2018
NF-κB-Chromatin Interactions Drive Diverse Phenotypes by Modulating Transcriptional Noise
Wong VC, Bass VL, Bullock ME, Chavali AK, Lee REC, Mothes W, Gaudet S, Miller-Jensen K. NF-κB-Chromatin Interactions Drive Diverse Phenotypes by Modulating Transcriptional Noise. Cell Reports 2018, 22: 585-599. PMID: 29346759, PMCID: PMC5812697, DOI: 10.1016/j.celrep.2017.12.080.Peer-Reviewed Original ResearchConceptsTranscriptional noiseIntegration sitesDiverse phenotypesRNA polymerase II regulationNoisy gene expressionGenomic integration sitesLive-cell imagingNF-κB activationChromatin environmentChromatin stateViral activationChromatin interactionsTranscript abundanceTranscription factor nuclear factor κBDivergent phenotypesGene expressionNoisy expressionNF-κBTranscript numbersNuclear factor κBPhenotypeTumor necrosis factorFactor κBActivationExpression
2014
Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma
Kusne Y, Carrera-Silva EA, Perry AS, Rushing EJ, Mandell EK, Dietrich JD, Errasti AE, Gibbs D, Berens ME, Loftus JC, Hulme C, Yang W, Lu Z, Aldape K, Sanai N, Rothlin CV, Ghosh S. Targeting aPKC disables oncogenic signaling by both the EGFR and the proinflammatory cytokine TNFα in glioblastoma. Science Signaling 2014, 7: ra75. PMID: 25118327, PMCID: PMC4486020, DOI: 10.1126/scisignal.2005196.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinogenesisDrug Delivery SystemsEnzyme-Linked Immunosorbent AssayEpidermal Growth FactorErbB ReceptorsErlotinib HydrochlorideFlow CytometryFluorescent Antibody TechniqueGlioblastomaHumansImmunoblottingImmunohistochemistryImmunoprecipitationKaplan-Meier EstimateMiceNF-kappa BParacrine CommunicationProtein Kinase CQuinazolinesReverse Transcriptase Polymerase Chain ReactionSignal TransductionTumor Necrosis Factor-alphaConceptsAtypical protein kinase CEpidermal growth factor receptorEGFR kinase inhibitorsHuman glioblastoma tumor cellsReceptor tyrosine kinasesProtein kinase CTNFα-dependent activationKinase inhibitorsTranscription factor nuclear factor κBGlioblastoma tumor cellsGrowth factor receptorKinase activityMolecular approachesTyrosine kinaseKinase CNuclear factor κBFactor receptorGlioblastoma microenvironmentFactor κBProinflammatory cytokine TNFαAbundanceTumor necrosis factorGlioblastoma therapyTumor growthGrade IV glioblastoma
2010
Bifurcation of Toll-Like Receptor 9 Signaling by Adaptor Protein 3
Sasai M, Linehan MM, Iwasaki A. Bifurcation of Toll-Like Receptor 9 Signaling by Adaptor Protein 3. Science 2010, 329: 1530-1534. PMID: 20847273, PMCID: PMC3063333, DOI: 10.1126/science.1187029.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Protein Complex 3Adaptor Protein Complex beta SubunitsAnimalsCells, CulturedCytokinesCytoplasmic VesiclesDendritic CellsEndosomesInterferon Regulatory Factor-7Interferon Type ILysosomal-Associated Membrane Protein 2MacrophagesMembrane Transport ProteinsMiceMice, Inbred C57BLMyeloid Differentiation Factor 88OligodeoxyribonucleotidesProtein TransportRecombinant Fusion ProteinsSignal TransductionTNF Receptor-Associated Factor 3Toll-Like Receptor 9Transcriptional ActivationVesicle-Associated Membrane Protein 3ConceptsI interferonTLR9 signalsEndosomal Toll-like receptors 7Toll-like receptor 9 signalingToll-like receptor 7Protein 3Type I IFNsDependent proinflammatory cytokinesInterferon regulatory factor 7I IFNsProinflammatory cytokine genesType I interferonNuclear factor κBRegulatory factor 7Viral nucleic acidsProinflammatory cytokinesReceptor 7Factor κBCytokine genesTLR9Adaptor protein 3Intracellular mechanismsFactor 7Viral pathogensReceptor trafficking
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