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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/RAof4eJx58RVYuOrAipX5o0WcvudcaXU5GU7oBiMjSdFg#_5 http://resource.belframework.org/belframework/1.0/knowledge/small_corpus.bel http://purl.org/pav/version 1.6 http://www.tkuhn.ch/bel2nanopub/RAof4eJx58RVYuOrAipX5o0WcvudcaXU5GU7oBiMjSdFg#_4 http://www.w3.org/ns/prov#value The mitogenic and chemotactic effects of VEGF in ECs are mediated mainly through VEGFR2 (76). VEGFR2 is activated through ligandstimulated receptor dimerization and transphosphorylation (autophosphorylation) of tyrosine residues in the cytoplasmic kinase domain. At present, tyrosine residues 951 and 996 in the kinase insert domain, and 1054 and 1059 in the kinase catalytic domain, have been identified as autophosphorylation sites for VEGFR2 in a bacterial expression system (30). 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