Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Alterations in Tight- and Adherens-Junction Proteins Related to Glaucoma Mimicked in the Organotypically Cultivated Mouse Retina Under Elevated Press…

2020

Purpose To scrutinize alterations in cellular interactions and cell signaling in the glaucomatous retina, mouse retinal explants were exposed to elevated pressure. Methods Retinal explants were prepared from C57bl6 mice and cultivated in a pressure chamber under normotensive (atmospheric pressure + 0 mm Hg), moderately elevated (30 mm Hg), and highly elevated (60 mm Hg) pressure conditions. The expression levels of proteins involved in the formation of tight junctions (zonula occludens 1 [ZO-1], occludin, and claudin-5) and adherens junctions (VE-cadherin and β-catenin) and in cell-signaling cascades (Cdc42 and activated Cdc42 kinase 1 [ACK1]), as well as the expression levels of the growth…

0301 basic medicineelevated pressureBlotting WesternVimentinReal-Time Polymerase Chain ReactionOccludinRetinaTight JunctionsAdherens junctionMice03 medical and health scienceschemistry.chemical_compoundOrgan Culture Techniques0302 clinical medicineAntigens CDOccludinmedicinecell signalingAnimalscell contactsEye Proteinscdc42 GTP-Binding ProteinReceptorretina explantsmousebeta CateninRetinabiologyTight junctionGlial fibrillary acidic proteinChemistryGlaucomaRetinalAdherens JunctionsProtein-Tyrosine KinasesCadherinsImmunohistochemistryCell biologyMice Inbred C57BLAtmospheric Pressure030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisZonula Occludens-1 Proteinbiology.proteinInvestigative Opthalmology & Visual Science
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Tyro3 Contributes to Retinal Ganglion Cell Function, Survival and Dendritic Density in the Mouse Retina

2020

Retinal ganglion cells (RGCs) are the only output neurons of the vertebrate retina, integrating signals from other retinal neurons and transmitting information to the visual centers of the brain. The death of RGCs is a common outcome in many optic neuropathies, such as glaucoma, demyelinating optic neuritis and ischemic optic neuropathy, resulting in visual defects and blindness. There are currently no therapies in clinical use which can prevent RGC death in optic neuropathies; therefore, the identification of new targets for supporting RGC survival is crucial in the development of novel treatments for eye diseases. In this study we identify that the receptor tyrosine kinase, Tyro3, is crit…

0301 basic medicineinner plexiform layergenetic structuresdendritesNerve fiber layerTAM receptorelectroretinogramBiologyRetinal ganglionlcsh:RC321-57103 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineOptic neuritislcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchRetinaoptical coherence tomographymedicine.diagnostic_testreceptor tyrosine kinasesGeneral NeuroscienceRetinalInner plexiform layermedicine.diseaseeye diseases030104 developmental biologymedicine.anatomical_structurechemistryRetinal ganglion cellsense organsNeuroscience030217 neurology & neurosurgeryNeuroscienceElectroretinographyFrontiers in Neuroscience
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Phosphorylated immunoreceptor tyrosine-based activation motifs and integrin cytoplasmic domains activate spleen tyrosine kinase via distinct mechanis…

2018

Spleen tyrosine kinase (Syk) is involved in cellular adhesion and also in the activation and development of hematopoietic cells. Syk activation induced by genomic rearrangement has been linked to certain T-cell lymphomas, and Syk inhibitors have been shown to prolong survival of patients with B-cell lineage malignancies. Syk is activated either by its interaction with a double-phosphorylated immunoreceptor tyrosine-based activation motif (pITAM), which induces rearrangements in the Syk structure, or by the phosphorylation of specific tyrosine residues. In addition to its immunoreceptor function, Syk is activated downstream of integrin pathways, and integrins bind to the same region in Syk a…

0301 basic medicinekinaasitCell signalingentsyymitIntegrinsintegrinIntegrinAmino Acid MotifsMutation MissenseSykPeptidechemical and pharmacologic phenomenaBiochemistryspleen tyrosine kinase (Syk)environment and public healthBiokemia solu- ja molekyylibiologia - Biochemistry cell and molecular biology03 medical and health sciencesProtein DomainsLääketieteen bioteknologia - Medical biotechnologyenzyme kineticshemic and lymphatic diseasescell signalingHumansSyk KinaseTyrosinePhosphorylationCell adhesionMolecular Biologychemistry.chemical_classificationsoluviestintäintegriinit030102 biochemistry & molecular biologybiologyChemistryta1182hemic and immune systemsCell Biology3. Good healthCell biologyEnzyme Activationenzymes and coenzymes (carbohydrates)030104 developmental biologyAmino Acid SubstitutionCytoplasmbiology.proteinPhosphorylationPeptidessurface plasmon resonance (SPR)Signal Transduction
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New 3-Aryl-2-(2-Thienyl)acrylonitriles with High Activity against Hepatoma Cells

2021

New 2-(thien-2-yl)-acrylonitriles with putative kinase inhibitory activity were prepared and tested for their antineoplastic efficacy in hepatoma models. Four out of the 14 derivatives were shown to inhibit hepatoma cell proliferation at (sub-)micromolar concentrations with IC50 values below that of the clinically relevant multikinase inhibitor sorafenib, which served as a reference. Colony formation assays as well as primary in vivo examinations of hepatoma tumors grown on the chorioallantoic membrane of fertilized chicken eggs (CAM assay) confirmed the excellent antineoplastic efficacy of the new derivatives. Their mode of action included an induction of apoptotic capsase-3 activity, whil…

0301 basic medicinelcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5SpectroscopyMolecular StructureKinaseChemistryLiver NeoplasmsGeneral MedicineHep G2 CellshepatomaComputer Science ApplicationsCAM assayMolecular Docking SimulationChorioallantoic membraneBiochemistry030220 oncology & carcinogenesistyrphostinTyrosine kinasemedicine.drugSorafenibCarcinoma HepatocellularthiopheneThiophenesCatalysisArticleInorganic ChemistryVEGFR inhibition03 medical and health sciencesStructure-Activity RelationshipIn vivomedicineHumansPhysical and Theoretical ChemistryMode of actionMolecular BiologyProtein Kinase InhibitorsCell ProliferationAcrylonitrileDose-Response Relationship DrugOrganic Chemistrymolecular dockingVascular Endothelial Growth Factor Receptor-2anticancer drugs030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisDocking (molecular)Drug Screening Assays AntitumorInternational Journal of Molecular Sciences
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Liquid Biopsy in Gastrointestinal Stromal Tumor

2017

Over the past 15 years, gastrointestinal stromal tumors (GISTs) have emerged from a poorly understood neoplasm to a well-defined tumor entity. Starting from 2000, the discovery of gain-of-function mutations involving KIT or PDGFRα (platelet-derived growth factor-α) genes and the development of tyrosine kinase inhibitors (TKIs), such as imatinib, revolutionized dramatically the management of GISTs. Due to the almost continual emergence of new data about biological complexity of GISTs and more sophisticated whole-genome technologies, to date, the role of molecular biology is clinically important to drive therapeutic decision making.

0301 basic medicinemedicine.medical_specialtyStromal cellbusiness.industryGeneral surgeryImatinibTherapeutic decision makingmedicine.diseasedigestive system diseases03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisCancer researchMedicineNeoplasmGastrointestinal stromal tumors (GISTs)Liquid biopsyStromal tumorbusinessneoplasmsTyrosine kinasemedicine.drug
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NKp30 isoforms and NKp30 ligands are predictive biomarkers of response to imatinib mesylate in metastatic GIST patients

2016

International audience; Despite effective targeted therapy acting on KIT and PDGFRA tyrosine kinases, gastrointestinal stromal tumors (GIST) escape treatment by acquiring mutations conveying resistance to imatinib mesylate (IM). Following the identification of NKp30-based immunosurveillance of GIST and the off-target effects of IM on NK cell functions, we investigated the predictive value of NKp30 isoforms and NKp30 soluble ligands in blood for the clinical response to IM. The relative expression and the proportions of NKp30 isoforms markedly impacted both event-free and overall survival, in two independent cohorts of metastatic GIST. Phenotypes based on disbalanced NKp30B/NKp30C ratio (Del…

0301 basic medicinemedicine.medical_treatmentImmunologyPDGFRATargeted therapy03 medical and health sciences0302 clinical medicinemedicineImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyneoplasmsOriginal ResearchTumor microenvironmentGiSTbusiness.industryCancermedicine.diseasedigestive system diseases3. Good healthImmunosurveillance030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisImmunologyCancer research[SDV.IMM]Life Sciences [q-bio]/ImmunologybusinessTyrosine kinase
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NUOVI AGENTI TERAPEUTICI PER IL TRATTAMENTO DI PATOLOGIE EMATOLOGICHE

2019

La presente invenzione si riferisce al campo di nuove molecole tetracicliche, aventi un sistema tetraciclico, e loro impiego come medicamenti di patologie ematologiche in particolare per il trattamento della leucemia mieloide acuta (AML) in pazienti emizigoti FLT3/ITD resistenti alle terapie convenzionali.

2H-Imidazo [2'1':23][13]thiazolo[45-e]isoindol-8-yl)phenyl]ureas Acute myeloid leukemia (AML) Internal tandem duplication (ITD) FMS-like tyrosine kinase 3 (FLT3) FLT3/ITDSettore CHIM/08 - Chimica Farmaceutica
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NEW THERAPEUTIC AGENTS FOR THE TREATMENT OF HAEMATOLOGICAL PATHOLOGIES

2021

2H-Imidazo [2'1':23][13]thiazolo[45-e]isoindol-8-yl-phenylureas Acute myeloid leukemia (AML) Internal tandem duplication (ITD) FMS-like tyrosine kinase 3 (FLT3) FLT3/ITD
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An in-depth evaluation of acalabrutinib for the treatment of mantle-cell lymphoma

2020

Introduction: Regimens involving intensive immuno-chemotherapy, followed by high-dose therapy and autologous stem cell transplant represent the standard treatment for younger fit patients with mantle cell lymphoma (MCL). Targeted approaches (i.e. ibrutinib, bortezomib, and lenalidomide) represent the backbone of therapy for relapsed cases. Areas covered: Acalabrutinib is a novel small molecule with a butynamide moiety specifically designed to irreversibly inhibit Bruton tyrosine kinase (BTK), which is more potent and selective than ibrutinib. Relevant publications have been identified through literature searches using the terms 'mantle cell lymphoma' and 'acalabrutinib'. Expert opinion: Aca…

Acalabrutinib; BTK; MCL; therapy; Agammaglobulinaemia Tyrosine Kinase; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Benzamides; Humans; Lymphoma Mantle-Cell; Protein Kinase Inhibitors; PyrazinesOncologymedicine.medical_specialtyLymphomaAntineoplastic AgentsLymphoma Mantle-Cell03 medical and health scienceschemistry.chemical_compound0302 clinical medicineimmune system diseaseshemic and lymphatic diseasesInternal medicineAntineoplastic Combined Chemotherapy ProtocolsAgammaglobulinaemia Tyrosine KinaseHumansMedicineBruton's tyrosine kinasePharmacology (medical)Protein Kinase InhibitorsLenalidomidePharmacologytherapy.therapybiologyAcalabrutinibbusiness.industryBortezomibStandard treatmentMCLGeneral MedicineMantle-Cellmedicine.diseaseClinical trialchemistryBTKPyrazines030220 oncology & carcinogenesisIbrutinibBenzamidesbiology.proteinAcalabrutinibMantle cell lymphomabusiness030217 neurology & neurosurgerymedicine.drugExpert Opinion on Pharmacotherapy
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Novel mutations of the MET proto-oncogene in papillary renal carcinomas.

1999

Hereditary papillary renal carcinoma (HPRC) is characterized by multiple, bilateral papillary renal carcinomas. Previously, we demonstrated missense mutations in the tyrosine kinase domain of the MET proto-oncogene in HPRC and a subset of sporadic papillary renal carcinomas. In this study, we screened a large panel of sporadic papillary renal carcinomas and various solid tumors for mutations in the MET proto-oncogene. Summarizing these and previous results, mutations of the MET proto-oncogene were detected in 17/129 sporadic papillary renal carcinomas but not in other solid tumors. We detected five novel missense mutations; three of five mutations were located in the ATP-binding region of t…

AdenomaModels MolecularCancer ResearchProtein ConformationDNA Mutational AnalysisMolecular Sequence DataHereditary Papillary Renal Cell CarcinomaBiologymedicine.disease_causeTransfectionProto-Oncogene MasReceptor tyrosine kinaseMiceAdenosine TriphosphateNeoplastic Syndromes HereditaryProto-OncogenesGeneticsCarcinomamedicineMissense mutationAnimalsHumansPoint MutationAmino Acid SequencePhosphorylationCodonMolecular BiologyKidneyMutationBinding SitesSequence Homology Amino AcidPoint mutation3T3 CellsDNA NeoplasmProto-Oncogene Proteins c-metmedicine.diseaseCarcinoma PapillaryKidney NeoplasmsNeoplasm Proteinsmedicine.anatomical_structureCell Transformation NeoplasticCancer researchbiology.proteinMutagenesis Site-DirectedTyrosine kinaseProtein Processing Post-TranslationalSequence AlignmentOncogene
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