Search results for "Kinase"

showing 10 items of 2635 documents

Emerging Therapies in Immune Thrombocytopenia

2021

Immune thrombocytopenia (ITP) is a rare autoimmune disorder caused by peripheral platelet destruction and inappropriate bone marrow production. The management of ITP is based on the utilization of steroids, intravenous immunoglobulins, rituximab, thrombopoietin receptor agonists (TPO-RAs), immunosuppressants and splenectomy. Recent advances in the understanding of its pathogenesis have opened new fields of therapeutic interventions. The phagocytosis of platelets by splenic macrophages could be inhibited by spleen tyrosine kinase (Syk) or Bruton tyrosine kinase (BTK) inhibitors. The clearance of antiplatelet antibodies could be accelerated by blocking the neonatal Fc receptor (FcRn), while n…

TPO-RAlcsh:MedicineSykReview03 medical and health sciencesClassical complement pathway0302 clinical medicinehemic and lymphatic diseasesMedicineBruton's tyrosine kinasePlateletB celldesialylationbiologybusiness.industrylcsh:RBTK inhibitorAutoantibodyGeneral MedicineFcRnmedicine.anatomical_structureimmune thrombocytopeniaSyk inhibitor030220 oncology & carcinogenesisImmunologybiology.proteinRituximabAntibodybusiness030215 immunologymedicine.drugJournal of Clinical Medicine
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Hematopoietic stem cell quiescence and function are controlled by the CYLD–TRAF2–p38MAPK pathway

2015

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

TRAF2Tumor suppressor geneMAP Kinase Signaling SystemImmunologyRegulatorBiologyp38 Mitogen-Activated Protein KinasesArticleMicemedicineAnimalsImmunology and AllergyMice KnockoutRegulation of gene expressionNF-kappa BHematopoietic stem cellCell BiologyHematopoietic Stem CellsTNF Receptor-Associated Factor 2PhenotypeDeubiquitinating Enzyme CYLDCell biologyCysteine EndopeptidasesHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutationStem cellJournal of Experimental Medicine
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Focal DNA Copy Number Changes in Neuroblastoma Target MYCN Regulated Genes

2013

Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system cells. Recurrent genomic alterations include MYCN and ALK amplification as well as recurrent patterns of gains and losses of whole or large partial chromosome segments. A recent whole genome sequencing effort yielded no frequently recurring mutations in genes other than those affecting ALK. However, the study further stresses the importance of DNA copy number alterations in this disease, in particular for genes implicated in neuritogenesis. Here we provide additional evidence for the importance of focal DNA copy number gains and losses, which are predominantly observed in MYCN amplified tumors. A focal 5 kb…

TRANSCRIPTIONAL TARGETNeuroblastoma/geneticsPsychologie appliquéeMedizinlcsh:MedicineChromosomal DisordersNeuroblastoma0302 clinical medicineRGS Proteins/geneticsGene duplicationMolecular Cell BiologyBasic Cancer ResearchTUMOR-SUPPRESSORALK KINASElcsh:ScienceNeurological TumorsGeneticsRegulation of gene expressionOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinACTIVATING MUTATIONSMultidisciplinaryCancer Risk FactorsHomozygoteChromosomal Deletions and DuplicationsNuclear ProteinsGenomicsSciences bio-médicales et agricolesSignaling in Selected DisciplinesCANCEROncogene Proteins/geneticsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisMedicineRNA Long NoncodingBiologieResearch ArticleSignal TransductionEXPRESSIONDNA Copy Number VariationsGenetic Causes of CancerDown-RegulationGenomicsBiologyMolecular Genetics03 medical and health sciencesGenome Analysis ToolsNeuroblastomaCell Line TumormicroRNAmedicineGeneticsCancer GeneticsHumansGene RegulationGeneneoplasmsBiology030304 developmental biologyOncogenic SignalingN-MYCTHERAPEUTIC TARGETRECEPTORMICRORNAlcsh:RBiology and Life SciencesChromosomeCancers and NeoplasmsHuman Geneticsmedicine.diseaseNuclear Proteins/geneticsMicroRNAs/geneticsMicroRNAsPediatric Oncologylcsh:QGenome Expression AnalysisN-MycRGS ProteinsPLoS ONE
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Fibronectin-bound α5β1 integrins sense load and signal to reinforce adhesion in less than a second

2017

Integrin-mediated mechanosensing of the extracellular environment allows cells to control adhesion and signalling. Whether cells sense and respond to force immediately upon ligand-binding is unknown. Here, we report that during adhesion initiation, fibroblasts respond to mechanical load by strengthening integrin-mediated adhesion to fibronectin (FN) in a biphasic manner. In the first phase, which depends on talin and kindlin as well as on the actin nucleators Arp2/3 and mDia, FN-engaged α5β1 integrins activate focal adhesion kinase (FAK) and c-Src in less than 0.5 s to steeply strengthen α5β1- and αV-class integrin-mediated adhesion. When the mechanical load exceeds a certain threshold, fib…

Talin0301 basic medicineTime FactorsMaterials scienceIntegrinNanotechnologyMechanotransduction CellularActin-Related Protein 2-3 ComplexCSK Tyrosine-Protein KinaseFocal adhesionMice03 medical and health sciencesCell AdhesionAnimalsGeneral Materials ScienceMechanotransductionCell adhesionActinMice KnockoutbiologyCell adhesion moleculeMechanical EngineeringGeneral ChemistryAdhesionFibroblastsCondensed Matter PhysicsFibronectinsCell biologyFibronectinsrc-Family Kinases030104 developmental biologyMechanics of MaterialsFocal Adhesion Kinase 1biology.proteinApplications of AFM; integrins; Mechanotransduction; Microscopy; Nanoscale biophysicsIntegrin alpha5beta1Nature Materials
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The high-performance technology CRISPR/Cas9 improves knowledge and management of acute myeloid leukemia

2021

Knowledge on acute myeloid leukemia pathogenesis and treatment has progressed recently, but not enough to provide ideal management. Improving the prognosis of acute myeloid leukemia patients depends on advances in molecular biology for the detection of new therapeutic targets and the production of effective drugs. The CRISPR/Cas9 technology allows gene insertions and deletions and it is the first step in investigating the function of their encoded proteins. Thus, new experimental models have been developed and progress has been made in understanding protein metabolism, antitumor activity, leukemic cell maintenance, differentiation, growth, apoptosis, and self-renewal, the combined pathogene…

TechnologyCD38acute myeloid leukemiamedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologycd38bcl2chemistry.chemical_compoundcrispr/cas9flt3 inhibitorshemic and lymphatic diseasesmedicineCRISPRHumansMidostaurinProtein Kinase InhibitorsCell ProliferationMutationCas9business.industryCell growthRMyeloid leukemiamedicine.diseaseidh2LeukemiaLeukemia Myeloid Acutechemistryfms-Like Tyrosine Kinase 3MutationCancer researchMedicineCRISPR-Cas SystemsbusinessBiomedical Papers
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Sustained activation of mTOR pathway in embryonic neural stem cells leads to development of tuberous sclerosis complex-associated lesions

2011

SummaryTuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by hamartomatous neurological lesions that exhibit abnormal cell proliferation and differentiation. Hyperactivation of mTOR pathway by mutations in either the Tsc1 or Tsc2 gene underlies TSC pathogenesis, but involvement of specific neural cell populations in the formation of TSC-associated neurological lesions remains unclear. We deleted Tsc1 in Emx1-expressing embryonic telencephalic neural stem cells (NSCs) and found that mutant mice faithfully recapitulated TSC neuropathological lesions, such as cortical lamination defects and subependymal nodules (SENs). These alterations were caused by enhanced gen…

Telencephaloncongenital hereditary and neonatal diseases and abnormalitiesCellular differentiationNeuroepithelial CellsEmbryonic DevelopmentBiologyTuberous Sclerosis Complex 1 Proteinmurine modelCerebral VentriclesMiceNeural Stem CellsCell MovementTuberous SclerosismedicineGeneticsAnimalsAnimals; Animals Newborn; Cell Differentiation; Cell Movement; Cell Proliferation; Cerebral Ventricles; Embryonic Development; Embryonic Stem Cells; Epilepsy; Gene Silencing; Gene Targeting; Megalencephaly; Mice; Mutation; Neural Stem Cells; Neuroepithelial Cells; Neurons; TOR Serine-Threonine Kinases; Telencephalon; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins; Signal TransductionGene SilencingNeural cellPI3K/AKT/mTOR pathwayEmbryonic Stem CellsCell ProliferationNeuronsEpilepsymTOR; Neural Stem Cells; Tuberous Sclerosis; murine modelTOR Serine-Threonine KinasesTumor Suppressor ProteinsCell DifferentiationCell BiologyNewbornEmbryonic stem cellNeural stem cellMegalencephalyCell biologynervous system diseasesNeuroepithelial cellmedicine.anatomical_structureAnimals NewbornImmunologyGene TargetingMutationmTORMolecular MedicineTSC1TSC2Signal Transduction
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Activation of classical protein kinase C reduces the expression of human cationic amino acid transporter 3 (hCAT-3) in the plasma membrane

2005

We have previously shown that activation of PKC (protein kinase C) results in internalization of hCAT-1 [human CAT-1 (cationic amino acid transporter 1)] and a decrease in arginine transport [Rotmann, Strand, Martiné and Closs (2004) J. Biol. Chem. 279, 54185–54192]. However, others found increased transport rates for arginine in response to PKC activation, suggesting a differential effect of PKC on different CAT isoforms. Therefore we investigated the effect of PKC on hCAT-3, an isoform expressed in thymus, brain, ovary, uterus and mammary gland. In Xenopus laevis oocytes and human U373MG glioblastoma cells, hCAT-3-mediated L-arginine transport was significantly reduced upon treatment with…

TeratocarcinomaArginineXenopusDown-RegulationArginineBiochemistryEnzyme activatorAntibody SpecificityCell Line TumorTumor Cells CulturedAnimalsHumansMolecular BiologyProtein Kinase CProtein kinase CCationic Amino Acid Transporter 1Arginine transportbiologyActivator (genetics)Cell MembraneBiological TransportCell BiologyFusion proteinEnzyme ActivationBiochemistryTetradecanoylphorbol AcetateOocytesbiology.proteinTetradecanoylphorbol AcetateCATIONIC AMINO ACID TRANSPORTER 3GlioblastomaResearch ArticleBiochemical Journal
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Retinoic Acid Induces Apoptosis-Associated Neural Differentiation of a Murine Teratocarcinoma Cell Line

2002

Abstract: Incubation with all-trans retinoic acid (RA) induces PCC7-Mz1 embryonic carcinoma cells to cease proliferation and to develop into a tissue-like pattern of neuronal, astroglial, and fibroblast-like derivatives over a period of several days. Concomitant with the induction of differentiation by RA, a sizable fraction of the Mz1 stem cells detaches and dies, with the maximal level of cell death achieved after 10 h of RA treatment. This RA-induced cell death fulfills all criteria of apoptosis, including nuclear condensation, intranucleosomal DNA degradation, expression of cysteine aspases (caspases), and the formation of apoptotic bodies. Apoptosis could be suppressed by the pan-caspa…

TeratocarcinomaProgrammed cell deathCellular differentiationRetinoic acidApoptosisTretinoinBiochemistryMiceCellular and Molecular Neurosciencechemistry.chemical_compoundGAP-43 ProteinTumor Cells CulturedAnimalsProtein Kinase CProtein kinase CCaspaseNeuronsbiologyCell DifferentiationGenes bcl-2Cell biologyGene Expression RegulationchemistryBiochemistryCell cultureApoptosisPhorbolbiology.proteinJournal of Neurochemistry
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Ciprofibrate stimulates protein kinase C-dependent phosphorylation of an 85 kDa protein in rat Fao hepatic derived cells

2000

The effect of ciprofibrate on early events of signal transduction was previously studied in Fao cells. Protein kinase C (PKC) assays performed on permeabilized cells showed a more than two-fold increase in PKC activity in cells treated for 24 h with 500 microM ciprofibrate. To show the subsequent effect of this increase on protein phosphorylation, the in vitro phosphorylation on particulate fractions obtained from Fao cells was studied. Among several modifications, the phosphorylation of protein(s) with an apparent molecular mass of 85 kDa was investigated. This modification appeared in the first 24 h of treatment with 500 microM ciprofibrate. It was shown to occur on Ser/Thr residue(s). It…

ThreonineBiochemistryCell LineSubstrate SpecificityMAP2K7Clofibric AcidSerinemedicineAnimalsProtein phosphorylationPhosphorylationProtein Kinase CProtein kinase CbiologyKinaseCyclin-dependent kinase 2Fibric AcidsGeneral MedicinePhosphoproteinsMolecular biologyRatsMolecular WeightLiverBiochemistrybiology.proteinPhosphorylationPeroxisome ProliferatorsCiprofibrateSignal transductionmedicine.drugBiochimie
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Serine- and Threonine/Valine-Dependent Activation of PDK and Tor Orthologs Converge on Sch9 to Promote Aging

2014

Dietary restriction extends longevity in organisms ranging from bacteria to mice and protects primates from a variety of diseases, but the contribution of each dietary component to aging is poorly understood. Here we demonstrate that glucose and specific amino acids promote stress sensitization and aging through the differential activation of the Ras/cAMP/PKA, PKH1/2 and Tor/S6K pathways. Whereas glucose sensitized cells through a Ras-dependent mechanism, threonine and valine promoted cellular sensitization and aging primarily by activating the Tor/S6K pathway and serine promoted sensitization via PDK1 orthologs Pkh1/2. Serine, threonine and valine activated a signaling network in which Sch…

ThreonineCancer ResearchAgingSerineMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataGene Expression Regulation FungalMolecular Cell BiologySerineSignaling in Cellular ProcessesThreonineGenetics (clinical)Cellular Stress Responses0303 health sciencesageing longevity Sch9 Tor Pkhs nutrients amino acidssurvival stress resistanceMechanisms of Signal TransductionValineCell biologyBiochemistryPhosphorylationSignal transductionResearch ArticleSignal TransductionSaccharomyces cerevisiae Proteinslcsh:QH426-470Adenylyl Cyclase Signaling PathwayLongevityP70-S6 Kinase 1Ras SignalingSaccharomyces cerevisiaeBiologyMicrobiologySignaling Pathways3-Phosphoinositide-Dependent Protein Kinases03 medical and health sciencesModel OrganismsStress PhysiologicalGeneticsAnimalsGene NetworksProtein kinase AMolecular BiologyTranscription factorBiologyEcology Evolution Behavior and Systematics030304 developmental biologySerine/threonine-specific protein kinase[SDV.GEN]Life Sciences [q-bio]/GeneticsCyclic AMP-Dependent Protein Kinaseslcsh:GeneticsGlucoseFoodTor SignalingProtein Kinases030217 neurology & neurosurgeryTranscription Factors
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