Source:http://www.reactome.org/biopax/48887BiochemicalReaction1819
| Predicate | Object |
|---|---|
| rdf:type | |
| biopax3:comment |
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.,
Reviewed: Ezzat, S, 2012-05-15
|
| biopax3:xref | |
| biopax3:dataSource | |
| biopax3:displayName |
p-BCR-pFGFR1 recruits GRB2:GAB2
|
| biopax3:left | |
| biopax3:right |