Search results for " tyrosine"

showing 10 items of 256 documents

Consensus guidelines for the detection of immunogenic cell death

2014

Apoptotic cells have long been considered as intrinsically tolerogenic or unable to elicit immune responses specific for dead cell-associated antigens. However, multiple stimuli can trigger a functionally peculiar type of apoptotic demise that does not go unnoticed by the adaptive arm of the immune system, which we named "immunogenic cell death" (ICD). ICD is preceded or accompanied by the emission of a series of immunostimulatory damage-associated molecular patterns (DAMPs) in a precise spatiotemporal configuration. Several anticancer agents that have been successfully employed in the clinic for decades, including various chemotherapeutics and radiotherapy, can elicit ICD. Moreover, defect…

HSV-1 herpes simplex virus type IΔψm mitochondrial transmembrane potentialmedicine.medical_treatmentDAMP damage-associated molecular patterndetectionFLT3LG fms-related tyrosine kinase 3 ligandReviewmember 3calreticulinEukaryotic translation initiation factor 2ARFP red fluorescent protein0302 clinical medicineMOMP mitochondrial outer membrane permeabilizationImmunology and AllergyGFP green fluorescent proteinHMGB10303 health scienceseducation.field_of_studyToll-like receptorBAK1 BCL2-antagonist/killer 1H2B histone 2Bendoplasmic reticulum stre3. Good healthBAX BCL2-associated X proteinXBP1 X-box binding protein 1cell deathOncologyPDIA3 protein disulfide isomerase family A030220 oncology & carcinogenesisendoplasmic reticulum stressImmunogenic cell deathHSP heat shock proteinimmunotherapyTLR Toll-like receptorautophagyATF6 activating transcription factor 6ImmunologyICD immunogenic cell deathEIF2A eukaryotic translation initiation factor 2AGuidelinesBiologyBCL2 B-cell CLL/lymphoma 2 proteinER endoplasmic reticulumPI propidium iodideATP release03 medical and health sciencesImmune systemimmunogenicmedicineIFN interferonAntigen-presenting celleducation030304 developmental biologyCALR calreticulinDamage-associated molecular patternImmunotherapyCTL cytotoxic T lymphocyteHMGB1 high mobility group box 1IL interleukinG3BP1 GTPase activating protein (SH3 domain) binding protein 1APC antigen-presenting cellCancer cellImmunologyDiOC6(3) 33′-dihexyloxacarbocyanine iodideDAPI 4′6-diamidino-2-phenylindoleOncoImmunology
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Macrophage MerTK promotes profibrogenic cross-talk with hepatic stellate cells via soluble mediators

2022

Background & aims: Activation of Kupffer cells and recruitment of monocytes are key events in fibrogenesis. These cells release soluble mediators which induce the activation of hepatic stellate cells (HSCs), the main fibrogenic cell type within the liver. Mer tyrosine kinase (MerTK) signaling regulates multiple processes in macrophages and has been implicated in the pathogenesis of non-alcoholic steatohepatitis-related fibrosis. In this study, we explored if MerTK activation in macrophages influences the profibrogenic phenotype of HSCs. Methods: Macrophages were derived from THP-1 cells or differentiated from peripheral blood monocytes towards MerTK+/CD206+/CD163+/CD209- macrophages. Th…

HepatologyCM conditioned medium ECM extracellular matrix Gas-6 Gas-6 growth arrest-specific gene 6 HSC(s) hepatic stellate cells KC(s) Kupffer cell(s) M-CSF macrophage colony-stimulating factor M2c-like macrophages MerTK Myeloid-epithelial-reproductive tyrosine kinase NAFLD non-alcoholic fatty liver disease NASH NASH non-alcoholic steatohepatitis PMA phorbol 12-myristate 13-acetate TGFβ1 transforming growth factor-β1 THP-1 TIMP1 tissue inhibitor of metalloproteinase 1 VEGF-A vascular endothelial growth factor-A liver fibrosis siRNA small-interfering RNAGas-6; liver fibrosis; M2c-like macrophages; NASH; THP-1GastroenterologyInternal MedicineImmunology and AllergyJHEP Reports
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Origin of metazoan adhesion molecules and adhesion receptors as deduced from cDNA analyses in the marine sponge Geodia cydonium: a review.

1997

The phylogenetic relationships of the kingdom Animalia (Metazoa) have long been questioned. Whether the lowest eukaryotic multicellular organisms, the metazoan phylum Porifera (sponges), independently evolved multicellularity from a separate protist lineage (polyphyly of animals) or whether they were derived from the same protist group as the other animal phyla (monophyly) remains unclear. Analyses of the genes that are typical for multicellularity, e.g. those coding for adhesion molecules (galectin) and adhesion receptors (receptor tyrosine kinase, integrin receptor, receptors featuring scavenger receptor cysteine-rich domains) or elements involved in signal transduction pathways (G-protei…

HistologyDNA ComplementaryMembrane GlycoproteinsbiologyCell adhesion moleculeProtistMembrane ProteinsCell Biologybiology.organism_classificationmedicine.disease_causeReceptor tyrosine kinasePathology and Forensic MedicineCell biologyPoriferaSuberites domunculaSpongeBiochemistryPlatelet Glycoprotein GPIb-IX Complexbiology.proteinmedicineAnimalsSignal transductionReceptorCell Adhesion MoleculesGalectinCell and tissue research
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Towards an understanding of the molecular basis of immune responses in sponges: The marine demospongeGeodia cydonium as a model

1999

The phylogenetic position of the phylum Porifera (sponges) is near the base of the kingdom Metazoa. During the last few years, not only rRNA sequences but, more importantly, cDNA/genes that code for proteins have been isolated and characterized from sponges, in particular from the marine demosponge Geodia cydonium. The analysis of the deduced amino acid sequences of these proteins allowed a molecular biological approach to the question of the monophyly of the Metazoa. Molecules of the extracellular matrix/basal lamina, with the integrin receptor, fibronectin, and galectin as prominent examples, and of cell-surface receptors (tyrosine kinase receptor), elements of sensory systems (crystallin…

HistologybiologyCell adhesion moleculeIntegrinbiology.organism_classificationReceptor tyrosine kinaseFibronectinMedical Laboratory TechnologySpongeDemospongeBiochemistrybiology.proteinAnatomySignal transductionInstrumentationGalectinMicroscopy Research and Technique
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Redox signaling and histone acetylation in acute pancreatitis

2011

Histone acetylation via CBP/p300 coordinates the expression of proinflammatory cytokines in the activation phase of inflammation, particularly through mitogen-activated protein kinases (MAPKs), nuclear factor-κB (NF-κB), and signal transducers and activators of transcription (STAT) pathways. In contrast, histone deacetylases (HDACs) and protein phosphatases are mainly involved in the attenuation phase of inflammation. The role of reactive oxygen species (ROS) in the inflammatory cascade is much more important than expected. Mitochondrial ROS act as signal-transducing molecules that trigger proinflammatory cytokine production via inflammasome-independent and inflammasome-dependent pathways. …

Histone AcetyltransferasesMitochondrial ROSAcetylationProtein tyrosine phosphataseBiologyEndoplasmic Reticulum StressBiochemistryChromatin remodelingProinflammatory cytokineHistonesOxidative StressHistoneGene Expression RegulationPancreatitisAcetylationPhysiology (medical)Acute Diseasebiology.proteinCancer researchAnimalsHumansPhosphorylationOxidation-ReductionProtein Processing Post-TranslationalSignal TransductionFree Radical Biology and Medicine
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EGFR tyrosine kinase inhibitor therapy continuation with high-dose hypofractionated radiotherapy in EGFR-mutated non-small cell lung cancer (NSCLC) p…

2020

e21580 Background: EGFR tyrosine kinase inhibitors (TKIs) represent the standard first-line therapy for advanced non-small cell lung cancer (NSCLC) patients with activating EGFR mutations. However, despite initial marked responses, tumors invariably develop acquired resistance to TKIs. Oligoprogression is commonly observed during treatment with oncogene-directed therapies, including EGFR TKIs, and refers to patients who experience disease progression only in limited sites as a result of heterogeneous mechanisms of resistance. The use of local ablative treatments for these resistant lesions may extend the duration of TKI therapy and potentially improve long-term disease control and survival…

Hypofractionated RadiotherapyCancer Researchbusiness.industrynon-small cell lung cancer (NSCLC)Diseasemedicine.diseaseEGFR Tyrosine Kinase Inhibitor TherapyEGFR Tyrosine Kinase Inhibitorsrespiratory tract diseasesOncologyEgfr mutationCancer researchMedicineNon small cellbusinessJournal of Clinical Oncology
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AML-associated Flt3 kinase domain mutations show signal transduction differences compared with Flt3 ITD mutations

2005

Activating mutations of Flt3 are found in approximately one third of patients with acute myeloid leukemia (AML) and are an attractive drug target. Two classes of Flt3 mutations occur: internal tandem duplications (ITDs) in the juxtamembrane and point mutations in the tyrosine kinase domain (TKD). We and others have shown that Flt3-ITD induced aberrant signaling including strong activation of signal transducer and activator of transcription 5 (STAT5) and repression of CCAAT/estradiol-binding protein α (c/EBPα) and Pu.1. Here, we compared the signaling properties of Flt3-ITD versus Flt3-TKD in myeloid progenitor cells. We demonstrate that Flt3-TKD mutations induced autonomous growth of 32D ce…

ImmunologyApoptosisBiologymedicine.disease_causeBiochemistryCell Linefluids and secretionsProto-Oncogene Proteinshemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansPoint MutationMyeloid CellsPhosphorylationProtein kinase BProtein kinase CMutationPoint mutationAutophosphorylationIntracellular Signaling Peptides and ProteinsReceptor Protein-Tyrosine Kinaseshemic and immune systemsCell BiologyHematologyMilk ProteinsStaurosporineMolecular biologyProtein Structure TertiaryDNA-Binding ProteinsMuridaefms-Like Tyrosine Kinase 3Leukemia MyeloidTandem Repeat SequencesAcute Diseaseembryonic structuresFms-Like Tyrosine Kinase 3Mutagenesis Site-DirectedTrans-ActivatorsSignal transductionTyrosine kinaseSignal TransductionTranscription FactorsBlood
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Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

2005

Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is unclear but is of major significance for the development of future therapeutic strategies. We searched for mechanisms of resistance in 6 patients with AML who had relapses upon PKC412 treatment. In an …

ImmunologyMutation MissenseBiologyBiochemistrychemistry.chemical_compoundIn vivoRecurrencehemic and lymphatic diseasesHumansProtein Kinase InhibitorsProtein Kinase CQuizartinibKinaseMyeloid leukemiaCell BiologyHematologyProtein-Tyrosine KinasesStaurosporineEnzyme ActivationProtein kinase domainchemistryfms-Like Tyrosine Kinase 3Drug Resistance NeoplasmLeukemia MyeloidFms-Like Tyrosine Kinase 3Acute DiseaseCancer researchTyrosine kinaseCrenolanibBlood
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Cross-Inhibition of Interferon-Induced Signals by GM-CSF Through a Block in Stat1 Activation

2007

We investigated the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on biologic signals induced by interferon-alpha (IFN-alpha) and IFN-gamma. In hematopoietic cell lines, IFN-induced signaling was investigated by Western blotting, electrophoretic mobility shift assays (EMSA), flow cytometry, protein-tyrosine phosphatase (PTP) assays, and RT-PCR. GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced Stat1 tyrosine phosphorylation in a time-dependent manner. EMSA showed that GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced IFN-gamma activator sequence (GAS) binding activity. As a consequence, IFN-induced transcription of the early response gene, IFN-stimulated…

ImmunologyPhosphataseSuppressor of Cytokine Signaling ProteinsProtein tyrosine phosphataseBiologyCell Linechemistry.chemical_compoundVirologyGranulocyte Colony-Stimulating FactorHumansPhosphorylationHistocompatibility Antigens Class IGranulocyte-Macrophage Colony-Stimulating FactorTyrosine phosphorylationDNACell BiologyMolecular biologySTAT1 Transcription FactorIRF1chemistryTyrosine kinase 2PhosphorylationInterleukin-3InterferonsSignal transductionInterferon Regulatory Factor-1Signal TransductionTranscription FactorsProto-oncogene tyrosine-protein kinase SrcJournal of Interferon & Cytokine Research
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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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