Search results for "src"

showing 10 items of 50 documents

Selective Inhibition of STAT3 with Respect to STAT1: Insights from Molecular Dynamics and Ensemble Docking Simulations

2016

STAT3 protein, which is known to be involved in cancer development, is a promising target for anticancer therapy. Successful inhibitors of STAT3 should not affect an activity of closely related protein STAT1, which makes their development challenging. The mechanisms of selectivity of several existing STAT3 inhibitors are not clear. In this work, we studied molecular mechanisms of selectivity of 13 experimentally tested STAT3 inhibitors by means of extensive molecular dynamics and ensemble docking simulations. It is shown that all studied inhibitors bind to the large part of the protein surface in an unspecific statistical manner. The binding to the dimerization interface of the SH2 domain, …

STAT3 Transcription Factor0301 basic medicine[ SDV.BBM.BP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsStereochemistryGeneral Chemical Engineering[SDV.CAN]Life Sciences [q-bio]/CancerMolecular Dynamics SimulationLibrary and Information SciencesBiologySelective inhibitionSH2 domain01 natural sciencesMolecular Docking SimulationSubstrate Specificity[ SDV.CAN ] Life Sciences [q-bio]/Cancersrc Homology Domains03 medical and health sciencesMolecular dynamics[SDV.SP.MED]Life Sciences [q-bio]/Pharmaceutical sciences/Medication[CHIM]Chemical SciencesSTAT1STAT3ComputingMilieux_MISCELLANEOUS010405 organic chemistry[ SDV.SP.MED ] Life Sciences [q-bio]/Pharmaceutical sciences/MedicationGeneral Chemistry0104 chemical sciences3. Good healthComputer Science ApplicationsMolecular Docking Simulation[SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry Molecular Biology/BiophysicsSTAT1 Transcription Factor030104 developmental biologyDocking (molecular)Biophysicsbiology.proteinSelectivity
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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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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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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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The yopJ locus is required for Yersinia-mediated inhibition of NF-kappaB activation and cytokine expression: YopJ contains a eukaryotic SH2-like doma…

1998

Upon exposure to bacteria, eukaryotic cells activate signalling pathways that result in the increased expression of several defence-related genes. Here, we report that the yopJ locus of the enteropathogen Yersinia pseudotuberculosis encodes a protein that inhibits the activation of NF-kappaB transcription factors by a mechanism(s), which prevents the phosphorylation and subsequent degradation of the inhibitor protein IkappaB. Consequently, eukaryotic cells infected with YopJ-expressing Yersinia become impaired in NF-kappaB-dependent cytokine expression. In addition, the blockage of inducible cytokine production coincides with yopJ-dependent induction of apoptosis. Interestingly, the YopJ pr…

Transcriptional Activationmedicine.medical_treatmentMolecular Sequence DataApoptosisBiologySH2 domainTransfectionMicrobiologysrc Homology DomainsGenes ReportermedicineYersinia pseudotuberculosisHumansAmino Acid SequenceMolecular BiologyGeneTranscription factorCells CulturedSrc homology domainVirulenceTumor Necrosis Factor-alphaMacrophagesNF-kappa BYersiniosisGene Expression Regulation Bacterialbiology.organism_classificationmedicine.diseaseFlow CytometryMolecular biologyCell biologyCytokineYersinia pseudotuberculosisPhosphorylationCytokinesBacterial Outer Membrane ProteinsHeLa CellsPlasmidsMolecular microbiology
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Abstract 4372: Chronic myeloid leukemia (CML) exosomes promote angiogenesis in a Src-dependent fashion in vitro and in vivo

2012

Abstract CML is an uncontrolled proliferation of bone marrow myeloid cells driven by the constitutively active fusion product tyrosine kinase BCR/ABL. Angiogenesis, the formation of new blood vessels from pre-existing vasculature, is newly recognized as a factor in CML progression. Exosomes, released by a broad spectrum of cells, are microvesicles that play an important role in cell-to-cell communication both in physiological and pathological conditions. The role of exosomes released by CML cells in angiogenesis is emerging; however, little is known about the mechanisms involved in this process. We first isolated and characterized exosomes released by K562 CML cells and we demonstrated thei…

Tube formationCancer Researchmedicine.medical_specialtyAngiogenesisbusiness.industryImatinibExosomeMicrovesiclesDasatinibEndocrinologyOncologyhemic and lymphatic diseasesInternal medicineCancer researchmedicinebusinessTyrosine kinasemedicine.drugProto-oncogene tyrosine-protein kinase SrcCancer Research
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Pharmacogenomic identification of small molecules for lineage specific manipulation of subventricular zone germinal activity

2017

Strategies for promoting neural regeneration are hindered by the difficulty of manipulating desired neural fates in the brain without complex genetic methods. The subventricular zone (SVZ) is the largest germinal zone of the forebrain and is responsible for the lifelong generation of interneuron subtypes and oligodendrocytes. Here, we have performed a bioinformatics analysis of the transcriptome of dorsal and lateral SVZ in early postnatal mice, including neural stem cells (NSCs) and their immediate progenies, which generate distinct neural lineages. We identified multiple signaling pathways that trigger distinct downstream transcriptional networks to regulate the diversity of neural cells …

animal diseasesGene Identification and AnalysisGenetic NetworksAPC-PAIDMiceNeural Stem CellsCell SignalingLateral VentriclesDatabases GeneticGene Regulatory NetworksBiology (General)WNT Signaling CascadeNotch SignalingOrganic CompoundsBB/M029379/1GenomicsSignaling CascadesOligodendrogliaChemistryBBSRCPhysical Sciences[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Network AnalysisNeurovetenskaperSignal TransductionResearch ArticleBiotechnologyComputer and Information SciencesSignal InhibitionQH301-705.5NeurogenesisResearch and Analysis MethodsSmall Molecule LibrariesGenetics/dk/atira/pure/core/subjects/biomedicalsciencesAnimalsAdultsCell LineageComputer Simulation[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Molecular Biology TechniquesMolecular BiologyOrganic ChemistryGene MappingChemical CompoundsNeurosciencesBiology and Life SciencesRCUKBiomedical SciencesCell BiologyNerve RegenerationSignaling NetworksGene Expression Regulationnervous systemSmall MoleculesAge GroupsPeople and PlacesPopulation GroupingsTranscriptome
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Mechanisms involved in lipid accumulation and apoptosis induced by 1-nitropyrene in Hepa1c1c7 cells

2011

International audience; 1-Nitropyrene (1-NP) is a nitro-polycyclic aromatic hydrocarbon (nitro-PAH) present in diesel exhaust and bound to particular matter in urban air. We show that 1-NP and the referent PAH benzo(a)pyrene (BP) induce apoptosis and a lipid accumulation dependent on cytochrome P450 1A1-metabolites in mouse hepatoma cells, whereas 1-amino-pyrene had no effect. The caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone (Z-VAD-fmk), inhibits 1-NP-induced apoptosis, but failed to alter 1-NP-triggered lipid accumulation determined by Nile red staining. We further show that cholesterol and fatty acid contents are modified after nitro-PAH exposure and that 1…

endoplasmic-reticulum stressMESH: PyrenesHepatoma cellsliver-cellsactivated protein-kinaseApoptosisAMP-Activated Protein KinasesToxicologyMESH: Liver Neoplasms ExperimentalMicechemistry.chemical_compoundMESH: CholesterolLiver Neoplasms ExperimentalMESH: AnimalsMESH: AMP-Activated Protein KinasesStearoyl-CoA desaturase 1CaspaseMESH: Lipid Metabolismchemistry.chemical_classificationhuman macrophages0303 health sciencesPyrenesbiology8-tetrachlorodibenzo-p-dioxin tcdd030302 biochemistry & molecular biologyGeneral Medicineinhibition[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]CholesterolBiochemistry[SDV.TOX]Life Sciences [q-bio]/ToxicologyCaspaseslipids (amino acids peptides and proteins)stearoyl-coaStearoyl-CoA DesaturaseMESH: Cell Line Tumor[SDV.BC]Life Sciences [q-bio]/Cellular Biology03 medical and health sciencesMESH: Benzo(a)pyreneCell Line Tumor1-NitropyreneBenzo(a)pyreneAnimalsFatty acidsProtein kinase AMESH: Mice030304 developmental biologyaromatic-hydrocarbonsMESH: CaspasesCholesterolMESH: Apoptosisc-srcFatty acidAMPKCytochrome P450Lipid MetabolismMolecular biologychemistryApoptosisMESH: Stearoyl-CoA Desaturasebiology.proteinStearoyl-CoA desaturase-1desaturaseToxicology Letters
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Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.

2018

Cardiovascular diseases (CVDs), including atherosclerosis, are globally the leading cause of death. Key factors contributing to onset and progression of atherosclerosis include the pro-inflammatory cytokines Interferon (IFN)a and IFN? and the Pattern Recognition Receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT)s. Searches for compounds targeting the pTyr-SH2 interaction area of STAT3, yielded many small molecules, including STATTIC and STX-0119. However, many of these inhibitors do not seem STAT3-specific. We hypothesized that multi-STAT-inhibitors that simultaneously block STAT1, STAT2, and STAT3 activit…

lcsh:Immunologic diseases. Allergy0301 basic medicineMaleIn silicoImmunologyGene ExpressionBiologystatIn silico dockingCell LineSmall Molecule Librariessrc Homology Domains03 medical and health sciencesCVDs treatment strategyImmunology and AllergyAnimalsHumansvascular inflammationSTAT1STAT2STAT3Vascular inflammationCells CulturedOriginal ResearchOxadiazolesGene Expression ProfilingSTATPattern recognition receptorin silico dockingFarmaciaAtherosclerosisCyclic S-OxidesMice Inbred C57BLSTAT Transcription Factors030104 developmental biologyCardiovascular DiseasesTLR4biology.proteinSTAT proteinCancer researchQuinolinesmulti-STAT inhibitorsMulti-STAT inhibitorslcsh:RC581-607Genome-Wide Association StudySignal TransductionFrontiers in immunology
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A MiR-142-3p/EGR2 Feedback Circuitry In Human CSF-1 Driven Differentiation of Monocytes Into Macrophages

2011

Abstract Abstract 2366 Colony-stimulating factor-1 (CSF-1 or M-CSF) triggers the differentiation of human peripheral blood monocytes into macrophages through and integrated cytokine/transcription factors circuitry. Using microarray profiling to explore the role of microRNAs (miRNAs) in this molecular circuitry, we identified the down-regulation of miR-142-3p in human macrophages obtained from CSF-1-treated monocytes. We show that miR-142-3p is a repressor of the transcription factor EGR2 (Early Growth Response 2) through direct 3'UTR interactions. Interestingly, EGR2 binds the promoter of the pre-miR-142-3p gene to negatively regulate its expression, identifying a self-regulatory feedback l…

medicine.medical_treatmentImmunologyRepressorChronic myelomonocytic leukemiaCell BiologyHematologyBiologyColony-stimulating factormedicine.diseaseBiochemistryCell biologyCytokinemicroRNAmedicineGeneTranscription factorProto-oncogene tyrosine-protein kinase SrcBlood
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