Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Signal transduction pathways involved in the mechanical responses to protease-activated receptors in rat colon.

2002

Recording simultaneously in vitro the changes of endoluminal pressure (index of circular muscle activity) and isometric tension (index of longitudinal muscle activity), we examined the mechanisms responsible for the apamin-sensitive relaxant and contractile responses induced by protease-activated receptor (PAR)-1 and PAR-2 activating peptides, SFLLRN-NH2 and SLIGRL-NH2, respectively, in rat colon. In the circular muscle, the inhibitory effects of SFLLRN-NH2 and SLIGRL-NH2 were significantly reduced by ryanodine, an inhibitor of Ca2+ release from the sarcoplasmic reticulum, but unaffected by 1-[6-[[17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122), a phosph…

Intracellular FluidMalemedicine.medical_specialtyColonGenisteinBiologyIn Vitro Techniqueschemistry.chemical_compoundInternal medicinemedicineAnimalsReceptor PAR-2Receptor PAR-1Rats WistarReceptorProtein kinase CPharmacologyPhospholipase CRyanodine receptorNeural InhibitionRatsEndocrinologychemistryType C PhospholipasesMolecular MedicineCalciumReceptors ThrombinSignal transductionmedicine.symptomExtracellular SpaceTyrosine kinaseMuscle contractionMuscle ContractionSignal TransductionThe Journal of pharmacology and experimental therapeutics
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Not all KIT 557/558 codons mutations have the same prognostic influence on recurrence-free survival: breaking the exon 11 mutations in gastrointestin…

2021

Background: Although the gastrointestinal stromal tumor (GIST) genotype is not currently included in risk-stratification systems, a growing body of evidence shows that the pathogenic variant (PV) type and codon location hold a strong prognostic influence on recurrence-free survival (RFS). This information has particular relevance in the adjuvant setting, where an accurate prognostication could help to better identify high-risk tumors and guide clinical decision-making. Materials and Methods: Between January 2005 and December 2020, 96 patients with completely resected GISTs harboring a KIT proto-oncogene receptor tyrosine kinase ( KIT) exon 11 PV were included in the study. We analyzed the t…

KIT proto-oncogene receptor tyrosine kinaseGiSTbusiness.industryplatelet-derived growth factor receptor alphaPlatelet-Derived Growth Factor Receptor AlphaNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasegastrointestinal stromal tumorExon557/558 deletionOncologyRecurrence free survivalGenotypeCancer researchmedicinePrognostic biomarkerGastrointestinal stromal tumors (GISTs)Stromal tumorprognostic biomarkerbusinessRC254-282Therapeutic Advances in Medical Oncology
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Differential role of p38 mitogen activated protein kinase for cellular recovery from attack by pore-forming S. aureus alpha-toxin or streptolysin O.

2006

Following the observation that cells are able to recover from membrane lesions incurred by Staphylococcus aureus alpha-toxin and streptolysin O (SLO), we investigated the role of p38 in this process. p38 phosphorylation occurred in response to attack by both toxins, commencing within minutes after toxin treatment and waning after several hours. While SLO reportedly activates p38 via ASK1 and ROS, we show that this pathway does not play a major role for p38 induction in alpha-toxin-treated cells. Strikingly divergent effects of p38 blockade were noted depending on the toxin employed. In the case of alpha-toxin, inhibition of p38 within the time frame of its activation led to disruption of th…

KeratinocytesProgrammed cell deathStaphylococcus aureusCell Membrane Permeabilityp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologymedicine.disease_causeMAP Kinase Kinase Kinase 5Biochemistryp38 Mitogen-Activated Protein KinasesMicrobiologyHemolysin ProteinsAdenosine TriphosphateBacterial ProteinsProto-Oncogene ProteinsmedicineHumansASK1PhosphorylationMolecular BiologyCells CulturedPore-forming toxinToxinCell MembraneCell BiologyProtein-Tyrosine KinasesBlockadeCell biologyEnzyme ActivationStreptolysinsPhosphorylationStreptolysinBiochemical and biophysical research communications
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Studies of Jak/STAT3 expression and signalling in psoriasis identifies STAT3-Ser727 phosphorylation as a modulator of transcriptional activity

2013

Jak/Tyk proteins have recently aroused as possible therapeutic targets for the treatment of psoriasis. In psoriasis, these proteins signal through STAT molecules including STAT3, and STAT3 expression and activation has been shown augmented in psoriatic lesions. Here, we characterized the expression of Jak/Tyk proteins in lesional compared with non-lesional psoriatic skin. Jak1, Jak2 mRNA and protein and Tyk2 mRNA appeared to be downregulated, whereas Jak3 mRNA expression was increased. Moreover, STAT3 expression and activation was examined in psoriasis. STAT3 is activated at two phosphorylation sites: Tyr705 and Ser727. Both phosphorylation sites were phosphorylated in lesional psoriatic sk…

KeratinocytesSTAT3 Transcription FactorTranscription GeneticMAP Kinase Signaling SystemBiopsyp38 mitogen-activated protein kinasesPrimary Cell CultureGene ExpressionDermatologyBiochemistrystatInterleukin 20PsoriasisSerinemedicineHumansPsoriasisRNA MessengerPhosphorylationSTAT3Molecular BiologySkinTYK2 KinasebiologyInterleukin-6InterleukinsJanus Kinase 3Janus Kinase 1Janus Kinase 2medicine.diseaseTyrosine kinase 2biology.proteinCancer researchPhosphorylationTumor necrosis factor alphaSignal Transduction
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LS104, a Novel Kinase Inhibitor, Induces Apoptosis, Synergizes with Cytostatic Drugs and Is Targeting the Receptor Tyrosine Kinase FLT3.

2005

Abstract Fms-like tyrosine kinase 3 (FLT3), a member of the class III tyrosine kinase receptor family, is expressed in up to 90% of acute myeloid leukemia (AML). Activating mutations like internal tandem duplication (ITD) of the juxtamembrane domain and kinase domain point mutations are found in approximately 35% of AML-cases and are considered to represent an attractive therapeutic target. In this study, we report that the novel hydroxystyryl-acrylonitrile compound LS104 induces potent cytotoxic effects in FLT3 ITD-positive leukemic cells. As a cellular model to investigate FLT3-ITD specific effects we used 32D myeloid cells stably transfected with FLT3-ITD and wt-FLT3, respectively. In MT…

KinaseCell growthImmunologyTyrosine phosphorylationCell BiologyHematologyBiologymedicine.diseaseBiochemistryMolecular biologyReceptor tyrosine kinaseLeukemiachemistry.chemical_compoundchemistryAnnexinhemic and lymphatic diseasesembryonic structuresmedicinebiology.proteinKinase activityTyrosineBlood
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A novel molecular mechanism of primary resistance to FLT3-kinase inhibitors in AML

2009

Abstract Currently, FLT3 tyrosine kinase inhibitors (TKIs) are emerging as the most promising drug therapy to overcome the dismal prognosis of acute myelogenous leukemia (AML) patients harboring internal tandem duplications (ITDs) of FLT3. However, up-front drug resistance occurs in approximately 30% of patients, and molecular mechanisms of resistance are poorly understood. Here, we have uncovered a novel mechanism of primary resistance to FLT3 TKIs in AML: an FLT3 receptor harboring a nonjuxtamembrane ITD atypically integrating into the β-2 sheet of the first kinase domain (FLT3_ITD627E) induces dramatic up-regulation of the anti-apoptotic myeloid cell leukemia 1 protein (MCL-1). Using RNA…

KinaseMitogen-Activated Protein Kinase 3ImmunologySignal transducing adaptor proteinCell BiologyHematologyBiologyBiochemistryProtein kinase domainhemic and lymphatic diseasesTrk receptorFms-Like Tyrosine Kinase 3Cancer researchSignal transductionTyrosine kinaseBlood
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Phenolic-glycolipid-1 and lipoarabinomannan preferentially modulate TCR- and CD28-triggered proximal biochemical events, leading to T-cell unresponsi…

2012

Abstract Background Advanced stages of leprosy show T cell unresponsiveness and lipids of mycobacterial origin are speculated to modulate immune responses in these patients. Present study elucidates the role of phenolicglycolipid (PGL-1) and Mannose-capped lipoarabinomannan (Man-LAM) on TCR- and TCR/CD28- mediated signalling. Results We observed that lipid antigens significantly inhibit proximal early signalling events like Zap-70 phosphorylation and calcium mobilization. Interestingly, these antigens preferentially curtailed TCR-triggered early downstream signalling events like p38 phosphorylation whereas potentiated that of Erk1/2. Further, at later stages inhibition of NFAT binding, IL-2…

LipopolysaccharidesEndocrinology Diabetes and MetabolismT-LymphocytesClinical BiochemistryPGL-1Man-LAMGene ExpressionLymphocyte ActivationJurkat cellsJurkat CellsEndocrinologyT-cell activationIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesPromoter Regions Geneticlcsh:RC620-627Protein Kinase CImmunity CellularZAP-70 Protein-Tyrosine KinaseCD28hemic and immune systemsCell biologyMycobacterium lepraelcsh:Nutritional diseases. Deficiency diseasesmedicine.anatomical_structureHost-Pathogen InteractionsProtein BindingMAP Kinase Signaling SystemT cellReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyImmune systemCD28 AntigensLeprosymedicineHumansSecretionCalcium SignalingCell ProliferationBiochemistry medicalAntigens BacterialLipoarabinomannanNFATC Transcription FactorsResearchBiochemistry (medical)T-cell receptorInterleukin-2 Receptor alpha SubunitMycobacteriaGene Expression RegulationAnergyImmunologyLeukocytes MononuclearInterleukin-2GlycolipidsLipids in Health and Disease
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Identification and characterization of a novel Ets-2-related nuclear complex implicated in the activation of the human interleukin-12 p40 gene promot…

1997

Interleukin-12 (IL-12) is a proinflammatory cytokine produced by antigen-presenting cells in response to many microbial infections. IL-12 plays an important role in the generation of T helper type-1 cells, which favor cell-mediated immune response. IL-12 is composed of two different subunits, p40 and p35, whose expression can be regulated concomitantly or differentially. Monocytic cells, the major producers of IL-12, can be primed by interferon-gamma (IFN-gamma) to produce optimal amounts of IL-12 in response to LPS stimulation as a consequence of bacterial infection. The priming effect is exerted primarily at the transcriptional level on the p40 promoter in conjunction with the effects of …

LipopolysaccharidesTranscription GeneticSequence HomologyStimulationbiosynthesis/geneticsBiochemistryChromatography Affinitychemistry.chemical_compoundMiceAnimals Base Sequence Cell Line Cell Nucleus; metabolism Chromatography; Affinity DNA-Binding Proteins Humans Interferon-gamma; pharmacology Interleukin-12; biosynthesis/genetics Kinetics Lipopolysaccharides; pharmacology Mice Molecular Sequence Data Nuclear Proteins; isolation /&/ purification/metabolism Promoter Regions; Genetic Protein-Tyrosine Kinases; metabolism Proto-Oncogene Protein c-ets-2 Proto-Oncogene Proteins; isolation /&/ purification/metabolism Repressor Proteins Sequence Homology; Nucleic Acid Trans-Activators; isolation /&/ purification/metabolism Transcription Factors Transcription; Genetic; drug effectsPromoter Regions GeneticChromatographyNuclear ProteinsMethylationProtein-Tyrosine KinasesInterleukin-12DNA-Binding ProteinsTranscriptionMolecular Sequence DataBiologyProinflammatory cytokineCell LineProto-Oncogene Protein c-ets-2Promoter RegionsInterferon-gammaGeneticSequence Homology Nucleic AcidProto-Oncogene ProteinsAnimalsHumansMolecular BiologyTranscription factorCell NucleusMolecular massBase SequenceNucleic Acidisolation /&/ purification/metabolismPromoterCell BiologyMolecular biologyIn vitroRepressor ProteinsKineticschemistryAffinitydrug effectsTrans-ActivatorspharmacologymetabolismDNATranscription Factors
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Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
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