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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/RAfGnwWKPNf30VrZEzGId7ebsRgF6Px2cFhhzLIJzIdyo#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAfGnwWKPNf30VrZEzGId7ebsRgF6Px2cFhhzLIJzIdyo#_5 http://www.w3.org/ns/prov#value To dissect the biochemical mechanism(s) underlying the ability of these protein kinases to promote the cell division cycle, we used Western blotting to assess the effects of RAF and AKT on the expression of a number of proteins known to be targets of RAF or AKT signaling. Of the various immediate- early targets of RAF signaling that we analyzed (e.g., Fos, Jun, c-Myc, and HB-EGF), none showed evidence of cooperative regulation in response to coactivation of AKT and RAF (data not shown) (11, 33, 34). However, we observed cooperative effects of RAF and AKT on the expression of two key cell cycle regulators, cyclin D1 and p27Kip1. 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