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All Rights Reserved. http://resource.belframework.org/belframework/20131211/knowledge/small_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Small Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/small_corpus.bel http://purl.org/dc/terms/license Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License http://resource.belframework.org/belframework/20131211/knowledge/small_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RALc4oNB_es7G0TCvcmSZMr1ZJ39gT_DiKJsHFL3laPQQ#_7 http://resource.belframework.org/belframework/20131211/knowledge/small_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RALc4oNB_es7G0TCvcmSZMr1ZJ39gT_DiKJsHFL3laPQQ#_6 http://www.w3.org/ns/prov#value As shown in Fig. 3,d–e, incubation with the PKC inhibitor BIM I (as well as with the β1-neutralizing mAb) blocked dose-dependent VEGF-induced cell adhesion to fibronectin. This involvement of PKC in MM cell adhesion to fibronectin was further confirmed by a dose-dependent increment of adhesion triggered by PMA stimulation (Fig. 3d) similar to that induced by VEGF. 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