Search results for " K"

showing 10 items of 22846 documents

Identification of the integrin-binding site on coagulation factor VIIa required for proangiogenic PAR2 signaling.

2018

The tissue factor (TF) pathway serves both hemostasis and cell signaling, but how cells control these divergent functions of TF remains incompletely understood. TF is the receptor and scaffold of coagulation proteases cleaving protease-activated receptor 2 (PAR2) that plays pivotal roles in angiogenesis and tumor development. Here we demonstrate that coagulation factor VIIa (FVIIa) elicits TF cytoplasmic domain-dependent proangiogenic cell signaling independent of the alternative PAR2 activator matriptase. We identify a Lys-Gly-Glu (KGE) integrin-binding motif in the FVIIa protease domain that is required for association of the TF-FVIIa complex with the active conformer of integrin β1. A po…

0301 basic medicineCell signalingImmunologyIntegrinNeovascularization PhysiologicFactor VIIa030204 cardiovascular system & hematologyBiochemistryThromboplastinThrombosis and Hemostasis03 medical and health sciencesTissue factorMice0302 clinical medicineAnimalsHumansReceptor PAR-2Protein Interaction Domains and MotifsProtein Interaction MapsProtein kinase ACells CulturedIntegrin bindingBinding SitesbiologyChemistryIntegrin beta1Cell BiologyHematologyCell biologyCrosstalk (biology)030104 developmental biologyADP-Ribosylation Factor 6biology.proteinNIH 3T3 CellsPhosphorylationSignal transductionProtein BindingSignal TransductionBlood
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Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-β1-induced epithelial-to-mesenchymal transition in human non-small cell…

2020

AbstractIn human lung cancer progression, the EMT process is characterized by the transformation of cancer cells into invasive forms that migrate to other organs. Targeting to EMT-related molecules is emerging as a novel therapeutic approach for the prevention of lung cancer cell migration and invasion. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as an anti-proliferative target molecule to regulate the Wnt signaling pathway in several types of cancer cells. In the present study, we evaluated the inhibitory effect of a tyrosine kinase inhibitor sunitinib and the integrin-αVβ3targeted cyclic peptide (cRGDfK) on EMT in human lung cancer cells. Sunitinib strongly inhib…

0301 basic medicineCell signalingIntegrinsLung NeoplasmsProtein ExpressionCancer TreatmentSmad ProteinsSignal transductionLung and Intrathoracic TumorsTyrosine-kinase inhibitorAdenosine Triphosphate0302 clinical medicineCarcinoma Non-Small-Cell LungCatalytic DomainAntineoplastic Combined Chemotherapy ProtocolsMedicine and Health SciencesSunitinibWnt Signaling PathwayWNT Signaling CascadeMultidisciplinarySunitinibChemistryQRWnt signaling pathwaySignaling cascadesDrug SynergismExtracellular MatrixMolecular Docking SimulationOncology030220 oncology & carcinogenesisMedicineCellular Structures and OrganellesSignal transductionResearch Articlemedicine.drugCell biologySignal InhibitionEpithelial-Mesenchymal TransitionCell Survivalmedicine.drug_classScienceSMAD signalingProtein Serine-Threonine KinasesResearch and Analysis MethodsPeptides CyclicTransforming Growth Factor beta103 medical and health sciencesCell Line TumorGene Expression and Vector TechniquesCell AdhesionBiomarkers TumormedicineHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionMolecular Biology TechniquesLung cancerMolecular BiologyA549 cellMolecular Biology Assays and Analysis TechniquesBiology and life sciencesCancers and NeoplasmsIntegrin alphaVbeta3medicine.diseaseNon-Small Cell Lung Cancer030104 developmental biologyTGF-beta signaling cascadeA549 CellsTNIKCancer cellCancer researchPLOS ONE
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The Role of Nrf2 and PPARγ in the Improvement of Oxidative Stress in Hypertension and Cardiovascular Diseases

2020

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological change…

0301 basic medicineCell signalingNF-E2-Related Factor 2PhysiologyBlood PressureReviewOxidative phosphorylationmedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwaychemistry.chemical_classificationReactive oxygen speciesKelch-Like ECH-Associated Protein 1ChemistryGeneral MedicineKEAP1Antioxidant Response ElementsNFE2L2Cell biologyPPAR gammaOxidative Stress030104 developmental biologyCardiovascular DiseasesHypertensionReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressSignal TransductionPhysiological Research
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Polyphenols from Pennisetum glaucum grains induce MAP kinase phosphorylation and cell cycle arrest in human osteosarcoma cells

2019

Abstract Osteosarcoma is the most common bone tumor with a high prevalence among children and adolescents. Polyphenols are widely investigated for their chemopreventive and chemotherapeutic proprieties. In the present study, we explored the pro-apoptotic effects of pearl millet, Pennisetum glaucum, phenolic compounds (PGPC) on osteosarcoma U-2OS cells. Our results show that PGPC induced U-2OS cells death, in a dose dependent manner, with an IC50 of 80 μg/mL. Annexin-V and 7-AAD staining show that PGPC induced cell death mainly through caspase-dependent apoptosis as shown by a decrease in cell death when co-treated with pan-caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketon…

0301 basic medicineCell signalingProgrammed cell deathCell cycle checkpointp38 mitogen-activated protein kinases[SDV]Life Sciences [q-bio]Medicine (miscellaneous)Pearl milletCell cycle arrest03 medical and health sciences0404 agricultural biotechnologyTX341-641Intracellular calciumProtein kinase BPI3K/AKT/mTOR pathwayCaspase030109 nutrition & dieteticsNutrition and DieteticsbiologyNutrition. Foods and food supplyChemistryCyclin-dependent kinase 2Polyphenols04 agricultural and veterinary sciencesU-2OS cells040401 food scienceMolecular biology3. Good healthApoptosisbiology.proteinFood Science
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EphrinB2 repression through ZEB2 mediates tumour invasion and anti-angiogenic resistance.

2016

Diffuse invasion of the surrounding brain parenchyma is a major obstacle in the treatment of gliomas with various therapeutics, including anti-angiogenic agents. Here we identify the epi-/genetic and microenvironmental downregulation of ephrinB2 as a crucial step that promotes tumour invasion by abrogation of repulsive signals. We demonstrate that ephrinB2 is downregulated in human gliomas as a consequence of promoter hypermethylation and gene deletion. Consistently, genetic deletion of ephrinB2 in a murine high-grade glioma model increases invasion. Importantly, ephrinB2 gene silencing is complemented by a hypoxia-induced transcriptional repression. Mechanistically, hypoxia-inducible facto…

0301 basic medicineCell signalingScienceGeneral Physics and AstronomyRepressorDown-RegulationAngiogenesis InhibitorsEphrin-B2BiologyGeneral Biochemistry Genetics and Molecular BiologyArticleNeovascularization03 medical and health sciencesDownregulation and upregulationddc:570GliomamedicineGene silencingAnimalsHumansNeoplasm InvasivenessPsychological repressionZinc Finger E-box Binding Homeobox 2Regulation of gene expressionMice KnockoutMultidisciplinaryNeovascularization PathologicQGeneral ChemistryGliomamedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitXenograft Model Antitumor AssaysCell HypoxiaCell biologyUp-RegulationBevacizumabGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyDrug Resistance Neoplasmmedicine.symptomNature communications
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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Thymus-derived regulatory T cells are positively selected on natural self-antigen through cognate interactions of high functional avidity

2016

Regulatory T (Treg) cells expressing Foxp3 transcripton factor are essential for immune homeostasis. They arise in the thymus as a separate lineage from conventional CD4+Foxp3- T (Tconv) cells. Here, we show that the thymic development of Treg cells depends on the expression of their endogenous cognate self-antigen. The formation of these cells was impaired in mice lacking this self-antigen, while Tconv cell development was not negatively affected. Thymus-derived Treg cells were selected by self-antigens in a specific manner, while autoreactive Tconv cells were produced through degenerate recognition of distinct antigens. These distinct modes of development were associated with the expressi…

0301 basic medicineCell typeCancer ResearchEncephalomyelitis Autoimmune ExperimentalMultiple Sclerosis[SDV]Life Sciences [q-bio]ImmunologyReceptors Antigen T-CellEndogenyT-Cell Antigen Receptor Specificitychemical and pharmacologic phenomenaThymus GlandBiologymedicine.disease_causeAutoantigensT-Lymphocytes RegulatoryAutoimmunity03 medical and health sciencesMice0302 clinical medicineAntigenT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsHumansAvidityCTLA-4 AntigenReceptorClonal Selection Antigen-MediatedCells CulturedMice KnockoutCell growthFOXP3Forkhead Transcription Factorshemic and immune systemsPeptide Fragments[SDV] Life Sciences [q-bio]Mice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyMyelin-Oligodendrocyte Glycoprotein030215 immunology
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Cell-Type-Specific Responses to Interleukin-1 Control Microbial Invasion and Tumor-Elicited Inflammation in Colorectal Cancer.

2017

Summary Chronic inflammation drives the progression of colorectal cancer (CRC). Increased expression of interleukin (IL)-17A is associated with poor prognosis, and IL-17A blockade curbs tumor progression in preclinical models of CRC. Here we examined the impact of IL-1 signaling, a key regulator of the IL-17 pathway, in different cell types within the CRC microenvironment. Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth. T cell specific ablation of IL-1R1 decreased tumor-elicited inflammation dependent on IL-17 and IL-22, thereby reducing…

0301 basic medicineCell typeColorectal cancerCarcinogenesisNeutrophilsmedicine.medical_treatmentImmunologyMedizinInflammationBiologymedicine.disease_causeArticle03 medical and health sciencesMice0302 clinical medicineSalmonellamedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansCells CulturedInflammationMice KnockoutTumor microenvironmentSalmonella Infections AnimalInterleukinsInterleukin-17InterleukinReceptors Interleukin-1medicine.disease030104 developmental biologyInfectious DiseasesCytokineTumor progressionOrgan Specificity030220 oncology & carcinogenesisCancer researchmedicine.symptomCarcinogenesisColorectal NeoplasmsInterleukin-1Signal TransductionImmunity
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Spleen tyrosine kinase (SYK) is a potential target for the treatment of cutaneous lupus erythematosus patients

2016

Spleen tyrosine kinase (SYK) is a protein kinase involved in cell proliferation and the regulation of inflammatory pathways. Due to the increasing evidence that kinase inhibitors have potential as specific anti-inflammatory drugs, we have investigated the potential for SYK inhibition as a therapeutic target in autoimmune diseases, particularly cutaneous lupus erythematosus (CLE). Skin samples of patients with different CLE subtypes and appropriate controls were analysed for the expression of SYK and SYK-associated pro-inflammatory mediators via gene expression analysis and immunohistochemistry. The functional role of SYK in keratinocytes was investigated in vitro, using LE-typical pro-infla…

0301 basic medicineCell typeSykchemical and pharmacologic phenomenaDermatologyenvironment and public healthBiochemistry03 medical and health sciencesImmune systemDownregulation and upregulationLupus Erythematosus CutaneousmedicineHumansSyk KinasePhosphorylationMolecular BiologyCells CulturedInnate immune systemSystemic lupus erythematosusKinasebusiness.industryhemic and immune systemsmedicine.diseaseenzymes and coenzymes (carbohydrates)030104 developmental biologyCase-Control StudiesImmunologyCytokinesPhosphorylationbiological phenomena cell phenomena and immunitybusinessExperimental Dermatology
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Autophagy in the pathogenesis of ankylosing spondylitis

2016

The pathogenesis of ankylosing spondylitis (AS) is not well understood, and treatment options have met with limited success. Autophagy is a highly conserved mechanism of controlled digestion of damaged organelles within a cell. It helps in the maintenance of cellular homeostasis. The process of autophagy requires the formation of an isolation membrane. They form double-membraned vesicles called “autophagosomes” that engulf a portion of the cytoplasm. Beyond the role in maintenance of cellular homeostasis, autophagy has been demonstrated as one of the most remarkable tools employed by the host cellular defense against bacteria invasion. Autophagy also affects the immune system and thus is im…

0301 basic medicineCellAutophagy-Related ProteinsATG16L1Cellular homeostasisInflammationBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Pathogenesis03 medical and health sciencesImmune systemRheumatologyATG16L1; Autophagy; Inflammation; LRRK2; Pathogenesis; Spondyloarthritis; RheumatologyPathogenesiAutophagymedicineHomeostasisHumansSpondylitis AnkylosingATG16L1InflammationAutophagyLRRK2General MedicineCell biology030104 developmental biologymedicine.anatomical_structureCytoplasmSpondyloarthritimedicine.symptomClinical Rheumatology
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