Search results for " TYR"

showing 10 items of 362 documents

Western blotting as a method for studying cell-biomaterial interactions: The role of protein collection

2000

Research of cell-biomaterial interactions is building on knowledge and methods available in cell and molecular biology. Western blotting is one of the options to characterize protein expression in cell populations. Method transfer to biomaterial model systems is not trivial because of the structure that exists in many biomaterials, preventing the collection of cell lysate by mechanical means. In this technical report, we describe the influence of different protein collection methods in a model system for cell-biomaterial interactions, consisting of endothelial cells exposed to different stimuli. In particular, the influence of trypsinization before lysis, and handling complexity were determ…

Lysismedicine.diagnostic_testCellBiomedical EngineeringTyrosine phosphorylationProtein tyrosine phosphataseProtein degradationBiologyTrypsinizationBiomaterialsBlotchemistry.chemical_compoundmedicine.anatomical_structureBiochemistrychemistryWestern blotmedicineJournal of Biomedical Materials Research
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Coupling of endothelin receptors to the ERK/MAP kinase pathway. Roles of palmitoylation and G(alpha)q.

2001

Endothelins are potent mitogens that stimulate extracellular signal-regulated kinases (ERK/MAP kinases) through their cognate G-protein-coupled receptors, ET(A) and ET(B). To address the role of post-translational ET receptor modifications such as acylation on ERK activation and to identify relevant downstream effectors coupling the ET receptor to the ERK signaling cascades we have constructed a panel of palmitoylation-deficient ET receptor mutants with differential G(alpha) protein binding capacity. Endothelin-1 stimulation of wild-type ET(A) or ET(B) induced a fivefold to sixfold increase in ERK in COS-7 and CHO cells whereas full-length nonpalmitoylated ET(A) and ET(B) mutants failed to …

MAPK/ERK pathwayGs alpha subunitInsectaMAP Kinase Signaling SystemBlotting WesternMolecular Sequence DataPalmitic AcidSRC Family Tyrosine KinaseBiochemistryCell LineCricetinaeArrestinTumor Cells CulturedAnimalsHumansAmino Acid SequenceReceptorMitogen-Activated Protein Kinase 1KinaseChemistryReceptors EndothelinCell MembraneHeterotrimeric GTP-Binding ProteinsCell biologyEnzyme ActivationErbB ReceptorsType C PhospholipasesCOS CellsMutationcardiovascular systemMutagenesis Site-DirectedPhosphorylationGTP-Binding Protein alpha Subunits Gq-G11Mitogen-Activated Protein KinasesProto-oncogene tyrosine-protein kinase SrcEuropean journal of biochemistry
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Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro.

2009

Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML). However, development of resistance to FLT3 tyrosine kinase inhibitors (TKI), such as PKC412A, has been described recently. This observation may have an increasing impact on the duration of response and relapse rates in upcoming clinical trials employing FLT3-TKI. Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones. Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts. Combination of bot…

MAPK/ERK pathwayIndolesmedicine.drug_classAntineoplastic AgentsApoptosisTransfectionTyrosine-kinase inhibitorReceptor tyrosine kinaseCell Linefluids and secretionshemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein kinase Bbiologyhemic and immune systemsHematologyStaurosporineIn vitroLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3Drug Resistance NeoplasmTandem Repeat SequencesTrk receptorembryonic structuresFms-Like Tyrosine Kinase 3Cancer researchbiology.proteinTyrosine kinasepsychological phenomena and processesBritish journal of haematology
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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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Use of CDC2 from etoposide-treated cells as substrate to assay CDC25 phosphatase activity

1999

International audience; Cyclin-dependent kinases (CDKs) regulate the key transition of the cell cycle in all organisms. In response to Etoposide (VP-16) induced DNA damage, cells undergo a G2-phase arrest resulting in the accumulation of inactive CDK1 (CDC2) kinase complexes. Here we report that upon Etoposide treatment CDC2 is phosphorylated on tyrosine 15 and is dephosphorylated and activated in vitro by recombinant CDC25 phosphatase. We also show that inactive CDC2 kinase from Etoposide-treated cells can be used as a substrate in a sensitive two-step assay of CDC25 phosphatase. This assay, which is very simple to set-up, is based on the monitoring of CDC2 kinase activity after CDC25-depe…

MESH: HumansMESH: Phosphorylation[SDV]Life Sciences [q-bio]Cell Cycle Proteins[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]MESH: CDC2 Protein KinaseMESH: Tyrosine[SDV] Life Sciences [q-bio]AGENT ANTITUMORALenzymes and coenzymes (carbohydrates)MESH: Cell Cycle ProteinsMESH: cdc25 PhosphatasesCDC2 Protein KinaseMESH: HeLa CellsMESH: Phosphoprotein PhosphatasesPhosphoprotein PhosphatasesHumansTyrosinecdc25 PhosphatasesPhosphorylationbiological phenomena cell phenomena and immunityEtoposideHeLa CellsMESH: Etoposide
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Increased Level of Phosphotyrosine in Human Dendritic Cells under Stimulation with Contact Sensitizers but Not Irritants

1997

In the last years evidence was presented for the activation of dendritic cells (DC) under stimulation with contact sensitizers. Most data were obtained for murine Langerhans cells (LC) whereas in man blood-derived dendritic cells were found to be a more suitable model to study the mechanism of DC activation by haptens. The first observation was the upregulation of MHC class II molecules on murine Langerhans cells in vivo1 followed by their migration from the epidermis into regional lymph nodes2. Very early events during this activation include the upregulation of IL-1s in murine LC3 as well as the endocytotic activation of this cell type4. Based on the last observation attempts were made to…

MHC class IIEpidermis (botany)biologyChemistryCellProtein tyrosine phosphataseIn vitroCell biologymedicine.anatomical_structureDownregulation and upregulationImmunologymedicinebiology.proteinPhosphorylationSignal transduction
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Existence of muscarinic acetylcholine receptor (mAChR) and fibroblast growth factor receptor (FGFR) heteroreceptor complexes and their enhancement of…

2017

Abstract Background Recently, it was demonstrated that G-protein-coupled receptors (GPCRs) can transactivate tyrosine kinase receptors in absence of their ligands. In this work, driven by the observation that mAChRs and fibroblast growth factor receptors (FGFRs) share signalling pathways and regulation of brain functions, it was decided to explore whether mAChRs activation may transactivate FGFRs and, if so, to characterize the related trophic effects in cultured hippocampal neurons. Methods Oxotremorine-M transactivation of FGFRs and related trophic effects were tested in primary hippocampal neurons. Western blotting and in situ proximity ligation assay (PLA) were used to detect FGFR phosp…

Male0301 basic medicineHippocampusBiochemistryReceptor tyrosine kinaseReceptors G-Protein-CoupledRats Sprague-DawleyTransactivation0302 clinical medicineMuscarinic acetylcholine receptorNeural plasticityNeuronsNeuronal PlasticitybiologyReceptors MuscarinicCell biologyFibroblast growth factor receptorFibroblast Growth Factor 2Signal TransductionProto-oncogene tyrosine-protein kinase Srcmedicine.medical_specialtyNeuriteNeuronal OutgrowthBiophysicsHeteroreceptor03 medical and health sciencesHippocampuInternal medicinemedicineAnimalsReceptor Fibroblast Growth Factor Type 1Rats WistarMolecular BiologyTransactivationAnimalOxotremorineFibroblast growth factor receptor 1Receptor Muscarinic M1NeuronReceptors Fibroblast Growth FactorRatsFGFR1030104 developmental biologyEndocrinologyM1receptorBiophysicHeteroreceptor complexebiology.proteinRat030217 neurology & neurosurgeryBiochimica et Biophysica Acta (BBA) - General Subjects
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The comparison of outcomes from tyrosine kinase inhibitor monotherapy in second- or third-line for advanced non-small-cell lung cancer patients with …

2016

// Giuseppe Bronte 1, * , Tindara Franchina 2, * , Massimiliano Alu 3, * , Giovanni Sortino 1 , Claudia Celesia 1 , Francesco Passiglia 1 , Giuseppina Savio 3 , Agata Laudani 3 , Alessandro Russo 2 , Antonio Picone 2 , Sergio Rizzo 1 , Michele De Tursi 4 , Elisabetta Gambale 4 , Viviana Bazan 1 , Clara Natoli 4 , Livio Blasi 3 , Vincenzo Adamo 2 , Antonio Russo 1 1 Department of Surgical, Oncological and Oral Sciences, University of Palermo, Palermo, Italy 2 Medical Oncology Unit-AOOR Papardo-Piemonte, Messina and Department of Human Pathology, University of Messina, Messina, Italy 3 Medical Oncology Unit, A.R.N.A.S. Civico, Palermo, Italy 4 Department of Medical, Oral and Biotechnological …

Male0301 basic medicineOncologymedicine.medical_specialtyLung Neoplasmsmedicine.drug_classEGFRTyrosine kinase inhibitorKaplan-Meier EstimateTyrosine-kinase inhibitorErlotinib Hydrochloride03 medical and health sciences0302 clinical medicineGefitinibCarcinoma Non-Small-Cell LungInternal medicinemedicineHumansChemotherapyErlotinib HydrochlorideLung cancerProtein Kinase InhibitorsChemotherapy EGFR Non-small-cell lung cancer Tyrosine kinase inhibitor OncologyAgedRetrospective StudiesAged 80 and overPerformance statusbusiness.industryChemotherapy; EGFR; Non-small-cell lung cancer; Tyrosine kinase inhibitor; OncologyGefitinibRetrospective cohort studyMiddle Agedmedicine.diseaserespiratory tract diseasesSurgeryErbB ReceptorsClinical trialTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationQuinazolinesFemaleErlotinibbusinessNon-small-cell lung cancerResearch Papermedicine.drug
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Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice

2016

Acute pancreatitis (AP) is a common and devastating gastrointestinal disorder that causes significant morbidity. The disease starts as local inflammation in the pancreas that may progress to systemic inflammation and complications. Protein tyrosine phosphatase 1B (PTP1B) is implicated in inflammatory signaling, but its significance in AP remains unclear. To investigate whether PTP1B may have a role in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the effects of pancreatic PTP1B deficiency on cerulein- and arginine-induced acute pancreatitis. We report that PTP1B protein expression was increased in the early phase of AP in mice and rats. In addition, histological an…

Male0301 basic medicineWistarSystemic inflammationMedical and Health SciencesOral and gastrointestinalMicePathology2.1 Biological and endogenous factorsAetiologyNon-Receptor Type 1CancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 1Pancreatitis Acute NecrotizingReverse Transcriptase Polymerase Chain ReactionRegular Articlemedicine.anatomical_structureAcute NecrotizingGastrointestinal disorderAcute pancreatitisTumor necrosis factor alphamedicine.symptomPancreashormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyKnockoutInflammationPathology and Forensic MedicineProinflammatory cytokinePancreatic Cancer03 medical and health sciencesRare DiseasesInternal medicinemedicineAnimalsRats WistarAnimalbusiness.industrymedicine.diseaseRatsDisease Models Animal030104 developmental biologyEndocrinologyPancreatitisDisease ModelsPancreatitisProtein Tyrosine PhosphataseDigestive DiseasesbusinessThe American Journal of Pathology
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Prognostic value of FLT3 mutations in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline monochemother…

2011

Background Fms-like tyrosine kinase-3 (FLT3) gene mutations are frequent in acute promyelocytic leukemia but their prognostic value is not well established. Design and Methods We evaluated FLT3-internal tandem duplication and FLT3-D835 mutations in patients treated with all-trans retinoic acid and anthracycline-based chemotherapy enrolled in two subsequent trials of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) and Hemato-Oncologie voor Volwassenen Nederland (HOVON) groups between 1996 and 2005. Results FLT3-internal tandem duplication and FLT3-D835 mutation status was available for 306 (41%) and 213 (29%) patients, respectively. Sixty-eight (22%) and 20 (9%) pa…

MaleAIDA PROTOCOLGene mutationmedicine.disease_causeGastroenterologyLeukemia Promyelocytic AcuteRESIDUAL DISEASEhemic and lymphatic diseasesMOLECULAR SUBTYPESChildanthracyclinesMutationRemission InductionFLT3 mutationshemic and immune systemsHematologyMiddle AgedPrognosisall-trans retinoic acidLeukemiaTreatment Outcomeembryonic structuresFemaleTandem exon duplicationmedicine.drugAcute promyelocytic leukemiaAdultmedicine.medical_specialtyAdolescentAntineoplastic AgentsTretinoinACUTE MYELOID-LEUKEMIABiologyYoung AdultQUALITY-CONTROLTretinoinPOOR-PROGNOSISInternal medicinemedicineCoagulopathyHumansAgedprognostic factorsOriginal Articlesacute promyelocytic leukemiamedicine.diseaseSurvival AnalysisINTERNAL TANDEM DUPLICATIONRISK-ADAPTED TREATMENTPML/RAR-ALPHAfms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3ImmunologyPETHEMA GROUPMutation
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