2022
CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression
Zhang M, Liu ZZ, Aoshima K, Cai WL, Sun H, Xu T, Zhang Y, An Y, Chen JF, Chan LH, Aoshima A, Lang SM, Tang Z, Che X, Li Y, Rutter SJ, Bossuyt V, Chen X, Morrow JS, Pusztai L, Rimm DL, Yin M, Yan Q. CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression. Science Translational Medicine 2022, 14: eabf5473. PMID: 35108062, PMCID: PMC9003667, DOI: 10.1126/scitranslmed.abf5473.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBreast NeoplasmsCell Line, TumorFemaleHumansImmunosuppression TherapyMacrophagesMiceNeoplasm MetastasisNF-kappa BTranscription Factor RelATranscription FactorsConceptsBreast cancer metastasisReticuloendotheliosis viral oncogene homolog ACancer metastasisImmune suppressionM2 macrophagesWorse metastasis-free survivalMetastatic breast cancerMetastasis-free survivalV-rel avian reticuloendotheliosis viral oncogene homolog ACancer-related deathPrimary breast tumorsMultiple mouse modelsNF-κB signalingImmunocompetent settingNuclear factor-κB family membersMetastasis-promoting genesDistant metastasisMetastatic sitesPrimary tumorEffective therapyBreast cancerMetastasis treatmentMouse modelBreast tumorsMetastasis
2019
Endogenous Retrovirus-Derived Long Noncoding RNA Enhances Innate Immune Responses via Derepressing RELA Expression
Zhou B, Qi F, Wu F, Nie H, Song Y, Shao L, Han J, Wu Z, Saiyin H, Wei G, Wang P, Ni T, Qian F. Endogenous Retrovirus-Derived Long Noncoding RNA Enhances Innate Immune Responses via Derepressing RELA Expression. MBio 2019, 10: 10.1128/mbio.00937-19. PMID: 31363026, PMCID: PMC6667616, DOI: 10.1128/mbio.00937-19.Peer-Reviewed Original ResearchConceptsAntiviral immune responseImmune responseInnate immune responseNF-κB subunitsExpression of RelADeficient miceI interferonAntiviral responseVirus-induced cytokine productionHost genome instabilityEndogenous retrovirusesNF-κB signalingType I interferonRNA virus infectionViral RNA mimicViral loadCytokine productionViral challengeVirus infectionLong noncoding RNADeleterious roleRelA expressionViral replicationViral sensorsReduced expressionMicrofluidic platform enables live-cell imaging of signaling and transcription combined with multiplexed secretion measurements in the same single cells
Ramji R, Alexander AF, Muñoz-Rojas AR, Kellman LN, Miller-Jensen K. Microfluidic platform enables live-cell imaging of signaling and transcription combined with multiplexed secretion measurements in the same single cells. Integrative Biology 2019, 11: 142-153. PMID: 31242304, PMCID: PMC8672722, DOI: 10.1093/intbio/zyz013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodiesCell CommunicationChemokine CCL2Chemokine CCL3Chemokine CCL5Equipment DesignLab-On-A-Chip DevicesLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMicrofluidicsRAW 264.7 CellsSignal TransductionTranscription Factor RelATranscription, GeneticTumor Necrosis Factor-alphaConceptsLive-cell imagingCell variabilitySame single cellSingle-cell assaysTranscription dynamicsBacterial component lipopolysaccharideDownstream responsesPathogenic assaultFluorescent reportersProtein secretionSingle cellsCell processesBiological sourcesCCL3 secretionRelative levelsCellsInnate immune cellsTranslocation dynamicsBiological stepC secretionTranscriptionSecretionCCL5 secretionRelAReporterFold-Change Detection of NF-κB at Target Genes with Different Transcript Outputs
Wong VC, Mathew S, Ramji R, Gaudet S, Miller-Jensen K. Fold-Change Detection of NF-κB at Target Genes with Different Transcript Outputs. Biophysical Journal 2019, 116: 709-724. PMID: 30704857, PMCID: PMC6382958, DOI: 10.1016/j.bpj.2019.01.011.Peer-Reviewed Original ResearchConceptsFold-change detectionTarget genesTranscript outputStress-responsive gene transcriptionSingle-cell dataNF-κB target genesRelA nuclear translocationLive-cell imagingMicrofluidic cell-trapping deviceLow-abundance transcriptsTranscription factor nuclear factorNF-κBRNA FISHTranscriptional outputΚB motifTranscript abundanceGene transcriptionTranscriptionTranscript numbersCell trap deviceJurkat TCell typesGenesNF-κB signalingMultiple biological mechanisms
2018
Enhanced astrocyte responses are driven by a genetic risk allele associated with multiple sclerosis
Ponath G, Lincoln MR, Levine-Ritterman M, Park C, Dahlawi S, Mubarak M, Sumida T, Airas L, Zhang S, Isitan C, Nguyen TD, Raine CS, Hafler DA, Pitt D. Enhanced astrocyte responses are driven by a genetic risk allele associated with multiple sclerosis. Nature Communications 2018, 9: 5337. PMID: 30559390, PMCID: PMC6297228, DOI: 10.1038/s41467-018-07785-8.Peer-Reviewed Original ResearchConceptsMultiple sclerosisAstrocyte responseRisk variantsLocal autoimmune inflammationPeripheral immune cellsCentral nervous system cellsPeripheral immune systemCultured human astrocytesNervous system cellsNF-κB signalingCNS accessDysfunctional lymphocytesAstroglial functionAutoimmune inflammationLymphocytic infiltrateLymphocyte recruitmentImmune cellsGenetic risk allelesGenetic risk variantsMS lesionsMS susceptibilityHuman astrocytesLesion sizeImmune systemSystem cellsSolute Carrier Organic Anion Transporter Family Member 3A1 Is a Bile Acid Efflux Transporter in Cholestasis
Pan Q, Zhang X, Zhang L, Cheng Y, Zhao N, Li F, Zhou X, Chen S, Li J, Xu S, Huang D, Chen Y, Li L, Wang H, Chen W, Cai SY, Boyer JL, Chai J. Solute Carrier Organic Anion Transporter Family Member 3A1 Is a Bile Acid Efflux Transporter in Cholestasis. Gastroenterology 2018, 155: 1578-1592.e16. PMID: 30063921, PMCID: PMC6221191, DOI: 10.1053/j.gastro.2018.07.031.Peer-Reviewed Original ResearchConceptsBile duct ligationLiver tissueBile acidsHepatic levelsHepatoma cell lineFibroblast growth factor 19Cholestatic liver tissuesEfflux transportersCholic acid dietDevelopment of cholestasisGrowth factor 19Sprague-Dawley ratsShorter survival timeBile acid homeostasisHealthy liver tissueReal-time quantitative polymerase chain reactionNuclear factor κBCell linesQuantitative polymerase chain reactionHuman primary hepatocytesMessenger RNALiver injuryCa dietControl miceC57BL/6J miceSIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65
Li P, Jin Y, Qi F, Wu F, Luo S, Cheng Y, Montgomery RR, Qian F. SIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65. Frontiers In Cellular And Infection Microbiology 2018, 8: 113. PMID: 29686974, PMCID: PMC5900784, DOI: 10.3389/fcimb.2018.00113.Peer-Reviewed Original ResearchConceptsToll-like receptor 3Dengue virusInflammatory responseDENV infectionDengue disease severityNF-κB p65Innate immune responseNF-κB activationDomain of p65Overexpression of SIRT6Chemokine productionProinflammatory cytokinesDengue patientsInflammatory cytokinesP65 functionImmune responseLike receptorsDisease severityNegative regulatorReceptor 3Variable severityP65SIRT6CytokinesVirus
2016
Perivascular delivery of resolvin D1 inhibits neointimal hyperplasia in a rat model of arterial injury
Wu B, Mottola G, Chatterjee A, Lance KD, Chen M, Siguenza IO, Desai TA, Conte MS. Perivascular delivery of resolvin D1 inhibits neointimal hyperplasia in a rat model of arterial injury. Journal Of Vascular Surgery 2016, 65: 207-217.e3. PMID: 27034112, PMCID: PMC5040608, DOI: 10.1016/j.jvs.2016.01.030.Peer-Reviewed Original ResearchMeSH KeywordsAngioplasty, BalloonAnimalsAortaCardiovascular AgentsCarotid Artery DiseasesCell MovementCell ProliferationCells, CulturedCytoskeletonDisease Models, AnimalDocosahexaenoic AcidsDrug CarriersDrug CompoundingHyperplasiaInflammation MediatorsKi-67 AntigenLactic AcidMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaOxidative StressPoloxamerPolyglycolic AcidPolylactic Acid-Polyglycolic Acid CopolymerRats, Sprague-DawleyTime FactorsTranscription Factor RelAConceptsLocal perivascular deliveryPerivascular deliveryRat modelCarotid angioplastyNeointimal hyperplasiaResolvin D1Inflammatory pathwaysNeointimal formationArterial smooth muscle cell proliferationNuclear factor-κB activationEffects of RvD1Smooth muscle cell proliferationKi67 proliferation indexResolution of inflammationNegative vessel remodelingMuscle cell proliferationSmooth muscle cellsMuscle cell responseWrap groupArterial injuryRat aortaEvidence of cytotoxicityRvD1Lipid mediatorsProliferation index
2014
The Pro-Resolving Lipid Mediator Maresin 1 (MaR1) Attenuates Inflammatory Signaling Pathways in Vascular Smooth Muscle and Endothelial Cells
Chatterjee A, Sharma A, Chen M, Toy R, Mottola G, Conte MS. The Pro-Resolving Lipid Mediator Maresin 1 (MaR1) Attenuates Inflammatory Signaling Pathways in Vascular Smooth Muscle and Endothelial Cells. PLOS ONE 2014, 9: e113480. PMID: 25409514, PMCID: PMC4237455, DOI: 10.1371/journal.pone.0113480.Peer-Reviewed Original ResearchMeSH KeywordsCell AdhesionCells, CulturedCyclic AMPDocosahexaenoic AcidsDown-RegulationE-SelectinEndothelial CellsHumansMuscle, Smooth, VascularNADPH OxidasesNF-kappa BOxidative StressPhosphorylationReactive Oxygen SpeciesSignal TransductionTranscription Factor RelATumor Necrosis Factor-alphaU937 CellsUp-RegulationConceptsInflammatory signaling pathwaysBroad anti-inflammatory actionsMonocyte adhesionCyclic AMPTumor necrosis factor alphaAdhesion molecules E-selectinPro-resolving responseNF-κB p65 subunitPro-inflammatory mediatorsAnti-inflammatory actionPro-inflammatory signalsVascular smooth muscleNecrosis factor alphaAttenuation of TNFHuman saphenous vein ECsHuman vascular endothelialBioactive lipid mediatorsNF-κB activationSmooth muscle cellsTNF-α effectSignaling pathwaysBronchial epithelial cellsIntracellular cyclic AMPTime-dependent increaseVascular inflammationA Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines
Endo F, Nishizuka SS, Kume K, Ishida K, Katagiri H, Ishida K, Sato K, Iwaya T, Koeda K, Wakabayashi G. A Compensatory Role of NF-κB to p53 in Response to 5-FU–Based Chemotherapy for Gastric Cancer Cell Lines. PLOS ONE 2014, 9: e90155. PMID: 24587255, PMCID: PMC3937424, DOI: 10.1371/journal.pone.0090155.Peer-Reviewed Original ResearchMeSH KeywordsAntimetabolites, AntineoplasticCell Line, TumorCodonDrug Resistance, NeoplasmFluorouracilGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansNF-kappa BProtein BindingProtein TransportStomach NeoplasmsTranscription Factor RelATumor Suppressor Protein p53ConceptsGastric cancer cell linesCancer cell linesNF-κBAdjuvant chemotherapyPrediction markersCell linesNF-κB-dependent mannerGastric cancer patientsKnockdown of RelANF-κB bindingArg homozygosityCurative resectionRelapse rateCancer patientsGastric cancerPrediction biomarkersChemotherapyP65 subunitTP53 knockdownChemotherapeutic efficacyProtein levelsCompensatory roleP53Target protein levelsTreatment
2013
Regulation of HA14‐1 mediated oxidative stress, toxic response, and autophagy by curcumin to enhance apoptotic activity in human embryonic kidney cells
Ranjan K, Sharma A, Surolia A, Pathak C. Regulation of HA14‐1 mediated oxidative stress, toxic response, and autophagy by curcumin to enhance apoptotic activity in human embryonic kidney cells. BioFactors 2013, 40: 157-169. PMID: 23559532, DOI: 10.1002/biof.1098.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsApoptosisAutophagyBenzopyransCaspase 3CatalaseCell ProliferationCell SurvivalCurcuminDrug Resistance, NeoplasmDrug SynergismHEK293 CellsHumansMembrane Potential, MitochondrialNitrilesOxidative StressProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSuperoxide DismutaseTranscription Factor RelAConceptsHuman embryonic kidney cellsHA14-1Embryonic kidney cellsProcess of autophagyHEK 293T cellsOxidative stressAntiapoptotic protein Bcl-2Kidney cellsProtein Bcl-2Toxic responsePromotion of malignancyAugmentation of apoptosisGeneration of ROSSignaling mechanismAntiapoptotic proteinsCell deathCancerous cell linesApoptotic activityCell proliferationBcl-2Cell linesPathological consequencesROS generationApoptosisROS
2012
Chromatin accessibility at the HIV LTR promoter sets a threshold for NF-κB mediated viral gene expression
Miller-Jensen K, Dey SS, Pham N, Foley JE, Arkin AP, Schaffer DV. Chromatin accessibility at the HIV LTR promoter sets a threshold for NF-κB mediated viral gene expression. Integrative Biology 2012, 4: 661-671. PMID: 22555315, PMCID: PMC3362694, DOI: 10.1039/c2ib20009k.Peer-Reviewed Original ResearchConceptsChromatin accessibilityGene expressionChromatin environmentIntegration sitesHigher-order chromatin structureDifferent genomic environmentsLTR promoterRepressive histone marksDifferent chromatin environmentsOrder chromatin structureGene expression regulationTranscription factor inputsSame transcription factorDifferential gene expressionLevels of RelASelective gene expressionViral gene expressionViral integration sitesTranscription factor activationHIV gene regulationGenomic environmentHIV LTR promoterHistone marksChromatin featuresChromatin structure
2011
The PPE18 Protein of Mycobacterium tuberculosis Inhibits NF-κB/rel–Mediated Proinflammatory Cytokine Production by Upregulating and Phosphorylating Suppressor of Cytokine Signaling 3 Protein
Nair S, Pandey AD, Mukhopadhyay S. The PPE18 Protein of Mycobacterium tuberculosis Inhibits NF-κB/rel–Mediated Proinflammatory Cytokine Production by Upregulating and Phosphorylating Suppressor of Cytokine Signaling 3 Protein. The Journal Of Immunology 2011, 186: 5413-5424. PMID: 21451109, DOI: 10.4049/jimmunol.1000773.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, BacterialBacterial ProteinsBlotting, WesternCell LineCell SeparationCytokinesElectrophoretic Mobility Shift AssayFlow CytometryHumansImmunoprecipitationInflammationMacrophagesMycobacterium tuberculosisNF-kappa BPhosphorylationReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingSignal TransductionSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTranscription Factor RelATransfectionTuberculosisUp-RegulationConceptsTranscription factorsNF-κB/Rel transcription factorsNuclear translocationNF-κB/RelRel transcription factorsSubsequent intracellular survivalC-Rel transcription factorPhosphorylation sitesTyrosine phosphorylationSpecific knockdownSuccessful infectionIntracellular survivalRel subunitsCytokine signaling-3 (SOCS-3) proteinNovel mechanismIκB kinasePhosphorylationProteinNuclear levelsNF-κB activationSOCS3Phosphorylation of IκBαSuppressorTNF-α productionTranslocation
2009
Focal adhesion kinase modulates activation of NF-κB by flow in endothelial cells
Petzold T, Orr AW, Hahn C, Jhaveri KA, Parsons JT, Schwartz MA. Focal adhesion kinase modulates activation of NF-κB by flow in endothelial cells. American Journal Of Physiology - Cell Physiology 2009, 297: c814-c822. PMID: 19587216, PMCID: PMC2770750, DOI: 10.1152/ajpcell.00226.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell NucleusCells, CulturedEndothelial CellsEndothelium, VascularFocal Adhesion Protein-Tyrosine KinasesHydrogen PeroxideI-kappa B KinaseIntegrinsIntercellular Adhesion Molecule-1MiceNF-kappa BPhosphorylationProtein Transportrac GTP-Binding ProteinsReactive Oxygen SpeciesSignal TransductionStress, MechanicalTranscription Factor RelATumor Necrosis Factor-alphaConceptsFocal adhesion kinaseAdhesion kinaseNF-kappaBRac activationTranscriptional activityDependent genesEndothelial cellsIntegrin activationP65 NF-kappaB subunitDegradation of IkappaBReactive oxygen productionFluid shear stressNF-kappaB subunitsSerine 536Phosphorylation of p65Novel mechanismNF-kappaB activationKinaseNF-kappaB phosphorylationPhosphorylationActivationNF-κBOxygen productionHydrogen peroxideCellsResolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases
Panzer U, Steinmetz OM, Turner JE, Meyer-Schwesinger C, von Ruffer C, Meyer TN, Zahner G, Gómez-Guerrero C, Schmid RM, Helmchen U, Moeckel GW, Wolf G, Stahl RA, Thaiss F. Resolution of renal inflammation: a new role for NF-κB1 (p50) in inflammatory kidney diseases. American Journal Of Physiology. Renal Physiology 2009, 297: f429-f439. PMID: 19458123, DOI: 10.1152/ajprenal.90435.2008.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAcute DiseaseAnimalsAntilymphocyte SerumBlotting, SouthwesternCells, CulturedChemokinesDisease Models, AnimalEndothelial CellsGlomerulonephritisImmunohistochemistryKidney GlomerulusLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, KnockoutNephritisNF-kappa B p50 SubunitNF-kappa B p52 SubunitProtein MultimerizationRatsRats, WistarRemission, SpontaneousTime FactorsTranscription Factor RelATranscription Factor RelBConceptsNF-kappaBRenal inflammationTissue injuryNF-kappaB p50 knockout miceRenal inflammatory cell infiltrationHighest chemokine expressionP50 knockout miceRenal tissue injuryResolution of LPSGlomerular immune injuryInflammatory kidney diseasesInflammatory cell infiltrationRenal inflammatory diseaseProinflammatory gene expressionModel of glomerulonephritisTranscription factor NF-kappaBResolution periodImmune injuryRenal diseaseChemokine expressionAcute nephritisKidney diseaseCell infiltrationInflammatory diseasesInflammatory process
2005
Comment on "Oscillations in NF-κB Signaling Control the Dynamics of Gene Expression"
Barken D, Wang C, Kearns J, Cheong R, Hoffmann A, Levchenko A. Comment on "Oscillations in NF-κB Signaling Control the Dynamics of Gene Expression". Science 2005, 308: 52a-52a. PMID: 15802586, PMCID: PMC2821939, DOI: 10.1126/science.1107904.Peer-Reviewed Original Research
2000
PDZ Domain-dependent Suppression of NF-κB/p65-induced Aβ42 Production by a Neuron-specific X11-like Protein*
Tomita S, Fujita T, Kirino Y, Suzuki T. PDZ Domain-dependent Suppression of NF-κB/p65-induced Aβ42 Production by a Neuron-specific X11-like Protein*. Journal Of Biological Chemistry 2000, 275: 13056-13060. PMID: 10777610, DOI: 10.1074/jbc.c000019200.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCell LineCOS CellsDNA, ComplementaryGene Expression RegulationGene LibraryHumansLuciferasesNerve Tissue ProteinsNeuronsNF-kappa BNF-kappa B p50 SubunitPeptide FragmentsPrecipitin TestsProtein BindingProtein IsoformsProtein Structure, TertiaryTranscription Factor RelATranscription, GeneticTransfectionTwo-Hybrid System TechniquesConceptsNF-kappaB/p65X11-like proteinsAlzheimer's diseaseNF-kappaB/p50Progression of ADAmyloid precursor proteinSpecific therapyAbeta productionAβ42 productionAbeta42 productionNF-kappaBP65Neuronal cellsAmino acids 161Precursor proteinX11LAbeta42DiseaseRel homology domainSecretionX11L.P50LIN-10Transcription factorsTherapy
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