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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/RAaIyHHgOyHTcBL3vtN0fd051dsE8ciJoCSyYpH81lFfc#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RAaIyHHgOyHTcBL3vtN0fd051dsE8ciJoCSyYpH81lFfc#_4 http://www.w3.org/ns/prov#value The c-MET serves as an attractive therapeutic target in SCLC, as shown through small interfering RNA (siRNA) and selective prototype c-MET inhibitor SU11274, inhibiting the phosphorylation of c-MET itself and its downstream molecules such as AKT, S6 kinase, and ERK1/2. The HGF-stimulated phosphorylation of the following downstream phosphokinases was inhibited by SU11274: p-ERK1 [T202/Y204], p-ERK1/2 [T185/Y187], p-MEK1/2 [S221/S225], p38a p-MAP kinase [T180/Y182], p-AKT1 [S473], p-RB [S672], p-adducin-g [S662], and p-CREB [S133]). 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