Search results for "IκBα"

showing 9 items of 19 documents

Characterization of aging-associated up-regulation of constitutive nuclear factor-kappa B binding activity.

2001

Changes occur in gene expression during aging in vivo and in replicative senescence in vitro, suggesting that aging can affect gene regulation. We have recently observed age-related changes in ubiquitously expressed, oxidative stress-responsive nuclear factor-kappa B (NF-kappa B) pathway during aging. Here we report a significant age-related increase in nuclear NF-kappa B binding activity together with increased protein levels of p52 and p65 components in rat liver. An additional, higher molecular weight protein band seen in their western blots suggests that their post-translational modification (but not phosphorylation) occurs in liver, which might affect their nuclear localization and bin…

SenescenceAgingPhysiologyClinical BiochemistryBlotting WesternCell Cycle ProteinsNerve Tissue ProteinsIκB kinaseBiologyTransfectionBiochemistrySynaptotagminsCalcium-binding proteinGene expressionAnimalsRats WistarPromoter Regions GeneticMolecular BiologyCells CulturedGeneral Environmental ScienceRegulation of gene expressionMembrane GlycoproteinsCalcium-Binding ProteinsNF-kappa BCell BiologyBlotting NorthernMolecular biologyRatsUp-RegulationIκBαGene Expression RegulationLiverSynaptotagmin IGeneral Earth and Planetary SciencesPhosphorylationNuclear localization sequenceAntioxidantsredox signaling
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Attenuation of NF-κB Signaling Response to UVB Light during Cellular Senescence

1999

The ability of cells to adapt to environmental stresses undergoes a progressive reduction during aging. NF-kappaB-mediated signaling is a major defensive system against various environmental challenges. The aim of this study was to find out whether replicative senescence affects the response of the NF-kappaB signaling pathway to UVB light in human WI-38 and IMR-90 fibroblasts. The exposure of early passage fibroblasts to UVB light inhibited the proliferation and induced a flat phenotype similar to that observed in replicatively senescent fibroblasts not exposed to UVB light. The UVB radiation dose used (153 mJ/cm2) did not induce apoptosis in either early or late passage WI-38 fibroblasts. …

SenescenceP50Ultraviolet RaysLactams MacrocyclicBiologyCell LineBenzoquinonesHumansEnzyme InhibitorsProtein Kinase InhibitorsCellular SenescenceCell Line TransformedNF-kappa BQuinonesCell BiologyFibroblastsTyrphostinsMolecular biologyIκBαRifabutinApoptosisPhosphorylationTumor necrosis factor alphaSignal transductionNuclear localization sequenceSignal TransductionExperimental Cell Research
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Targeting V-ATPase in primary human monocytes by archazolid potently represses the classical secretion of cytokines due to accumulation at the endopl…

2014

The macrolide archazolid inhibits vacuolar-type H(+)-ATPase (V-ATPase), a proton-translocating enzyme involved in protein transport and pH regulation of cell organelles, and potently suppresses cancer cell growth at low nanomolar concentrations. In view of the growing link between inflammation and cancer, we investigated whether inhibition of V-ATPase by archazolid may affect primary human monocytes that can promote cancer by sustaining inflammation through the release of tumor-promoting cytokines. Human primary monocytes express V-ATPase, and archazolid (10-100nM) increases the vesicular pH in these cells. Archazolid (10nM) markedly reduced the release of pro-inflammatory (TNF-α, interleuk…

Vacuolar Proton-Translocating ATPasesmedicine.medical_specialtyp38 mitogen-activated protein kinasesInflammationBiologyEndoplasmic ReticulumBiochemistryMonocytesCell Linechemistry.chemical_compoundInternal medicinemedicineHumansSecretionPhosphorylationProtein kinase BDNA PrimersPharmacologyBase SequenceDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionEndoplasmic reticulumBafilomycinCell biologyIκBαEndocrinologySecretory proteinMicroscopy FluorescencechemistryCytokinesMacrolidesmedicine.symptomSignal TransductionBiochemical Pharmacology
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Sources, Chemistry, and Biological Potential of Ellagitannins and Ellagic Acid Derivatives

2019

Abstract The consumption of polyphenols is considered an important part of a healthy life style and is related to reducing the risk for diseases. Ellagitanins (e.g., vescalagin, punicalagin, and castalagin) and ellagic acid and its derived compounds (e.g., urolithin) have been receiving attention in recent years as bioactive substances. This class of phenolic substances can be found in berries, pomegranates, walnuts, almonds, and other plant material that is consumed as traditional medicine to treat inflammatory diseases. Human gut microbiota are considered to play an important role in the bioactivity of ellagic acid derivative activity due to the production of urolithin and its antiinflamm…

chemistry.chemical_classificationMAPK/ERK pathway0303 health sciences030309 nutrition & dieteticsNeurotoxicityPeroxisome proliferator-activated receptor04 agricultural and veterinary sciencesPharmacologymedicine.disease040401 food scienceUrolithin03 medical and health sciencesIκBαchemistry.chemical_compound0404 agricultural biotechnologychemistryPolyphenolmedicinePunicalaginEllagic acid
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Weaning induces NOS-2 expression through NF-κB modulation in the lactating mammary gland: importance of GSH

2005

Zaragozá, R; Miralles, VJ; Rus, AD; García, C; Carmena, R; García-Trevijano, ER; Barber, T; Pallardó, FV; Torres, L; Viña, JR. At the end of lactation the mammary gland undergoes involution, a process characterized by apoptosis of secretory cells and tissue remodelling. To gain insight into this process, we analysed the gene expression profile by oligonucleotide microarrays during lactation and after forced weaning. Up-regulation of inflammatory mediators and acute-phase response genes during weaning was found. Expression of IκBα (inhibitory κBα), a protein known to modulate NF-κB (nuclear factor-κB) nuclear translocation, was significantly up-regulated. On the other hand, there was a time-…

medicine.medical_specialtyMammary glandDown-RegulationNitric Oxide Synthase Type IIWeaninglactationBiologyBiochemistryNF-κBMammary Glands AnimalWestern blotnitric oxideInternal medicineLactationGene expressionmedicineGSHinvolutionWeaningAnimalsInvolution (medicine)Rats WistarPromoter Regions GeneticMolecular Biologymedicine.diagnostic_test:CIENCIAS DE LA VIDA::Bioquímica [UNESCO]Gene Expression ProfilingNF-kappa BUNESCO::CIENCIAS DE LA VIDA::BioquímicaCell BiologyGlutathioneRatsUp-RegulationIκBαProtein Transportmedicine.anatomical_structureEndocrinologyEnzyme InductionFemaleChromatin immunoprecipitationProtein BindingResearch Article
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Synergistic effects of fluticasone propionate and salmeterol on in vitro T-cell activation and apoptosis in asthma

2004

Background In asthma T cells are characterized by an increased activation state and by reduced apoptosis. Objective Because the clinical efficacy of inhaled corticosteroids combined with long-acting β 2 -agonists has been widely demonstrated in asthma, we studied, in vitro , the effect of fluticasone propionate (FP) and salmeterol alone and in combination on the activation and apoptosis of peripheral blood T cells (PBTs), on the expression of phosphorylated nuclear factor κB inhibitor (IκBα), and on the nuclear translocation of glucocorticoid receptor (GR) in PBTs from asthmatic subjects. Methods Apoptosis was evaluated on the basis of annexin V binding, whereas the expression of caspases 8…

medicine.medical_specialtyProgrammed cell deathAdolescentT cellT-LymphocytesImmunologyActive Transport Cell NucleusApoptosisAndrostadienes; Active Transport Cell Nucleus; NF-kappa B; Apoptosis; Humans; Albuterol; Receptors Glucocorticoid; Asthma; Child; Caspases; Lymphocyte Activation; Phosphorylation; I-kappa B Proteins; Adolescent; Drug Synergism; T-LymphocytesLymphocyte ActivationGlucocorticoid receptorReceptors GlucocorticoidNF-KappaB Inhibitor alphaAnnexinInternal medicinemedicineHumansImmunology and AllergyAlbuterolPhosphorylationChildSalmeterol XinafoateAndrostadieneChemistryActive Transport Cell NucleuNF-kappa BApoptosiDrug SynergismCaspaseAsthmaAndrostadienesIκBαEndocrinologymedicine.anatomical_structureApoptosisCaspasesFluticasoneI-kappa B ProteinI-kappa B ProteinsSalmeterolGlucocorticoidmedicine.drugHuman
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Inhibition of the NF-κB Signaling Pathway Mediates the Anti-inflammatory Effects of Petrosaspongiolide M

2003

Petrosaspongiolide M (PT) is a potent secretory phospholipase A(2) inhibitor and anti-inflammatory agent. This marine metabolite reduced the production of nitrite, prostaglandin E(2), and tumor necrosis factor-alpha in the mouse air pouch injected with zymosan. These effects were also observed in mouse peritoneal macrophages stimulated with zymosan. Inhibition of these inflammatory mediators was related to reductions in inducible nitric oxide synthase, cyclo-oxygenase-2, and tumor necrosis factor-alpha expression. Since nuclear factor-kappaB (NF-kappaB) appears to play a central role in the transcriptional regulation of these proteins by macrophages, we investigated the effects of PT on thi…

medicine.medical_treatmentAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiochemistryDinoprostoneMicechemistry.chemical_compoundPhospholipase A2NF-KappaB Inhibitor alphaCell MovementmedicineAnimalsRNA MessengerOleanolic AcidPhosphorylationNitritesPharmacologybiologyTumor Necrosis Factor-alphaZymosanNF-kappa BZymosanBiological TransportNF-κBDNACell biologyIsoenzymesNitric oxide synthaseIκBαCytokinechemistryBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesModels AnimalMacrophages Peritonealbiology.proteinCytokinesI-kappa B ProteinsTumor necrosis factor alphaNitric Oxide SynthaseSignal TransductionProstaglandin E
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Rho GTPases Are Involved in the Regulation of NF-κB by Genotoxic Stress

2001

A common cellular response to genotoxic agents and inflammatory cytokines is the activation of NF-kappaB. Here, we addressed the question of whether small GTPases of the Rho family are involved in the stimulation of NF-kappaB signaling by genotoxic agents or TNFalpha in HeLa cells. Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Furthermore, NF-kappaB-regulated gene expression stimulated by either UV irradiation or treatment with TNFalpha was abrogated by lovastatin pretreatment. This indicates that iso…

rho GTP-Binding ProteinsBacterial ToxinsClostridium difficile toxin BGenotoxic StressGTPaseBiologyProinflammatory cytokinechemistry.chemical_compoundBacterial ProteinsNF-KappaB Inhibitor alphamedicineHumansLovastatinTumor Necrosis Factor-alphaNF-kappa BNF-kappa B p50 SubunitNF-κBCell BiologyCell biologyDNA-Binding ProteinsIκBαchemistryDoxorubicinI-kappa B ProteinsTumor necrosis factor alphaLovastatinHeLa CellsSignal Transductionmedicine.drugExperimental Cell Research
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Inhibition of Protein Isoprenylation Impairs Rho-Regulated Early Cellular Response to Genotoxic Stress

2000

Activation of c-Jun N-terminal kinases (JNKs) and nuclear factor-kappaB (NF-kappaB) are early cellular responses to genotoxic stress involved in the regulation of gene expression. Pretreatment of cells with the hydroxymethyl glutaryl-CoA reductase inhibitor lovastatin blocked stimulation of JNK1 activity by UV irradiation and by treatment with the alkylating compound methyl methanesulfonate but did not affect activation of extracellular signal-regulated kinase 2 by UV light. Lovastatin also attenuated UV-induced degradation of the NF-kappaB inhibitor IkappaBalpha. The effects of lovastatin on UV-triggered stimulation of JNK1 as well as on IkappaBalpha degradation were reverted by cotreatmen…

rho GTP-Binding ProteinsProtein PrenylationStimulationClostridium difficile toxin BCHO CellsGenotoxic StressBiologychemistry.chemical_compoundCricetinaemedicineAnimalsHumansMitogen-Activated Protein Kinase 8LovastatinPharmacologyMutagenicity TestsKinaseFarnesyltransferase inhibitorNF-kappa BMethyl methanesulfonateCell biologyIκBαchemistryMolecular MedicineLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsMitogen-Activated Protein KinasesHeLa CellsSignal Transductionmedicine.drugMolecular Pharmacology
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