Search results for " Protein Kinase"

showing 10 items of 540 documents

The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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To the research of treatments for the typical calcific disease of old aortic valve in the omics era: Is the miR-195 a therapeutic signature via targe…

2020

Calcific aortic valve disease (CAVD) is the most frequent form of val-vular pathology [1,2], with high percentages of mortality and morbidityin Western populations, so much to be a very public health problem [2].Diverse millions of subjects are affected by CAVD and the major numberare old individuals (65- older), even if some have a younger age and aregenerally affected by congenital bicuspid aortic valve (BAV) disease[2,3]. CAVD in BAV individuals arises decades earlier respect to subjectswith the physiological tricuspid aortic valve [3]. Furthermore, it can leadto death if untreated with surgical aortic valve replacement or trans-catheter aortic valve implantation, its unique treatments […

Aortic valvemedicine.medical_specialtybicuspid aortic valvebusiness.industryp38 mitogen-activated protein kinasesDiseasemedicine.diseaseOmicsBicuspid aortic valvemedicine.anatomical_structuremiR-195Internal medicinemedicineCardiologyCardiology and Cardiovascular Medicinebusiness
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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

2014

Purpose Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. Methods Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (…

MaleRetinal Ganglion Cellsmedicine.medical_specialtyAgingSuperior ColliculiMAP Kinase Signaling SystemBlotting WesternRetinal ganglionRetinaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicinemedicineAnimalsAxonPhosphorylationMitogen-Activated Protein Kinase 7030304 developmental biologyBrain-derived neurotrophic factorMitogen-Activated Protein Kinase 10303 health sciencesRetinaMitogen-Activated Protein Kinase 3biologyChemistryBrain-Derived Neurotrophic FactorBrainAnatomyRatsmedicine.anatomical_structureEndocrinologynervous systemRetinal ganglion cellTrk receptorOptic Nerve InjuriesIntravitreal Injectionsbiology.proteinsense organsNeuroglia030217 neurology & neurosurgeryNeurotrophinInvestigative ophthalmologyvisual science
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Advances in Targeting Signal Transduction Pathways

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Lin Sun 1,2 , Nicole M. Davis 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Lucio Cocco 3 , Camilla Evangelisti 4 , Francesca Chiarini 4 , Alberto M. Martelli 3,4 , Massimo Libra 5 , Saverio Candido 5 , Giovanni Ligresti 5 , Grazia Malaponte 5 , Maria C. Mazzarino 5 , Paolo Fagone 5 , Marco Donia 5 , Ferdinando Nicoletti 5 , Jerry Polesel 6 , Renato Talamini 6 , Jorg Basecke 7 , Sanja Mijatovic 8 , Danijela Maksimovic-Ivanic 8 , Michele Milella 9 , Agostino Tafuri 10 , Joanna Dulinska-Litewka 11 , Piotr Laidler 11 , Antonio B. D’Assoro 12 , Lyudmyla Drobot 13 , Kazuo Umezawa 14 , Giuseppe Montalto 15 , Melchiorre Cer…

cancer stem cellsAMPKtherapy resistanceReviewsLibrary scienceAntineoplastic AgentsrafBiologyPI3Kampk03 medical and health sciences0302 clinical medicineCANCER STEM CELLSNeoplasmsAnimalsHumansUniversity medicalMolecular Targeted TherapyAkt; AMPK; Cancer stem cells; Metformin; MTOR; PI3K; Raf; Targeted therapy; Therapy resistanceTreatment resistanceProtein Kinase Inhibitors030304 developmental biology0303 health sciencesRoswell Park Cancer InstituteAktCancer stem cellAKTMTORAMP-ACTIVATED PROTEIN KINASE (AMPK)Raftargeted therapyMetformin3. Good healthGene Expression Regulation NeoplasticCell stressOncologyDrug Resistance NeoplasmDrug Designtargeted therapy; metformin; therapy resistance; pi3k; akt; ampk; cancer stem cells; raf; mtor030220 oncology & carcinogenesisMutationmTORMolecular targetsCancer researchmetforminSignal Transduction
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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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Specific and global regulation of mRNA stability during osmotic stress in Saccharomyces cerevisiae.

2009

Hyperosmotic stress yields reprogramming of gene expression in Saccharomyces cerevisiae cells. Most of this response is orchestrated by Hog1, a stress-activated, mitogen-activated protein kinase (MAPK) homologous to human p38. We investigated, on a genomic scale, the contribution of changes in transcription rates and mRNA stabilities to the modulation of mRNA amounts during the response to osmotic stress in wild-type and hog1 mutant cells. Mild osmotic shock induces a broad mRNA destabilization; however, osmo-mRNAs are up-regulated by increasing both transcription rates and mRNA half-lives. In contrast, mild or severe osmotic stress in hog1 mutants, or severe osmotic stress in wild-type cel…

BioquímicaMessenger RNASaccharomyces cerevisiae ProteinsTranscription GeneticOsmotic shockMRNA destabilizationRNA Stabilityp38 mitogen-activated protein kinasesSaccharomyces cerevisiaeMRNA stabilizationSaccharomyces cerevisiaeBiologybiology.organism_classificationMolecular biologyArticleGenètica molecularCell biologyOsmotic PressureGene Expression Regulation FungalGene expressionOsmotic pressureRNA MessengerMitogen-Activated Protein KinasesMolecular Biology
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Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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Molecular mechanisms of sorafenib action in liver cancer cells.

2012

Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …

SorafenibDNA ReplicationNiacinamideCarcinoma HepatocellularDNA RepairTranscription GeneticAngiogenesisCell SurvivalPyridinesApoptosisPharmacologyBiologysorafenib HCC mini-chromosome maintenance genes Dickkopf1 Harakiri Acheron/LARP6 YAP1 cell cycle microarray global gene expression analysisCell Line TumormedicineCell AdhesionHumansneoplasmsMolecular BiologyProtein Kinase InhibitorsCell ProliferationYAP1Neovascularization PathologicCell growthGene Expression ProfilingPhenylurea CompoundsBenzenesulfonatesCell CycleLiver NeoplasmsBiological TransportCell BiologyCell cycleSorafenibmedicine.diseasedigestive system diseasesMechanism of actionHepatocellular carcinomaProtein Biosynthesismedicine.symptomMitogen-Activated Protein KinasesLiver cancerDevelopmental Biologymedicine.drugSignal Transduction
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TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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