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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAofnbR-Uw9Hi8-h6e4m1VjHeYOvoHvr3Du8VSI2XuAJU#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAofnbR-Uw9Hi8-h6e4m1VjHeYOvoHvr3Du8VSI2XuAJU#_5 http://www.w3.org/ns/prov#value In this study, we report that S100A8, S100A9, and S100A8/A9 caused neutrophil chemotaxis at concentrations of 10(-12)-10(-9) M. S100A8, S100A9, and S100A8/A9 stimulated shedding of L-selectin, up-regulated and activated Mac-1, and induced neutrophil adhesion to fibrinogen in vitro. As shown in Fig. 3, MRPs induced shedding of L-selectin (CD62L) from the neutrophil surface. In contrast, expression of CD11b, but not CD51 was up-regulated following stimulation with MRPs. 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