p-BCR-pFGFR1 recruits GRB2:GAB2 Authored: Rothfels, K, 2012-02-09 Edited: Rothfels, K, 2012-05-16 Proliferation of BCR-FGFR1 fusion proteins is blocked by treatment with the PI3K inhibitor LY294002, suggesting the activation of this pathway downstream of BCR-FGFR1 phosphorylation. Y177 has been shown to be a binding site for GRB2 and to be required for the both the phosphorylation of GAB2 and the development of CML-like disease (Roumiantsev, 2004, Demiroglu, 2001). By analogy with studies in BCR-ABL, where mutation of Y177 abrogates recruitment of PI3K activity to the fusion protein (Sattler, 2002), this suggests that Y177 may serve as a docking site for a complex of GRB2:GAB1:PI3K in the context of BCR-FGFR1 as well. Pubmed11739186 Pubmed12124177 Pubmed15050920 Reactome Database ID Release 431839095 Reactome, http://www.reactome.org ReactomeREACT_121232 Reviewed: Ezzat, S, 2012-05-15 pY177-BCR1-p-FGFR1 mutant:GRB2:GAB2 GRB2:GAB2 pY177-BCR-p-FGFR1 fusion mutant dimer