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http://resource.belframework.org/belframework/1.0/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/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/RA0KbbZudseP2xTq_uP5AtkSi67WIyd9x13Eg8VEZUs1g#_7 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RA0KbbZudseP2xTq_uP5AtkSi67WIyd9x13Eg8VEZUs1g#_6 http://www.w3.org/ns/prov#value Figure 6 Notch function in cervical cancer. A theoretical model of how the tumour-suppressor properties of NOTCH1 can, in principle, be sidestepped in HPV-infected cervical cancer cells, allowing manifestation of growth-promoting properties of NOTCH1. Apart from HPV E6 and E7 proteins, cervical cancers frequently express increased levels of the phosphatidylinositol 3-kinase (PI3K) subunit p110? and ?Np63 as a result of amplification of the q26-29 locus of chromosome 3. Experiments show that Notch-induced PI3K confers resistance to anoikis in epithelial cells. 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