Search results for "src-Family Kinases"

showing 10 items of 11 documents

De novo design of protein kinase inhibitors by in silico identification of hinge region-binding fragments.

2013

Protein kinases constitute an attractive family of enzyme targets with high relevance to cell and disease biology. Small molecule inhibitors are powerful tools to dissect and elucidate the function of kinases in chemical biology research and to serve as potential starting points for drug discovery. However, the discovery and development of novel inhibitors remains challenging. Here, we describe a structure-based de novo design approach that generates novel, hinge-binding fragments that are synthetically feasible and can be elaborated to small molecule libraries. Starting from commercially available compounds, core fragments were extracted, filtered for pharmacophoric properties compatible w…

Binding SitesMolecular StructureProtein ConformationIntracellular Signaling Peptides and ProteinsArticlesProtein Serine-Threonine KinasesCrystallography X-RayMAP Kinase Kinase KinasesImmediate-Early ProteinsCSK Tyrosine-Protein KinaseMolecular Docking SimulationSmall Molecule Librariessrc-Family KinasesDrug DesignComputer SimulationProtein Kinase InhibitorsACS chemical biology
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Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
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Regulation of the tumor marker Fascin by the viral oncoprotein Tax of human T-cell leukemia virus type 1 (HTLV-1) depends on promoter activation and …

2015

AbstractAdult T-cell leukemia/lymphoma is a highly infiltrative neoplasia of CD4+ T-lymphocytes that occurs in about 5% of carriers infected with the deltaretrovirus human T-cell leukemia virus type 1 (HTLV-1). The viral oncoprotein Tax perturbs cellular signaling pathways leading to upregulation of host cell factors, amongst them the actin-bundling protein Fascin, an invasion marker of several types of cancer. However, transcriptional regulation of Fascin by Tax is poorly understood. In this study, we identified a triple mode of transcriptional induction of Fascin by Tax, which requires (1) NF-κB-dependent promoter activation, (2) a Tax-responsive region in the Fascin promoter, and (3) a p…

Transcriptional ActivationT-LymphocytesTaxmacromolecular substancesBiologyModels BiologicalFascinDownregulation and upregulationVirologyTranscriptional regulationmedicineHumansPromoter Regions GeneticProtein Kinase InhibitorsOncogeneFascinRegulation of gene expressionHuman T-lymphotropic virus 1NF‐kappa B (NF‐KB)Microfilament ProteinsNF-kappa BPromoterTumor virusTranscription regulationGene Products taxmedicine.diseasebiology.organism_classificationCell Transformation ViralPP2DeltaretrovirusLeukemiasrc-Family KinasesGene Expression RegulationHTLV-1ATLHuman T-lymphotropic virus 1Cancer researchbiology.proteinSignal transductionCarrier ProteinsSignal TransductionVirology
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Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src…

2017

International audience; We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho- Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in w…

0301 basic medicineMaleSomatic cellVascular MalformationsCutaneo-mucosal venous malformationsTyrosine Kinase Tie2Bioinformaticsmedicine.disease_causeGermlineMetastasisp-SrcExonPharmacology Toxicology and Pharmaceutics(all)General Pharmacology Toxicology and PharmaceuticsPhosphorylationCancerMedicine(all)MutationBrief ReportGeneral MedicineReceptor TIE-2[SDV.BDD.MOR] Life Sciences [q-bio]/Development Biology/Morphogenesis3. Good healthsrc-Family Kinases[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]FemaleProto-oncogene tyrosine-protein kinase SrcReceptorSrc[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]AdolescentDirect sequencingContext (language use)BiologyVegfGeneral Biochemistry Genetics and Molecular BiologyPermeability03 medical and health sciencesGermline mutationTEK gene[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN][ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansAmino Acid SequenceGeneMucous MembraneCell-Lines[ SDV ] Life Sciences [q-bio]Base SequenceBiochemistry Genetics and Molecular Biology(all)[SDV.BDD.MOR]Life Sciences [q-bio]/Development Biology/MorphogenesisGermline and somatic DNA030104 developmental biologyFaceMutationCancer researchSkin AbnormalitiesAngiogenesisPathwayJournal of negative results in biomedicine
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TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
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Identification and phenotypic characterization of a subpopulation of T84 human colon cancer cells, after selection on activated endothelial cells

2004

The extravasation of metastatic cells is regulated by molecular events involving the initial adhesion of tumor cells to the endothelium and subsequently the migration of the cells in the host connective tissue. The differences in metastatic ability could be attributed to properties intrinsic of the various primary tumor types. Thus, the clonal selection of neoplastic cells during cancer progression results in cells better equipped for survival and formation of colonies in secondary sites. A cell line (T84SF) exhibiting an altered phenotypic appearance was selected from a colon cancer cell line (T84) by repetitive plating on TNFα-activated human endothelial cells and subsequent selection for…

MaleUmbilical VeinsPhysiologyCellular differentiationClinical BiochemistryMice NudeApoptosisCell CommunicationMicechemistry.chemical_compoundCancer stem cellCell Line TumorCell AdhesionAnimalsHumansNeoplasm InvasivenessEnzyme InhibitorsNeoplasm MetastasisPhosphorylationCD40biologyCell growthTyrosine phosphorylationCell BiologyCell biologyEndothelial stem cellPhenotypesrc-Family KinaseschemistryCell cultureColonic NeoplasmsMetalloproteasesbiology.proteinTyrosineEndothelium VascularCell DivisionNeoplasm TransplantationProto-oncogene tyrosine-protein kinase SrcJournal of Cellular Physiology
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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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CNS Macrophages Control Neurovascular Development via CD95L.

2017

The development of neurons and vessels shares striking anatomical and molecular features, and it is presumably orchestrated by an overlapping repertoire of extracellular signals. CNS macrophages have been implicated in various developmental functions, including the morphogenesis of neurons and vessels. However, whether CNS macrophages can coordinately influence neurovascular development and the identity of the signals involved therein is unclear. Here, we demonstrate that activity of the cell surface receptor CD95 regulates neuronal and vascular morphogenesis in the post-natal brain and retina. Furthermore, we identify CNS macrophages as the main source of CD95L, and macrophage-specific del…

0301 basic medicineFas Ligand ProteinAngiogenesisMorphogenesisvesselmicrogliaBiologyGeneral Biochemistry Genetics and Molecular BiologyRetina03 medical and health sciencesangiogenesisMiceCell surface receptorExtracellularmedicineHuman Umbilical Vein Endothelial CellsNeuritesAnimalsHumansfas Receptorlcsh:QH301-705.5Cell ProliferationRetinaMicrogliaKinaseMacrophagesneurovascular developmentBrainNeurovascular bundle030104 developmental biologymedicine.anatomical_structurecortexsrc-Family Kinasesnervous systemlcsh:Biology (General)ImmunologySynapsesCD95CD95LNeuroscienceCNS macrophagesProtein BindingSignal TransductionCell reports
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Geldanamycin and its derivatives as Hsp90 inhibitors

2012

The Hsp90 molecule, one of the most abundant heat shock proteins in mammalian cells, maintains homeostasis and prevents stress-induced cellular damage. Hsp90 is expressed under normal conditions at a level of about 1-2 Percent of total proteins, while its expression increases 2-10 fold in cancer cells. The two main constitutively expressed isoforms of Hsp90 are known as Hsp90-alpha and Hsp90-beta, and their upregulation is associated with tumor progression, invasion and formation of metastases, as well as development of drug resistance. The Hsp90 is a key target for many newly established, potent anticancer agents containing Hsp90 N-terminal ATP binding inhibitors, such as geldanamycin, and…

IndolesLactams MacrocyclicCyclin-Dependent KinaseAntineoplastic AgentsTanespimycinBenzoquinoneModels BiologicalAntineoplastic Agentchemistry.chemical_compoundDownregulation and upregulationTransforming Growth Factor betaCyclin-dependent kinaseHeat shock proteinBenzoquinonespolycyclic compoundsAnimalsHumansHSP90 Heat-Shock ProteinsbiologyAnimalTriazolesGeldanamycinHsp90Cyclin-Dependent KinasesProto-Oncogene Proteins c-rafHSP90 Heat-Shock Proteinsrc-Family KinaseschemistryTumor progressionMutationCancer cellbiology.proteinCancer researchMacrolidesMacrolideTriazoleTumor Suppressor Protein p53Animals; Antineoplastic Agents; Benzoquinones; Cyclin-Dependent Kinases; HSP90 Heat-Shock Proteins; Humans; Lactams Macrocyclic; Macrolides; Models Biological; Mutation; Novobiocin; Proto-Oncogene Proteins c-raf; Transforming Growth Factor beta; Triazoles; Tumor Suppressor Protein p53; src-Family KinasesNovobiocinHumanFrontiers in Bioscience
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Activation of TRPC6 calcium channels by diacylglycerol (DAG)-containing arachidonic acid: A comparative study with DAG-containing docosahexaenoic acid

2006

We synthesized a diacylglycerol (DAG)-containing arachidonic acid, i.e., 1-stearoyl-2-arachidonyl-sn-glycerol (SAG), and studied its implication in the modulation of canonical transient receptor potential sub-type 6 (TRPC6) channels in stably-transfected HEK-293 cells. SAG induced the influx of Ca(2+), and also of other bivalent cations like Ba(2+) and Sr(2+), in these cells. SAG-evoked Ca(2+) influx was not due to its metabolites as inhibitors of DAG-lipase (RHC80267) and DAG-kinase (R50922) failed to inhibit the response of the same. To emphasise that SAG exerts its action via its DAG configuration, but not due to the presence of stearic acid at sn-1 position, we synthesized 1-palmitoyl-2…

Docosahexaenoic AcidsBiologyBiochemistryTRPC6DiglyceridesMicechemistry.chemical_compoundTransient receptor potential channelMembrane Microdomainsparasitic diseasesTRPC6 Cation ChannelAnimalsCells CulturedTRPC Cation ChannelsDiacylglycerol kinaseDose-Response Relationship DrugVoltage-dependent calcium channelGeneral MedicineRhc80267src-Family KinaseschemistryBiochemistrySU6656BiophysicsCalciumlipids (amino acids peptides and proteins)Arachidonic acidProto-oncogene tyrosine-protein kinase SrcBiochimie
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