Search results for "kappa"

showing 10 items of 419 documents

IKK-β inhibitors: An analysis of drug–receptor interaction by using Molecular Docking and Pharmacophore 3D-QSAR approaches

2010

Abstract The IKK kinases family represents a thrilling area of research because of its importance in regulating the activity of NF-kB transcription factors. The discovery of the central role played by IKK-β in the activation of transcription in response to apoptotic or inflammatory stimuli allowed to considerate its modulation as a promising tool for the treatment of chronic inflammation and cancer. To date, several IKK-β inhibitors have been discovered and tested. In this work, an analysis of the interactions between different classes of inhibitors and their biological target was performed, through the application of Molecular Docking and Pharmacophore/3D-QSAR approaches to a set of 141 in…

Models MolecularQuantitative structure–activity relationshipReceptors DrugMolecular Sequence DataQuantitative Structure-Activity RelationshipIκB kinaseComputational biologyPharmacologyBiologyMaterials ChemistryHumansAmino Acid SequenceNF-kBHomology modelingPhysical and Theoretical ChemistryProtein Kinase InhibitorsTranscription factorSpectroscopyIKK-betaIKK-beta inhibitors Molecular Docking Pharmacophore 3D-QSAR approachesBinding SitesPharmacophoreKinaseHomology modelingSettore CHIM/08 - Chimica FarmaceuticaComputer Graphics and Computer-Aided DesignI-kappa B KinaseMolecular DockingStructural Homology ProteinBiological targetDrug receptorPharmacophoreJournal of Molecular Graphics and Modelling
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In murine 3T3 fibroblasts, different second messenger pathways resulting in the induction of NO synthase II (iNOS) converge in the activation of tran…

1996

Transcription factor NF-kappaB is essential for the induction of nitric oxide synthase (NOS) II (iNOS) by bacterial lipopolysaccharide in murine macrophages (Xie, Q. W., Kashiwabara, Y., and Nathan, C. (1994) J. Biol. Chem. 269, 4705-4708). In 3T3 fibroblasts, agents other than cytokines are efficacious inducers of NOS II expression. In addition to cytokines such as interferon-gamma or tumor necrosis factor-alpha, protein kinase C-stimulating agents such as tetradecanoylphorbol-13-acetate, or cyclic AMP-elevating agents such as forskolin and 8-bromo-cAMP markedly increased NOS II mRNA (measured by Sl nuclease and RNase protection analyses), NOS II protein (determined by Western blotting), a…

Molecular Sequence DataBiochemistrySecond Messenger SystemsDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePyrrolidine dithiocarbamateTransforming Growth Factor betaAnimalsHumansAmino Acid SequenceRNA MessengerNuclear proteinProtein kinase AMolecular BiologyTranscription factorProtein Kinase CDNA PrimersForskolinbiologyBase SequenceNF-kappa BReceptor Protein-Tyrosine KinasesCell Biology3T3 CellsMolecular biologyCyclic AMP-Dependent Protein KinasesActinsNitric oxide synthasechemistryEnzyme InductionSecond messenger systembiology.proteinTumor necrosis factor alphaNitric Oxide SynthaseThe Journal of biological chemistry
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Defective stromal remodeling and neutrophil extracellular traps in lymphoid tissues favor the transition from autoimmunity to lymphoma

2013

Abstract Altered expression of matricellular proteins can become pathogenic in the presence of persistent perturbations in tissue homeostasis. Here, we show that autoimmunity associated with Fas mutation was exacerbated and transitioned to lymphomagenesis in the absence of SPARC (secreted protein acidic rich in cysteine). The absence of SPARC resulted in defective collagen assembly, with uneven compartmentalization of lymphoid and myeloid populations within secondary lymphoid organs (SLO), and faulty delivery of inhibitory signals from the extracellular matrix. These conditions promoted aberrant interactions between neutrophil extracellular traps and CD5+ B cells, which underwent malignant …

MyeloidLymphoid Tissue: immunologyLymphomaNeutrophilsChronic lymphocytic leukemiaAutoimmunityOsteonectin: geneticsCHRONIC LYMPHOCYTIC-LEUKEMIA; SYSTEMIC-LUPUS-ERYTHEMATOSUS; INHIBITORY RECEPTOR LAIR-1; KAPPA-B ACTIVATION; MARGINAL ZONE; INFLAMMATORY DISORDERS; MATRICELLULAR PROTEIN; SPARCMalignant transformationExtracellular matrixKAPPA-B ACTIVATIONLymphoma: immunologyMicehemic and lymphatic diseasesOsteonectinSYSTEMIC-LUPUS-ERYTHEMATOSUSNF-kappa B: immunologyCells CulturedTissue homeostasisB-LymphocytesCulturedNF-kappa BLymphoid Tissue: cytologyCell biologyCD5: immunologyExtracellular MatrixMutant Strainsmedicine.anatomical_structureINHIBITORY RECEPTOR LAIR-1OncologyCD95Stromal cellLymphoid TissueCellsBiologyCD95: geneticsCD5 AntigensINFLAMMATORY DISORDERSExtracellular Matrix: immunologymedicineAnimalsHumansfas ReceptorAntigensB-Lymphocytes: immunologyMATRICELLULAR PROTEINCHRONIC LYMPHOCYTIC-LEUKEMIASPARCLymphoma: geneticsNeutrophil extracellular trapsmedicine.diseaseAnimals; Antigens; Autoimmunity; B-Lymphocytes; B-Lymphocytes: immunology; CD5; CD5: immunology; CD95; CD95: genetics; Cells; Cultured; Extracellular Matrix; Extracellular Matrix: immunology; Humans; Lymphoid Tissue; Lymphoid Tissue: cytology; Lymphoid Tissue: immunology; Lymphoma; Lymphoma: genetics; Lymphoma: immunology; Mice; Mutant Strains; NF-kappa B; NF-kappa B: immunology; Neutrophils; Neutrophils: immunology; Osteonectin; Osteonectin: genetics; Osteonectin: immunologyMice Mutant StrainsCD5Neutrophils: immunologyOsteonectin: immunologyMARGINAL ZONELymphoma SPARC autoimmunityCD5
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Cycloamphilectenes, a new type of potent marine diterpenes: inhibition of nitric oxide production in murine macrophages.

2003

The inhibitory effect of a series of 6 cycloamphilectenes, novel marine diterpenes based on amphilectene skeletons and isolated from the Vanuatu sponge Axinella sp., on NO, PGE(2) and TNFalpha production in murine peritoneal macrophages was studied. These compounds reduced potently nitric oxide production in a concentration-dependent manner with IC(50) values in the submicromolar range (0.1-4.3 microM). Studies on intact cells and Western blot analysis showed that the more potent cycloamphilectenes reduced the expression of inducible nitric oxide synthase without affecting cyclo-oxygenase-2 expression. Among them cycloamphilectene 2, the unique compound bearing an exocyclic methylene group,…

NeutrophilsBlotting WesternNitric Oxide Synthase Type IIElectrophoretic Mobility Shift AssayIn Vitro TechniquesNitric OxideGeneral Biochemistry Genetics and Molecular BiologyDinoprostoneNitric oxidechemistry.chemical_compoundMiceStructure-Activity RelationshipWestern blotmedicineAnimalsEdemaHumansGeneral Pharmacology Toxicology and PharmaceuticsMethylenebiologymedicine.diagnostic_testPancreatic ElastaseTumor Necrosis Factor-alphaMacrophagesZymosanAnti-Inflammatory Agents Non-SteroidalAxinellaNF-kappa BMembrane ProteinsGeneral Medicinebiology.organism_classificationPoriferaNitric oxide synthaseIsoenzymesSpongechemistryBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide Synthasesbiology.proteinMacrophages PeritonealTumor necrosis factor alphaFemaleMarine ToxinsDiterpenesNitric Oxide SynthaseLife sciences
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Pharmacology of Ischemia-Reperfusion. Translational Research Considerations.

2016

Ischemia-reperfusion (IRI) is a complex physiopathological mechanism involving a large number of metabolic processes that can eventually lead to cell apoptosis and ultimately tissue necrosis. Treatment approaches intended to reduce or palliate the effects of IRI are varied, and are aimed basically at: inhibiting cell apoptosis and the complement system in the inflammatory process deriving from IRI, modulating calcium levels, maintaining mitochondrial membrane integrity, reducing the oxidative effects of IRI and levels of inflammatory cytokines, or minimizing the action of macrophages, neutrophils, and other cell types. This study involved an extensive, up-to-date review of the bibliography …

NeutrophilsIschemiaApoptosis030204 cardiovascular system & hematologyPharmacologyurologic and male genital diseasesAntioxidantsProinflammatory cytokineTranslational Research Biomedical03 medical and health sciences0302 clinical medicinemedicineHumanscardiovascular diseasesIschemic PreconditioningOpiate alkaloidurogenital systemMechanism (biology)business.industryTumor Necrosis Factor-alphaMacrophagesOpiate AlkaloidsfungiNF-kappa BComplement System Proteinsmedicine.diseaseApoptosis030220 oncology & carcinogenesisReperfusion InjuryAnesthetics InhalationIschemic preconditioningCytokinesSurgeryTumor necrosis factor alphaInflammation MediatorsbusinessReperfusion injuryJournal of investigative surgery : the official journal of the Academy of Surgical Research
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Involvement of PKC and NF-κB in Nitric Oxide Induced Apoptosis in Human Coronary Artery Smooth Muscle Cells

2001

Apoptosis of vascular smooth muscle cells is critically involved in progression of atherosclerosis and may prevent intimal hyperplasia in restenosis and vascular remodeling. Nitric oxide (NO) is known to induce apoptosis, but the signaling pathways still remain unclear. We investigated p53 accumulation, protein kinase C (PKC) activation and nuclear transcription factor (NF-kappaB) binding activity as possible signaling mechanisms of NO-induced apoptosis. Apoptosis was induced dose-dependently with the NO-donors sodiumnitroprusside (SNP: 232+/-48%) and SIN-1 (241+/-90% of actinomycin D induced apoptosis; means +/- SEM, *por =0.05 vs. control) in HSMC. Inhibition of PKC significantly attenuat…

Nitroprussidemedicine.medical_specialtyVascular smooth muscleIntimal hyperplasiaPhysiologyApoptosisDNA FragmentationNaphthalenesNitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundNF-KappaB Inhibitor alphaRestenosisInternal medicinemedicineHumansNitric Oxide DonorsEnzyme InhibitorsCells CulturedProtein Kinase CProtein kinase CCell Nucleusbusiness.industryNF-kappa BNF-κBStaurosporinemedicine.diseaseCoronary VesselsDNA-Binding Proteinsmedicine.anatomical_structurechemistryApoptosisMolsidomineCancer researchCardiologyI-kappa B ProteinsTumor Suppressor Protein p53businessArteryCellular Physiology and Biochemistry
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Validation of short term recall of mobile phone use for the Interphone study

2006

Aim: To validate short term recall of mobile phone use within Interphone, an international collaborative case control study of tumours of the brain, acoustic nerve, and salivary glands related to mobile telephone use. Methods: Mobile phone use of 672 volunteers in 11 countries was recorded by operators or through the use of software modified phones, and compared to use recalled six months later using the Interphone study questionnaire. Agreement between recalled and actual phone use was analysed using both categorical and continuous measures of number and duration of phone calls. Results: Correlations between recalled and actual phone use were moderate to high (ranging from 0.5 to 0.8 acros…

Observer Variationmedicine.medical_specialtyRecallbusiness.industryPublic Health Environmental and Occupational HealthReproducibility of ResultsAudiologyTerm (time)SurgeryCohen's kappaPhoneMobile phoneCase-Control StudiesMental RecallHumansMedicineOriginal ArticleGeometric meanbusinessCategorical variableCell PhoneKappaOccupational and Environmental Medicine
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Interassay and interobserver comparability study of four programmed death-ligand 1 (PD-L1) immunohistochemistry assays in triple-negative breast canc…

2021

Different immunohistochemical programmed death-ligand 1 (PD-L1) assays and scorings have been reported to yield variable results in triple-negative breast cancer (TNBC). We compared the analytical concordance and reproducibility of four clinically relevant PD-L1 assays assessing immune cell (IC) score, tumor proportion score (TPS), and combined positive score (CPS) in TNBC. Primary TNBC resection specimens (n = 104) were stained for PD-L1 using VENTANA SP142, VENTANA SP263, DAKO 22C3, and DAKO 28–8. PD-L1 expression was scored according to guidelines on virtual whole slide images by four trained readers. The mean PD-L1 positivity at IC-score ≥1% and CPS ≥1 ranged between 53% and 75% with th…

OncologyCPS combined positive scoreTC tumor cellsICI immune checkpoint inhibitorTriple Negative Breast NeoplasmsB7-H1 AntigenMedicineHER2 human epidermal growth factor receptor 2Triple-negative breast cancerRC254-282ICC intraclass correlation coefficientbiologyNeoplasms. Tumors. Oncology. Including cancer and carcinogensGeneral MedicineMSI microsatellite instabilityImmunohistochemistrypCR pathological complete responsePFS progression-free survivalImmunohistochemistryOriginal ArticleIC-ScoreIC immune cellsIHC immunohistochemistryProgrammed deathPD-L1medicine.medical_specialtyConcordanceTNBC triple-negative breast cancerOS overall survivalBreast cancerTriple-negative breast cancerPD-L1Internal medicineTPS tumor proportion scoreBiomarkers TumorHumansProgrammed death-ligand 1Reproducibilitybusiness.industryReproducibility of Resultsmedicine.diseaseITT intention to treatCI confidence intervalPD-L1 programmed death-ligand 1biology.proteinSurgeryCPSbusinessKappaTMB tumor mutational burdenBreast
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Comparative Analyses of Two Established Scores to Assess the Stability of Spinal Bone Metastases Before and After Palliative Radiotherapy

2021

Background and PurposeTo compare two validated spinal instability scores regarding the stabilizing effects and skeletal-related events (SREs) of palliative radiotherapy (RT) in patients with spinal bone metastases (SBM).Materials and MethodsTwo hundred eighty-two osteolytic SBM of lung or breast cancer patients were analyzed for stability before and following RT based on the Spinal Instability Neoplastic Score (SINS) or the Taneichi score. Score concordance was quantified by absolute agreement and Cohen’s kappa coefficient. SREs were defined as fractures or local progression after RT. OS was quantified as the time between the start of RT and death from any cause.ResultsAt 3 and 6 months aft…

OncologyCancer Researchmedicine.medical_specialtyFuture studiesConcordancemedicine.medical_treatmentCohen's kappaBreast cancerPalliative radiotherapyInternal medicinemedicineSINSRC254-282radiotherapyOriginal Researchbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensSpinal instabilityspinal bone metastasesmedicine.diseaseskeletal-related eventsRadiation therapyinstabilityOncologybusinessKappaFrontiers in Oncology
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