Search results for "NF-"

showing 10 items of 461 documents

Potential Therapeutic Applications of MDA-9/Syntenin-NF-κB-RKIP Loop in Human Liver Carcinoma

2019

Background Overexpression of MDA-9/Syntenin occurs in multiple human cancer cell lines and is associated with higher grade of tumor classification, invasiveness and metastasis. In some cases, its role in cancer biology depends on relationships between MDA-9/Syntenin and NF-κB. Objective This study aims to analyze the presence of a regulation loop like that between MDA-9/Syntenin - NF-κB - RKIP in human liver carcinoma. Methods Transient transfection was performed with siRNA anti-MDA-9/Syntenin. Expression of different factors was evaluated by Real time-PCR and Western blotting, while NF-κB activation by TransAM assay. Invasion capacity was analyzed by Matrigel Invasion Assay and the effects…

0301 basic medicineMDA-9/Syntenin NF-κB RKIP drug targets HA22T/VGH Hep3B HepG2Carcinoma HepatocellularCurcuminSynteninsPhosphatidylethanolamine Binding ProteinBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationAntineoplastic Combined Chemotherapy ProtocolsHumansGene silencingNeoplasm InvasivenessViability assayMolecular BiologyCell growthMatrigel Invasion AssayLiver NeoplasmsNF-kappa BNF-κBHep G2 CellsGeneral MedicineNeoplasm ProteinsBlot030104 developmental biologychemistryDoxorubicinCell cultureSettore BIO/14 - FarmacologiaCancer researchMolecular MedicineSignal Transduction030215 immunologyCurrent Molecular Medicine
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miR-128 Is Implicated in Stress Responses by Targeting MAFG in Skeletal Muscle Cells.

2017

MAFG (v-Maf avian musculoaponeurotic fibrosarcoma oncogene homolog G) is a bZIP-type transcriptional regulator that belongs to the small MAF (sMAFs) protein family. By interacting with other bZIP transcription factors, sMAFs can form homo- and heterodimers governing either repressive or activating transcriptional functions. As heterodimeric partner of Nrf2, MAFG positively influences the ARE-dependent antioxidant/xenobiotic pathways, at least in condition of a correct MAFG:Nrf2 balance. MicroRNAs (miRs) participate to different regulatory networks being involved as fine-tuning regulators of gene expression. However, the connections between cellular surveillance to stresses mediated by MAFG:…

0301 basic medicineMafG Transcription FactorMaleAgingProtein familyArticle SubjectNF-E2-Related Factor 2Muscle Fibers SkeletalBiologyTransfectionBiochemistryAntioxidants03 medical and health sciencesMiceGene expressionmicroRNATranscriptional regulationAnimalsHumanslcsh:QH573-671Gene3' Untranslated RegionsGeneticsBinding SitesOncogeneThree prime untranslated regionlcsh:CytologyHEK 293 cellsMembrane ProteinsCell BiologyGeneral MedicineMice Inbred C57BLRepressor ProteinsMicroRNAsOxidative Stress030104 developmental biologyHEK293 CellsHeme Oxygenase-1Research ArticleOxidative medicine and cellular longevity
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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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Klebsiella pneumoniae Lipopolysaccharides Serotype O2afg Induce Poor Inflammatory Immune Responses Ex Vivo

2021

Currently, Klebsiella pneumoniae is a pathogen of clinical relevance due to its plastic ability of acquiring resistance genes to multiple antibiotics. During K. pneumoniae infections, lipopolysaccharides (LPS) play an ambiguous role as they both activate immune responses but can also play a role in immune evasion. The LPS O2a and LPS O2afg serotypes are prevalent in most multidrug resistant K. pneumoniae strains. Thus, we sought to understand if those two particular LPS serotypes were involved in a mechanism of immune evasion. We have extracted LPS (serotypes O1, O2a and O2afg) from K. pneumoniae strains and, using human monocytes ex vivo, we assessed the ability of those LPS antigens to in…

0301 basic medicineMicrobiology (medical)SerotypeChemokineQH301-705.5Klebsiella pneumoniae<i>Klebsiella pneumoniae</i>030106 microbiologyMicrobiologyArticleNF-κBMicrobiology03 medical and health scienceschemistry.chemical_compoundImmune systemAntigenVirologyantimicrobial resistanceBiology (General)Pathogenimmune evasionbiologylipopolysaccharideNF-κBSettore CHIM/06 - Chimica Organicalipopolysaccharidesbiology.organism_classificationKlebsiella pneumoniae030104 developmental biologychemistrynosocomial infectionbiology.proteinlipids (amino acids peptides and proteins)Ex vivoMicroorganisms
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The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
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The murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated trans…

2017

The type I interferon (IFN) response is imperative for the establishment of the early antiviral immune response. Here we report the identification of the first type I IFN antagonist encoded by murine cytomegalovirus (MCMV) that shuts down signaling following pattern recognition receptor (PRR) sensing. Screening of an MCMV open reading frame (ORF) library identified M35 as a novel and strong negative modulator of IFNβ promoter induction following activation of both RNA and DNA cytoplasmic PRR. Additionally, M35 inhibits the proinflammatory cytokine response downstream of Toll-like receptors (TLR). Using a series of luciferase-based reporters with specific transcription factor binding sites, …

0301 basic medicineMuromegalovirusPhysiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMiceWhite Blood Cells0302 clinical medicineCell SignalingTranscription (biology)InterferonAnimal CellsImmune PhysiologyMedicine and Health SciencesMembrane Receptor SignalingBiology (General)Enzyme-Linked ImmunoassaysReceptorConnective Tissue CellsbiologyToll-Like ReceptorsPattern recognition receptorNF-kappa BImmune Receptor SignalingEnzymesThe murine cytomegalovirus M35 protein antagonizes type I IFN induction downstream of pattern recognition receptors by targeting NF-κB mediated transcription.Connective TissueReceptors Pattern RecognitionCytomegalovirus InfectionsInterferon Type ISignal transductionCellular TypesAnatomyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.OxidoreductasesLuciferasemedicine.drugProtein BindingSignal TransductionResearch ArticleViral proteinQH301-705.5Immune CellsImmunologyResearch and Analysis MethodsTransfectionMicrobiology03 medical and health sciencesViral ProteinsMuromegalovirusVirologyGeneticsmedicineAnimalsImmunoassaysMolecular Biology TechniquesMolecular BiologyBlood CellsMacrophagesBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Biology and Life SciencesProteinsNF-κBInterferon-betaCell BiologyRC581-607Fibroblastsbiology.organism_classificationMolecular biology030104 developmental biologyBiological TissuechemistryEnzymologyImmunologic TechniquesParasitologyInterferonsImmunologic diseases. AllergySpleen030215 immunology
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Arsenic promotes NF-Κb-mediated fibroblast dysfunction and matrix remodeling to impair muscle stem cell function

2016

Abstract Arsenic is a global health hazard that impacts over 140 million individuals worldwide. Epidemiological studies reveal prominent muscle dysfunction and mobility declines following arsenic exposure; yet, mechanisms underlying such declines are unknown. The objective of this study was to test the novel hypothesis that arsenic drives a maladaptive fibroblast phenotype to promote pathogenic myomatrix remodeling and compromise the muscle stem (satellite) cell (MuSC) niche. Mice were exposed to environmentally relevant levels of arsenic in drinking water before receiving a local muscle injury. Arsenic-exposed muscles displayed pathogenic matrix remodeling, defective myofiber regeneration …

0301 basic medicineMyoblastSatellite Cells Skeletal MuscleCellSkeletal muscleBiologyMuscle DevelopmentArticleMyoblasts03 medical and health sciencesMiceStem CellmedicineAnimalsHumansMyocyteRegenerationFibroblastMuscle stem cellMyofibroblastMyogenesisAnimalStem CellsRegeneration (biology)arsenicNF-kappa BTranscription Factor RelASkeletal muscleGene Expression Regulation DevelopmentalCell BiologyFibroblastsCell biology030104 developmental biologymedicine.anatomical_structureMyogenesiImmunologyFibroblastMolecular MedicineStem cellMyofibroblastHumanSignal TransductionDevelopmental Biology
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Nrf2 expression driven by Foxp3 specific deletion of Keap1 results in loss of immune tolerance in mice

2020

European journal of immunology 50(4), 515-524 (2020). doi:10.1002/eji.201948285

0301 basic medicineNF-E2-Related Factor 2T cellImmunologyAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes Regulatorydigestive systemenvironment and public healthImmune toleranceImmunomodulationMice03 medical and health sciences0302 clinical medicineImmune systemImmune TolerancemedicineAnimalsHomeostasisImmunology and AllergyTranscription factorPI3K/AKT/mTOR pathwayInflammationMice KnockoutKelch-Like ECH-Associated Protein 1ChimeraEffectorTOR Serine-Threonine KinasesPeripheral toleranceFOXP3Forkhead Transcription Factorshemic and immune systemsrespiratory systemCell biologyMice Inbred C57BLOxidative Stress030104 developmental biologymedicine.anatomical_structure030215 immunology
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NOD-like receptors: major players (and targets) in the interface between innate immunity and cancer

2019

Innate immunity comprises several inflammation-related modulatory pathways which receive signals from an array of membrane-bound and cytoplasmic pattern recognition receptors (PRRs). The NLRs (NACHT (NAIP (neuronal apoptosis inhibitor protein), C2TA (MHC class 2 transcription activator), HET-E (incompatibility locus protein from Podospora anserina) and TP1 (telomerase-associated protein) and Leucine-Rich Repeat (LRR) domain containing proteins) relate to a large family of cytosolic innate receptors, involved in detection of intracellular pathogens and endogenous byproducts of tissue injury. These receptors may recognize pathogen-associated molecular patterns (PAMPs) and/or danger-associated…

0301 basic medicineNOD1InflammasomesBiophysicsNLR ProteinsReview ArticleRECEPTORESBiochemistry46NOD2NLR Proteins45NLRInflammasome03 medical and health sciences0302 clinical medicineNeoplasmsMHC class INOD1medicineAnimalsHumansNF-kBReceptorMolecular BiologyReview ArticlesCancerInflammationInnate immune systembiologyPathogen-Associated Molecular Pattern MoleculesPattern recognition receptorNF-kappa BInflammasomeCell Biology3910Immunity InnateCell biology030104 developmental biology030220 oncology & carcinogenesisReceptors Pattern Recognitionbiology.proteinNAIPmedicine.drug
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PPMS onset upon adalimumab treatment extends the spectrum of anti-TNF-α therapy-associated demyelinating disorders

2020

Since their introduction in 1999, anti-tumour necrosis factor-α (anti-TNF-α) therapies have been suspected repeatedly to be associated with the occurrence of central nervous system (CNS) demyelinating disorders, including multiple sclerosis (MS). However, recent publications were restricted to descriptions of monophasic demyelinating events or cases of relapsing–remitting MS (RRMS). We here provide the first case report of primary progressive MS (PPMS) onset upon anti-TNF-α therapy as well as a literature review of previously published cases of anti-TNF-α therapy-associated MS onset. The 51-year old male patient was treated with adalimumab due to psoriasis arthritis. About 18 months after …

0301 basic medicineNecrosisCentral nervous systemprimary progressive multiple sclerosisPrimary Progressive Multiple SclerosisCase ReportAnti-TNF-alpha therapylcsh:RC346-42903 medical and health sciences0302 clinical medicineadalimumabmedicineAdalimumabanti-TNF-alpha therapyDemyelinating DisorderAnti tnf α therapylcsh:Neurology. Diseases of the nervous systemPharmacologybusiness.industry030104 developmental biologymedicine.anatomical_structureNeurologyImmunologyNeurology (clinical)medicine.symptombusiness030217 neurology & neurosurgerymedicine.drugTherapeutic Advances in Neurological Disorders
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