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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/RAEoOiq9TrreW8g8xnbVzaa_sBBdGY7rr49TaYm2DdmTw#_6 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAEoOiq9TrreW8g8xnbVzaa_sBBdGY7rr49TaYm2DdmTw#_5 http://www.w3.org/ns/prov#value IL-18 treatment markedly increased phospho-ATF-2 (Thr71) levels in HCMEC, and this effect was blocked by the IL-18BPa/Fc chimera (Fig. 5A). Furthermore, treatment with the p38PMAPK inhibitor SB203580 strongly inhibited IL-18-mediated ATF-2 phosphorylation (Fig. 5B). Inhibition of p38MAPK also attenuated p65 phosphorylation (Fig. 5C) and NF-?B-driven reporter gene activity (Fig. 5D). 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