| created | [InstanceEdit:1839079] Rothfels, K, 2011-10-27 |
| dbId | 1839077 |
| displayName | Activation of the PI3K signaling pathway has been demonstrat... |
| modified | [InstanceEdit:2085549] Rothfels, K, 2012-02-03 |
| schemaClass | Summation |
| text | 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). |
| (summation) |
© 2026 Reactome