FGFR1 fusion proteins recruit PIK3R1 Activation 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). Authored: Rothfels, K, 2012-02-09 Edited: Rothfels, K, 2012-05-16 Pubmed11689702 Pubmed11739186 Pubmed15050920 Pubmed15448205 Pubmed18412956 Reactome Database ID Release 431839078 Reactome, http://www.reactome.org ReactomeREACT_120762 Reviewed: Ezzat, S, 2012-05-15 p-FGFR1 fusion mutant dimers p-FGFR1 fusion mutant dimers:PIK3R1