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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA7qvApdOXJreV1CYr_xLbzpCjoaMWTWH1DBQkp-MBtVM#_4 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RA7qvApdOXJreV1CYr_xLbzpCjoaMWTWH1DBQkp-MBtVM#_3 http://www.w3.org/ns/prov#value NHBE cells were pretreated with 0.5 to 5 ?M BAY 11-7082 before hyperoxic exposure. BAY 11-7082 is an irreversible NF-?B inhibitor that inhibits the IKK pathway to phosphorylate I?B, which is then degraded [24] and [25]. Figure 3 shows that pretreatment of NHBE cells with BAY 11-7082 accelerated hyperoxia-induced cell death. This accelerated loss of cell viability is independent of the presence of 0.5% DMSO, the vehicle for BAY 11-7082, because the extents of cell viability upon exposure to hyperoxia were similar in cells with or without 0.5% DMSO (Fig. 3). In contrast, an increase in the dose of BAY 11-7082 resulted in an incremental loss of cell viability in hyperoxia, indicating that inhibition of NF-?B can induce an accelerated, dose-dependent cell killing effect. 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