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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/description Approximately 61,000 statements. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/rights Copyright (c) 2011-2012, Selventa. 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/RAC3dc1uk6OZg4xFwJmVTTA-a1aOiOaJycumdS7oDguuw#_8 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAC3dc1uk6OZg4xFwJmVTTA-a1aOiOaJycumdS7oDguuw#_7 http://www.w3.org/ns/prov#value The data in Figure 1D suggested that a second aV integ- rin, aVb5, which has been implicated in angiogenesis, may also be activated by VEGF165. Therefore, we sought concento determine if still other integrins implicated in angio- genesis, a5b1, a fibronectin receptor (Bloch et al., 1997), and a2b1, a collagen receptor (Senger et al., 1997), might be activated by VEGF165. In cell migration assays, VEGF165 markedly stimulated HUVEC movement onto effibronectin (see Figure 3A). The migrating cells exhibited extensive spreading, much more so than for their aVb3- mediated migration onto vitronectin (see Figure 2A). shown in Figure 3B, VEGF165-enhanced migration was only partly dependent upon aVb3 activation (partial inhi- bition by c7E3) and partly dependent upon a5b1; mAb JBS5 to a5b1 produced marked inhibition. The combina- tion of mAbs c7E3 and JBS5 produced full inhibition cell migration. Thus, integrin a5b1 also can be activated tranwhen HUVECs are stimulated with VEGF165. A similar conclusion was reached with regard to VEGF165 activa- tion of integrin a2b1 using Type I collagen as a matrix (Figure 3C). The role of a2b1 in this migration was con- firmed using blocking mAb BHA2.1. 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