Search results for "NF-"

showing 10 items of 461 documents

Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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Nuclear Factor Kappa B Signaling Complexes in Acute Inflammation.

2020

[Significance]: Nuclear factor kappa B (NF-κB) is a master regulator of the inflammatory response and represents a key regulatory node in the complex inflammatory signaling network. In addition, selective NF-κB transcriptional activity on specific target genes occurs through the control of redox-sensitive NF-κB interactions.

0301 basic medicineRedox signalingPhysiologyClinical BiochemistryRepressorCREBInteractomeBiochemistry03 medical and health sciencesCoactivatorHumansSTAT3Transcription factorMolecular BiologyGeneral Environmental ScienceInflammation030102 biochemistry & molecular biologybiologyChemistryActivator (genetics)NF-kappa BCell Biology3. Good healthCell biology030104 developmental biologyGene Expression RegulationMultiprotein ComplexesAcute DiseaseSTAT proteinbiology.proteinGeneral Earth and Planetary SciencesDisease SusceptibilitySignaling complexesCarrier ProteinsBiomarkersProtein BindingSignal TransductionAntioxidantsredox signaling
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The Good and Bad of Nrf2: An Update in Cancer and New Perspectives in COVID-19

2021

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a well-known transcription factor best recognised as one of the main regulators of the oxidative stress response. Beyond playing a crucial role in cell defence by transactivating cytoprotective genes encoding antioxidant and detoxifying enzymes, Nrf2 is also implicated in a wide network regulating anti-inflammatory response and metabolic reprogramming. Such a broad spectrum of actions renders the factor a key regulator of cell fate and a strategic player in the control of cell transformation and response to viral infections. The Nrf2 protective roles in normal cells account for its anti-tumour and anti-viral functions. However, Nrf2 over…

0301 basic medicineRegulatorAnti-Inflammatory AgentsDiseaseReviewenvironment and public healthNF-κBAntioxidantschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaNeoplasmsoxidative stressBiology (General)SpectroscopyGeneral Medicinerespiratory systemComputer Science ApplicationsChemistrycell death030220 oncology & carcinogenesisSignal transductionSignal TransductionQH301-705.5NF-E2-Related Factor 2Context (language use)BiologyCatalysisNrf2Inorganic Chemistry03 medical and health sciencesmedicinecancerAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyTranscription factorQD1-999Organic ChemistryCancerCOVID-19NF-κBmedicine.diseaseCOVID-19 Drug Treatment030104 developmental biologychemistryinflammationCytokine stormNeuroscienceInternational Journal of Molecular Sciences
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Molecular evolution of antioxidant and hypoxia response in long-lived, cancer-resistant blind mole rats: The Nrf2-Keap1 pathway.

2015

The Nrf2-Keap1 pathway is crucial for the cellular antioxidant and hypoxia response in vertebrates. Deciphering its modifications in hypoxia-adapted animals will help understand its functionality under environmental stress and possibly allow for knowledge transfer into biomedical research. The blind mole rat Spalax, a long-lived cancer-resistant rodent, lives in burrows underground and is adapted to severely hypoxic conditions. Here we have conducted a bioinformatical survey of Spalax core genes from the Nrf2-Keap1 pathway on the coding sequence level in comparison to other hypoxia-tolerant and -sensitive rodents. We find strong sequence conservation across all genes, illustrating the pathw…

0301 basic medicineRodentSpalaxNF-E2-Related Factor 2Molecular Sequence DataConserved sequenceEvolution Molecular03 medical and health sciencesbiology.animalNeoplasmsGene expressionGeneticsAnimalsAmino Acid SequencePeptide sequenceGeneConserved SequenceGeneticsKelch-Like ECH-Associated Protein 1030102 biochemistry & molecular biologybiologyMole RatsIntracellular Signaling Peptides and ProteinsGeneral Medicinebiology.organism_classificationPhenotypeKEAP1Cell HypoxiaRatsOxidative Stress030104 developmental biologySequence AlignmentGene
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The angiotensin‐(1‐7)/Mas receptor axis protects from endothelial cell senescence via klotho and Nrf2 activation

2019

Endothelial cell senescence is a hallmark of vascular aging that predisposes to vascular disease. We aimed to explore the capacity of the renin-angiotensin system (RAS) heptapeptide angiotensin (Ang)-(1-7) to counteract human endothelial cell senescence and to identify intracellular pathways mediating its potential protective action. In human umbilical vein endothelial cell (HUVEC) cultures, Ang II promoted cell senescence, as revealed by the enhancement in senescence-associated galactosidase (SA-β-gal+) positive staining, total and telomeric DNA damage, adhesion molecule expression, and human mononuclear adhesion to HUVEC monolayers. By activating the G protein-coupled receptor Mas, Ang-(1…

0301 basic medicineSenescenceAgingNF-E2-Related Factor 2medicine.medical_treatmentCellBiologyKlothoReceptors G-Protein-Coupled03 medical and health sciences0302 clinical medicineheme oxygenase‐1medicineHuman Umbilical Vein Endothelial CellsHumansReceptorKlothoKlotho ProteinsCells CulturedCellular SenescenceGlucuronidaseangiotensin‐(1‐7)Original PaperNuclear factor (erythroid-derived 2)-like 2nuclear factor (erythroid‐derived 2)‐like 2Vascular agingCell BiologyAngiotensin-(1-7)FarmaciaOriginal PapersPeptide FragmentsEndothelial senescenceCell biologyEndothelial stem cell030104 developmental biologyCytokinemedicine.anatomical_structureHeme oxygenase-1cardiovascular systemHuman umbilical vein endothelial cellAngiotensin I030217 neurology & neurosurgeryIntracellular
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Balanced Bcl-3 expression in murine CD4+T cells is required for generation of encephalitogenic Th17 cells

2017

The function of NF-κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl-3, an atypical member of the IκB family. By using a murine model of conditional Bcl-3 overexpression specifically in T cells, we observed impairment in the development of Th2, Th1 and Th17 cells. High expression of Bcl-3 promoted CD4+ T-cell survival, but at the same time suppressed proliferation in response to TCR stimulation, resulting in reduced CD4+ T-cell expansion. As a consequence, T cell specific overexpression of Bcl-3 led to reduced inflammation in the small intestine of mice applied with anti-CD3 in a model of gut inflammation. Moreover, impaired Th17-cell develop…

0301 basic medicineT cellMultiple sclerosisImmunologyT-cell receptorStimulationInflammationNF-κBBiologymedicine.diseaseSmall intestineCell biology03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structurechemistryImmunologymedicineTranscriptional regulationImmunology and Allergymedicine.symptomEuropean Journal of Immunology
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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer’s disease

2018

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or …

0301 basic medicineTime Factorsmedicine.medical_treatmentHippocampusCell CountPharmacologymedicine.disease_causeHippocampuslcsh:RC346-429Superoxide Dismutase-10302 clinical medicineNeuroinflammationNF-kBMicrogliaGeneral NeuroscienceMicrofilament ProteinsROSPro-inflammatory cytokineIFNβ1amedicine.anatomical_structureCytokineNeurologyIL-10CytokinesFemalemedicine.symptomAlzheimer's diseaseInterferon beta-1aPro-inflammatory cytokinesImmunologyAβ 1-42InflammationProinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceHippocampuAlzheimer DiseaseGlial Fibrillary Acidic ProteinmedicineAnimalsAβ1-42Rats WistarSODMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationInflammationAmyloid beta-PeptidesNeuroscience (all)Superoxide Dismutasebusiness.industryResearchCalcium-Binding ProteinsRecognition Psychologymedicine.diseasePeptide FragmentsRatsDisease Models Animal030104 developmental biologyLipid PeroxidationCognition DisordersReactive Oxygen Speciesbusiness030217 neurology & neurosurgeryOxidative stressJournal of Neuroinflammation
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NF-κB and Disease

2020

The role of NF-κB in all diseases characterized by an inflammatory process, from cancer to autoimmune diseases, is known, but—precisely because it is involved in many diseases—this transcriptional factor continues to attract scientific research and the new knowledge that emerges is fundamental in highlighting the therapeutic potential that this factor can have in the various diseases in which it is involved [...]

0301 basic medicineTranscriptional factorDiseaseCatalysislcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansMolecular Targeted TherapyPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyNF-kB diseasebusiness.industryOrganic ChemistryNF-kappa BCancerNF-κBGeneral Medicinemedicine.diseaseComputer Science Applicationsn/aEditorial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Gene Expression Regulationchemistry030220 oncology & carcinogenesisCancer researchDisease SusceptibilitybusinessBiomarkersSignal TransductionInternational Journal of Molecular Sciences
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Inhibition of NF-κB pathway in LPS-stimulated THP-1 monocytes and COX-2 activity in vitro by berry pomace extracts from five Vaccinium species

2020

BACKGROUND: Berry processing residues called pomaces are rich in polyphenols, sugars, organic acids, and minerals. Polyphenols are reported to reduce the risk of non-communicable diseases, including cardiovascular diseases, cancer, and diabetes mellitus, owing to their anti-inflammatory activity. OBJECTIVE: We aimed to assess the anti-inflammatory properties of five Vaccinium spp. berry pomace extracts using LPS-stimulated THP-1 monocytes and a COX-2 inhibition assay. METHODS: THP-1 monocytes were pre-incubated with chemically characterized bilberry, blueberry, American cranberry, bog cranberry, and lingonberry pomace extracts following LPS stimulation. NF-κB nuclear translocation was asses…

0301 basic medicinebiologyChemistryPomaceSoil ScienceNF-κBPlant ScienceBerryHorticulturebiology.organism_classificationBiochemistryMolecular biologyIn vitro03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisTHP1 cell lineAgronomy and Crop ScienceFood ScienceVacciniumJournal of Berry Research
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Loss of MCL1 function sensitizes the MDA-MB-231 breast cancer cells to rh-TRAIL by increasing DR4 levels.

2019

Triple-negative breast cancer (TNBC) is a form of BC characterized by high aggressiveness and therapy resistance probably determined by cancer stem cells. MCL1 is an antiapoptotic Bcl-2 family member that could limit the efficacy of anticancer agents as recombinant human tumor necrosis factor related apoptosis-inducing ligand (rh-TRAIL). Here, we investigated MCL1 expression in TNBC tissues and cells. We found MCL1 differentially expressed (upregulated or downregulated) in TNBC tissues. Furthermore, in comparison to the human mammary epithelial cells, we found that MDA-MB-231 cells show similar messenger RNA levels but higher MCL1 protein levels, whereas it resulted downregulated in MDA-MB-…

0301 basic medicinecancer stem cellIndolesPhysiologyCell SurvivalClinical BiochemistryCellPopulationApoptosisTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineCancer stem cellSettore BIO/10 - BiochimicaCell Line Tumormedicinerh-TRAILBiomarkers TumorGene silencingHumansViability assayGene SilencingeducationCell ShapeCell ProliferationMembrane Potential Mitochondrialeducation.field_of_studySulfonamidesChemistryCell growthCell CycleCell BiologyCell cycleRecombinant ProteinsGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing Ligand030104 developmental biologymedicine.anatomical_structureMCL1ApoptosisDR4 receptor030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerMyeloid Cell Leukemia Sequence 1 ProteinJournal of cellular physiology
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