV) and cellular actin assembly, in order to limit the acute phase of the infection. Most strikingly, SIK2 is not exclusively acting locally on actin assembly associated with the SCV but impacts the actin cytoskeleton architecture in its entirety upon Salmonella infection. Our work provides a mechanistic framework for how the actin cytoskeleton is regulated and h…

ProteomicsSalmonellaactin cytoskeletonImmunoblottingArp2/3 complexSalmonella infectionmacromolecular substancesProtein Serine-Threonine Kinasesmedicine.disease_causeBiochemistry03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineXenophagyAnimalsHumansArp2/3 complexProtein Interaction MapsPhosphorylationActinCells Cultured030304 developmental biologyActin nucleation0303 health sciencesMultidisciplinarybiologyEpithelial CellsBiological Sciencesmedicine.diseaseActin cytoskeletonHCT116 CellsPhosphoproteinsActinsCell biologySalmonella-containing vacuoleHEK293 CellsFormins407Host-Pathogen Interactionsbiology.proteinRNA Interference030217 neurology & neurosurgeryhost–pathogen interactionsHeLa CellsSignal TransductionProceedings of the National Academy of Sciences of the United States of America
researchProduct

Mitochondrial proteomics profile points oxidative phosphorylation as main target for beauvericin and enniatin B mixture

2020

Abstract Beauvericin (BEA) and enniatin B (EN B) are non-legislated Fusarium mycotoxins usually found in cereal and cereal-based products all around the world. By the proteomic analysis of mitochondria enriched extracts from Jurkat cells exposed for 24 h to three concentrations of BEA:EN B (0.01–0.1–0.5 μM), a number of 1821 proteins (202 mitochondrial) were identified and relatively quantified. 340 proteins (59 mitochondrial) were statistically significant altered in our samples (Anova p-value ≤ 0.05 and fold change (FC) ≥1.5). The protein mitochondrial translational release factor 1 like (MTRF1L) was the most abundant protein in the three mycotoxin exposures studied. The mycotoxins mixtur…

ProteomicsTranscription GeneticOxidative phosphorylationMitochondrionToxicologyProteomicsRibosomeJurkat cellsOxidative PhosphorylationElectron TransportMitochondrial ProteinsJurkat Cells03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyDepsipeptidesHumans030304 developmental biology0303 health sciencesfood and beverages04 agricultural and veterinary sciencesGeneral Medicine040401 food scienceBeauvericinFold changeMitochondriachemistryBiochemistryBacterial outer membraneFood ScienceFood and Chemical Toxicology
researchProduct

Multi-laboratory experiment PME11 for the standardization of phosphoproteome analysis

2022

6 p.-2 fig.-2 tab.

ProteomicsenrichmentStandardizationProteomeComputer scienceCellbiologiMass-spectrometryBiophysics610 Medicine & healthComputational biologyBioinformatik och systembiologiProteòmicaProteomics:Chemical Phenomena::Biochemical Phenomena::Phosphorylation [PHENOMENA AND PROCESSES]BiochemistryExperimentFosforilació:Natural Science Disciplines::Biological Science Disciplines::Biochemistry::Proteomics [DISCIPLINES AND OCCUPATIONS]:Investigative Techniques::Epidemiologic Methods::Epidemiologic Research Design::Reproducibility of Results [ANALYTICAL DIAGNOSTIC AND THERAPEUTIC TECHNIQUES AND EQUIPMENT]Inter-laboratoryPhosphorylationquality controlEpidemiologia610 Medicine & healthBioinformatics and Systems BiologyFosfoproteïnes:fenómenos químicos::fenómenos bioquímicos::fosforilación [FENÓMENOS Y PROCESOS]:disciplinas de las ciencias naturales::disciplinas de las ciencias biológicas::bioquímica::proteómica [DISCIPLINAS Y OCUPACIONES]PhosphoproteomicsBiochemistry and Molecular BiologyReproducibility of ResultsCell BiologyReference Standards:técnicas de investigación::métodos epidemiológicos::diseño de la investigación epidemiológica::reproducibilidad de los resultados [TÉCNICAS Y EQUIPOS ANALÍTICOS DIAGNÓSTICOS Y TERAPÉUTICOS]NormalitzacióPhosphoproteinsStandardizationReference samplePhosphoproteomeProteomeLaboratory experimentLaboratoriesBiokemi och molekylärbiologi
researchProduct

B-Raf Acts via the ROCKII/LIMK/Cofilin Pathway To Maintain Actin Stress Fibers in Fibroblasts

2004

Members of the Raf family of serine/threonine protein kinases have been well studied in a variety of organisms ranging from Drosophila to humans. Three raf homologues (raf-1, B-raf, and A-raf) exist in mammals, while a single prototypic homologue exists in lower organisms. A wealth of genetic and biochemical data have indicated that Raf family members are signaling kinases that are integral components of the conserved Ras/Raf/MEK/ERK signaling cascade. Following activation by Ras-dependent mechanisms, Raf protein kinases act as mitogen-activated protein (MAP) kinase kinase kinases, which phosphorylate and activate the type 1/2 MAP kinase kinases, also known as MEK1/2. These dual-specificity…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwaymacromolecular substancesProtein Serine-Threonine KinasesTransfectionCell LineProto-Oncogene Proteins B-rafLim kinaseMiceCell MovementStress FibersAnimalsHumansPhosphorylationKinase activityCell Growth and DevelopmentMolecular BiologyRho-associated protein kinaseCytoskeletonrho-Associated KinasesbiologyKinaseMicrofilament ProteinsIntracellular Signaling Peptides and ProteinsLim KinasesCell BiologyFibroblastsMolecular biologyActinsCell biologyProto-Oncogene Proteins c-rafActin Depolymerizing FactorsMitogen-activated protein kinasebiology.proteinProto-Oncogene Proteins c-rafMitogen-Activated Protein KinasesProtein KinasesSignal TransductionMolecular and Cellular Biology
researchProduct

Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.

2012

Reactive oxygen species (ROS) are involved in the pathogenesis of many inflammatory diseases such as chronic obstructive pulmonary disease (COPD). They can alter the expression of genes involved in cellular damage by activating transcription factors, including the NF-κB and the activator protein 1 (AP-1). Phosphodiesterase type 4 (PDE4) inhibitors have anti-inflammatory and antioxidant effects, as described in in vivo and in vitro COPD models. This study analysed the effects of piclamilast, a selective PDE4 inhibitor, on modulating the global gene expression profile in A549 cells exposed to H(2)O(2).Changes in gene expression were analysed using high-density Affymetrix microarrays and valid…

Proto-Oncogene Proteins c-junPyridinesActivating transcription factorApoptosisBiologymedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundPulmonary Disease Chronic ObstructiveIn vivoAnnexinCell Line TumorGene expressionmedicineHumansRNA MessengerPhosphorylationCell ProliferationOligonucleotide Array Sequence AnalysisA549 cellGene Expression ProfilingNF-kappa BGeneral MedicineCell Cycle CheckpointsHydrogen PeroxideMolecular biologyTranscription Factor AP-1chemistryGene Expression RegulationAlveolar Epithelial CellsBenzamidesPhosphodiesterase 4 InhibitorsSignal transductionReactive Oxygen SpeciesPiclamilastOxidative stressSignal TransductionFree radical research
researchProduct

Mitochondrial complex I: new insights from inhibitor assays

2000

The NADH:ubiquinone oxidoreductase (complex I) of the mitochondrial respiratory chain is by far the most complicated of the proton-translocating enzymes involved in the oxidative phosphorylation. Many clues regarding both electron transfer and proton translocation are still unknown. In this sense, inhibitor assays are relevant and useful pieces for elaborating a suitable model to explain the elusive bioenergetic mechanism of this enzyme. This short review presents the most recent advances in inhibitor studies and highlights the major controversies.

Proton translocationchemistry.chemical_classificationNADH-Ubiquinone OxidoreductaseMechanism (biology)Cell BiologyPlant ScienceGeneral MedicineOxidative phosphorylationBiologyMitochondrial respiratory chainEnzymeBiochemistrychemistryOxidoreductaseMitochondrial Complex IProtoplasma
researchProduct

Oxidative Stress and Respiratory System: Pharmacological and Clinical Reappraisal of N-Acetylcysteine

2014

Abstract The large surface area for gas exchange makes the respiratory system particularly susceptible to oxidative stress-mediated injury. Both endogenous and exogenous pro-oxidants (e.g. cigarette smoke) trigger activation of leukocytes and host defenses. These mechanisms interact in a ìmultilevel cycleî responsible for the control of the oxidant/antioxidant homeostasis. Several studies have demonstrated the presence of increased oxidative stress and decreased antioxidants (e.g. reduced glutathione [GSH]) in subjects with chronic obstructive pulmonary disease (COPD), but the contribution of oxidative stress to the pathophysiology of COPD is generally only minimally discussed. The aim of t…

Pulmonary and Respiratory MedicineChronic ObstructiveAntioxidantantioxidantNeutrophilsmedicine.medical_treatmentAntioxidant; Copd exacerbation; Lung function; Small airways; Acetylcysteine; Antioxidants; Bronchitis Chronic; Disease Progression; Expectorants; Forced Expiratory Volume; Hospitalization; Humans; Macrophages; Neutrophils; Pulmonary Disease Chronic Obstructive; Reactive Oxygen Species; Respiratory Physiological Phenomena; Oxidative Stress; Pulmonary and Respiratory MedicineAntioxidant; Copd exacerbation; Lung function; Small airways; Acetylcysteine; Antioxidants; Bronchitis Chronic; Disease Progression; Expectorants; Forced Expiratory Volume; Hospitalization; Humans; Macrophages; Neutrophils; Pulmonary Disease Chronic Obstructive; Reactive Oxygen Species; Respiratory Physiological Phenomena; Oxidative StressOxidative phosphorylationReviewSettore MED/10 - Malattie Dell'Apparato Respiratoriomedicine.disease_causeAntioxidantsAcetylcysteinePulmonary Diseasechemistry.chemical_compoundPulmonary Disease Chronic ObstructiveCOPD exacerbationForced Expiratory VolumemedicineHumansRespiratory systemChronicBronchitisExpectorantschemistry.chemical_classificationCOPDReactive oxygen speciessmall airwaysbusiness.industryMacrophageslung functionGlutathionemedicine.diseaseAcetylcysteineBronchitis ChronicHospitalizationOxidative StresschemistryImmunologyDisease ProgressionRespiratory Physiological PhenomenabusinessReactive Oxygen SpeciesOxidative stressmedicine.drug
researchProduct

Regulation of endothelial nitric oxide synthase (eNOS) in myocardium subjected to cardioplegic arrest.

2009

BACKGROUND: Nitric oxide (NO) production by both coronary endothelial cells and cardiomyocytes is thought to play a significant role in myocardial pathophysiology following ischemia/reperfusion (I/R). METHODS: In thirteen pigs subjected to 1 hour cardioplegic arrest (CA) on CPB, left ventricular (LV) biopsies were collected prior to CPB (baseline), at 60 min CPA, at 15 and 30 min reperfusion on CPB, and at 120 min post CPB. LV specimens were immunocytochemically stained against phospho-eNOS Ser1177 , phospho-eNOS Thr495 , phosphorylated ERK1/2, and AKT/PKB. Four additional pigs without CA served as controls. Cardiomyocytes were quantitatively investigated using TV densitometry (gray units: …

Pulmonary and Respiratory MedicineMaleThreoninemedicine.medical_specialtyTime FactorsNitric Oxide Synthase Type IIISwineHeart VentriclesIschemiaEnos phosphorylationVentricular Function LeftNitric oxidechemistry.chemical_compoundEnosInternal medicinemedicineSerineAnimalsPhosphorylationProtein kinase BMitogen-Activated Protein Kinase 1Cardiopulmonary BypassMitogen-Activated Protein Kinase 3Endothelial nitric oxide synthasebiologybusiness.industryMyocardiummedicine.diseasebiology.organism_classificationImmunohistochemistryMyocardial ContractionPathophysiologyEnzyme ActivationEndocrinologychemistryModels AnimalCardiologyHeart Arrest InducedPhosphorylationSurgeryFemaleCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktThe Thoracic and cardiovascular surgeon
researchProduct

Aclidinium inhibits human lung fibroblast to myofibroblast transition

2011

Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition. Methods Human bronchial fibroblasts were stimulated with carbachol (10 −8 to 10 −5  M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10 −9 to 10 −7  M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyCarbacholChronic Obstructive Pulmonary DiseaseBronchiMuscarinic AntagonistsBiologyCholinergic AgonistsCollagen Type ITransforming Growth Factor beta1Downregulation and upregulationWestern blotanticholinergicCell MovementInternal medicinemedicineCOPDHumans1506RNA MessengerAutocrine signallingFibroblastMyofibroblastsCells CulturedCell Proliferationmedicine.diagnostic_testDose-Response Relationship Drugairway epitheliumCell Differentiationasthmainterstitial fibrosisFibroblastsAdenosineMolecular biologymyofibroblastActinsUp-RegulationEndocrinologymedicine.anatomical_structurePhosphorylationFibroblastCarbacholMyofibroblastmedicine.drugTropanesThorax
researchProduct