Statements in which the resource exists.
SubjectPredicateObjectContext
http://www.reactome.org/bio...rdf:typebiopax3:BiochemicalReactionlld:biopax3
http://www.reactome.org/bio...biopax3:commentEdited: Rothfels, K, 2012-05-16lld:biopax3
http://www.reactome.org/bio...biopax3:commentReviewed: Ezzat, S, 2012-05-15lld:biopax3
http://www.reactome.org/bio...biopax3:commentAuthored: Rothfels, K, 2012-02-09lld:biopax3
http://www.reactome.org/bio...biopax3:commentActivation of the PI3K signaling pathway has been demonstrated for a number of FGFR1 fusion proteins and inhibitors of this pathway impair the proliferative and survival function of the fusions (Guasch, 2001; Demiroglu, 2001; Chen, 2004; Lelievre, 2008). FGFR1 fusions lack the FRS2-binding site of the full length protein, so the mechanism of PI3K recruitment is unclear. Unlike BCR-FGFR1, which has been shown to recruit GRB2 through the BCR Y177 site, GRB2 did not co-precipitate with the ZMYM2-FGFR1 fusion (Roumianetsev, 2004). In the case of FOP-FGFR1, Y730 has been shown to be required for the recruitment of the p85 subunit of PI3K; however, CEP110-FGFR1, which contains Y730 in the context of the same pYXXM motif, was not shown to recruit p85 at the centrosome (Guasch, 2001).lld:biopax3
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http://www.reactome.org/bio...biopax3:displayNameFGFR1 fusion proteins recruit PIK3R1lld:biopax3
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