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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/RATe3ing9Y1UDXAeZtz9i3YvbNBSFs4MTCsxDO48jMhz0#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RATe3ing9Y1UDXAeZtz9i3YvbNBSFs4MTCsxDO48jMhz0#_5 http://www.w3.org/ns/prov#value However, it is p27 that seems to be the primary target of SKP2, given that Skp2 ko mice show a marked accumulation of p27 (REF. 24), and that prominent cellular phenotypes apparent in Skp2 00 mice (see Supplementary information S1 (table)) including nuclear enlargement, polyploidy and an increased number of centrosomes that are probably caused by overreplication of chromosomes and centrosomes disappear in Skp2 ko p27 ko double mutant mice. The oncogenic potential of SKP2 has also been shown in transgenic mouse models 35,36. Furthermore, Ras signalling induces SKP2 expression through the binding of GA-binding protein, an Ets-family transcription factor, to the SKP2 promoter37. 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