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All Rights Reserved. http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Small Corpus Document http://resource.belframework.org/belframework/1.0/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/1.0/knowledge/small_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RA-0MEkPYDhb298btN_oqdhLVhi_91pNNS205Y8VxEqS4#_5 http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/version 1.6 http://www.tkuhn.ch/bel2nanopub/RA-0MEkPYDhb298btN_oqdhLVhi_91pNNS205Y8VxEqS4#_4 http://www.w3.org/ns/prov#value Adhesion of HT-29 cells on a monolayer of HUVEC pretreated with TNFα was dependent on E-selectin expression but was independent of SAPK2/p38 activity of both HUVEC and tumor cells. The adhesion of HT-29 cells to E-selectin-expressing HUVEC led to the activation of SAPK2/p38 in the tumor cells as reflected by the increased phosphorylation of the actin-polymerizing factor HSP27 by mitogen-activated protein kinase 2/3, a direct target of SAPK2/p38. Moreover, a recombinant E-selectin/Fc chimera quickly increased the activation of SAPK2/p38 in HT-29 cells. 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