Search results for "NF-kappa B p50 Subunit"

showing 10 items of 10 documents

Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes

2009

Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and dec…

Cartilage Articularmedicine.medical_specialtyAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiologyBiochemistryp38 Mitogen-Activated Protein KinasesChondrocyteArticleGene Expression Regulation EnzymologicGlucocorticoid receptorChondrocytesReceptors GlucocorticoidInternal medicineGene expressionmedicineHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulationCell Line TransformedPharmacologyRegulation of gene expressionNF-kappa B p50 SubunitRNA-Binding ProteinsInterferon-Stimulated Gene Factor 3Janus Kinase 2Cell biologyNitric oxide synthaseEndocrinologymedicine.anatomical_structureCell cultureEnzyme Inductionbiology.proteinTrans-ActivatorsCytokinesZearalenoneSignal transduction
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SPARC is a new myeloid-derived suppressor cell marker licensing suppressive activities

2019

Myeloid-derived suppressor cells (MDSC) are well-known key negative regulators of the immune response during tumor growth, however scattered is the knowledge of their capacity to influence and adapt to the different tumor microenvironments and of the markers that identify those capacities. Here we show that the secreted protein acidic and rich in cysteine (SPARC) identifies in both human and mouse MDSC with immune suppressive capacity and pro-tumoral activities including the induction of epithelial-to-mesenchymal transition (EMT) and angiogenesis. In mice the genetic deletion of SPARC reduced MDSC immune suppression and reverted EMT. Sparc−/− MDSC were less suppressive overall and the granu…

STAT3 Transcription Factorlcsh:Immunologic diseases. Allergy0301 basic medicineEpithelial-Mesenchymal TransitionAngiogenesisImmunologyneutrophil extracellular trapsNitric Oxide Synthase Type IIInflammationExtracellular TrapsMice03 medical and health sciences0302 clinical medicineImmune systemBreast cancermedicineMyeloid-derived suppressor cellAnimalsHumansImmunology and AllergyOsteonectinOriginal ResearchMice KnockoutMice Inbred BALB CTumor microenvironmentArginaseChemistryNeutrophilNF-kappa B p50 SubunitSPARCNeutrophil extracellular trapsmyeloid-derived suppressor cells030104 developmental biologyCancer researchMyeloid-derived Suppressor CellTumor necrosis factor alphaSignal transductionmedicine.symptomlcsh:RC581-607Neutrophil extracellular trapBiomarkers030215 immunology
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Characterization of the Clinical and Immunologic Phenotype and Management of 157 Individuals with 56 Distinct Heterozygous NFKB1 Mutations

2020

Contains fulltext : 229571.pdf (Publisher’s version ) (Closed access) BACKGROUND: An increasing number of NFKB1 variants are being identified in patients with heterogeneous immunologic phenotypes. OBJECTIVE: To characterize the clinical and cellular phenotype as well as the management of patients with heterozygous NFKB1 mutations. METHODS: In a worldwide collaborative effort, we evaluated 231 individuals harboring 105 distinct heterozygous NFKB1 variants. To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling. RESU…

0301 basic medicineMaleNF-KAPPA-BMedizinlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Fluorescent Antibody TechniqueAutoimmunityDiseaseNUCLEAR-FACTORKaplan-Meier Estimatemedicine.disease_causeHypogammaglobulinemia0302 clinical medicineNFKB1 variants and mutations; autosomal dominant inheritance; common variable immunodeficiency; reduced penetrance; variable expressivityHDE PEDImmunology and Allergyvariants and mutationsNF-κB1-related phenotypeImmunodeficiencyIMMUNODEFICIENCY*NF-?B1-related phenotypeNFKB1 variants and mutations1184 Genetics developmental biology physiologycommon variable immunodeficiencyDisease ManagementMiddle AgedNF-kappa B1-related phenotypereduced penetrancePrognosisPenetranceImmunohistochemistryMagnetic Resonance Imaging3. Good healthPhenotypeNFKB1 variant*NFKB1 variant*common variable immunodeficiencyFemaleHaploinsufficiency*reduced penetranceNFKB1 mutationAdultHeterozygote*NFKB1 mutationImmunologyHAPLOINSUFFICIENCYArticle03 medical and health sciencesvariable expressivityautosomal dominantmedicineHumansGenetic Predisposition to DiseaseGenetic Association StudiesAgedbusiness.industryCommon variable immunodeficiencyNF-kappa B p50 SubunitNF-KAPPA-B1Immune dysregulationmedicine.diseaseautosomal dominant inheritance030104 developmental biologyBiological Variation PopulationImmunologyCELLSMutation*autosomal dominantPrimary immunodeficiency3111 BiomedicinebusinessTomography X-Ray ComputedBiomarkers030215 immunology
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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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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

2009

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-kappaB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-kappaB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-kappaB inhibits NF-kappaB-driven, M1-polariz…

LipopolysaccharidesP50Macrophage polarizationRegulatorInflammationBiologyImmune toleranceMiceCell polaritymedicineImmune ToleranceMacrophageAnimalsHumansCells CulturedMice KnockoutMultidisciplinaryMacrophagesCell PolarityNF-kappa B p50 SubunitNF-kappa B p50 SubunitInterferon-betaBiological SciencesCell biologyEndotoxinsSTAT1 Transcription FactorImmunologymedicine.symptom
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Tumor-Derived Prostaglandin E2 Promotes p50 NF-κB-Dependent Differentiation of Monocytic MDSCs

2020

Abstract Myeloid-derived suppressor cells (MDSC) include immature monocytic (M-MDSC) and granulocytic (PMN-MDSC) cells that share the ability to suppress adaptive immunity and to hinder the effectiveness of anticancer treatments. Of note, in response to IFNγ, M-MDSCs release the tumor-promoting and immunosuppressive molecule nitric oxide (NO), whereas macrophages largely express antitumor properties. Investigating these opposing activities, we found that tumor-derived prostaglandin E2 (PGE2) induces nuclear accumulation of p50 NF-κB in M-MDSCs, diverting their response to IFNγ toward NO-mediated immunosuppression and reducing TNFα expression. At the genome level, p50 NF-κB promoted binding …

0301 basic medicineCancer ResearchCellular differentiationProstaglandin E2 receptormedicine.medical_treatmentMelanoma ExperimentalApoptosisSettore MED/08 - Anatomia PatologicaNitric OxideDinoprostoneMonocytesInterferon-gammaMice03 medical and health sciences0302 clinical medicineImmune systemOxytocicsImmune ToleranceTumor Cells CulturedmedicineAnimalsHumansProstaglandin E2Cell ProliferationChemistryMyeloid-Derived Suppressor CellsNF-kappa B p50 SubunitCell DifferentiationImmunotherapyAcquired immune systemPancreatic Neoplasms030104 developmental biologyOncologyp50 NF-κB differentiation of monocytic MDSC.030220 oncology & carcinogenesisMyeloid-derived Suppressor CellCancer researchTumor necrosis factor alphaColorectal Neoplasmsmedicine.drugCancer Research
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Aging-induced Up-regulation of Nuclear Binding Activities of Oxidative Stress Responsive NF-kB Transcription Factor in Mouse Cardiac Muscle

1996

The accumulation of lipofuscin to cardiomyocytes is a classical parameter of aging and is believed to reflect oxidative stress. NF-kB transcription factor complex is one of the cellular sensors which responds to oxidative stress and regulates gene expression. Our purpose was to study whether aging affects the level and distribution of DNA binding activities of NF-kB transcription factors both in cardiac sarcoplasm and nuclear extracts. We used electrophoretic mobility shift assays (EMSA) to characterize the DNA binding activities of NF-kB and two other transcription factors. AP-1 and Sp-1, in the myocardium of 4 months and 24 months old male and female NMRI-mice. The protein levels of p50, …

MaleAgingP50Sp1 Transcription FactorSarcoplasmDown-RegulationTranscription factor complexBiologymedicine.disease_causeMiceNF-KappaB Inhibitor alphaGene expressionmedicineAnimalsMolecular BiologyTranscription factorCell NucleusMyocardiumNF-kappa BTranscription Factor RelACardiac muscleNF-kappa B p50 SubunitNF-kappa B p50 SubunitMolecular biologyUp-RegulationDNA-Binding ProteinsTranscription Factor AP-1Oxidative Stressmedicine.anatomical_structureFemaleI-kappa B ProteinsCardiology and Cardiovascular MedicineOxidative stressJournal of Molecular and Cellular Cardiology
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Differential Regulation of CCL22 Gene Expression in Murine Dendritic Cells and B Cells

2005

Abstract The activated T cell-attracting CC chemokine CCL22 is expressed by stimulated B cells and mature dendritic cells (DC). We have cloned and sequenced the complete mouse gene, including 4 kb of the 5′-flanking promoter region, and detected two distinct sites for initiation of transcription by 5′-RACE. Reporter gene assays indicate that the promoter reflects the specificity of the endogenous gene. Within the proximal promoter region, we identified potential binding sites for NF-κB, Ikaros, and a putative GC box. All three regions bind proteins. The NF-κB site was shown to specifically bind NF-κB subunits p50 and p65 from nuclear extracts of LPS-stimulated B cells, B cell line A20/2J, T…

Transcriptional ActivationSp1 Transcription FactorMolecular Sequence DataImmunologyCAAT boxBiologyCell LineMiceTransactivationGene expressionAnimalsImmunology and AllergyCloning MolecularProtein PrecursorsBinding sitePromoter Regions GeneticGeneChemokine CCL22B-LymphocytesMice Inbred BALB CReporter geneBinding SitesBinding proteinNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitPromoterDendritic CellsMolecular biologyDNA-Binding ProteinsMice Inbred C57BLGene Expression RegulationChemokines CCMutagenesis Site-DirectedNIH 3T3 CellsFemaleTranscription Initiation SiteThe Journal of Immunology
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Avarol inhibits TNF-a generation and NF-kB activation in human cells and in animal models

2007

Avarol is a marine sesquiterpenoid hydroquinone with interesting pharmacological properties including anti-inflammatory and antipsoriatic effects. In the present study we evaluated the pharmacological effect of avarol on some inflammatory parameters related to the pathogenesis of psoriasis. Avarol inhibited tumor necrosis factor-alpha (TNF-alpha) generation in stimulated human monocytes (IC(50) 1 microM) and TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB)-DNA binding in keratinocytes. In the mouse air pouch model, administration of avarol produced a dose-dependent reduction of TNF-alpha generation (ED(50) 9.2 nmol/pouch) as well as of interleukin (IL)-1beta, prostaglandin …

Keratinocytesmedicine.medical_specialtymedicine.medical_treatmentAnti-Inflammatory AgentsAntineoplastic AgentsBiologyPharmacologyMonocytesGeneral Biochemistry Genetics and Molecular BiologyCell LineMicechemistry.chemical_compoundDownregulation and upregulationIn vivoInternal medicinemedicineAnimalsHumansPsoriasisGeneral Pharmacology Toxicology and PharmaceuticsPeroxidaseInflammationHyperplasiaDose-Response Relationship DrugTumor Necrosis Factor-alphaNF-kappa B p50 SubunitInterleukinNF-κBGeneral MedicineDisease Models AnimalEndocrinologymedicine.anatomical_structureEicosanoidchemistryTetradecanoylphorbol AcetateFemaleTumor necrosis factor alphaEpidermisInflammation MediatorsKeratinocyteSesquiterpenesProstaglandin E
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Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis

2017

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, t…

AdultMale0301 basic medicineP50ScienceGeneral Physics and AstronomyBiologyT-Lymphocytes RegulatoryInflammatory bowel diseaseArticleGeneral Biochemistry Genetics and Molecular BiologyYoung Adult03 medical and health sciences0302 clinical medicineImmune systemB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsGene expressionmedicineAnimalsHumansColitisMice KnockoutRegulation of gene expressionMultidisciplinaryEffectorHEK 293 cellsQNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitGeneral ChemistryMiddle AgedColitismedicine.diseaseMice Inbred C57BLHEK293 Cells030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisImmunologyFemaleProtein BindingTranscription FactorsNature Communications
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