Cellular responses to activation of growth factor receptors is dictated by the repertoire of signaling molecules present within a given cell type. Weidentified a novel mechanism utilized by the CSF-1R for activating thephosphatidylinositol 3-kinase (PI3K)/Akt survival pathway in the 32D myeloidcell line (Fig. 1). Unlike thepreviously described pathway involving direct CSF-1R:PI3K binding, this novelmechanism is activated by a deletion mutant of CSF-1R (DKI) that cannot bind PI3K. Using both pharmacological and genetic approaches, wedetermined that the novel pathway involves a CSF-1R-Src-Gab2-PI3K link.
Recent exciting results in the lab point to an essential role for Gab2 in maintaining neural stem cell proliferation (self-renewal). Since a multitude of receptor tyrosine kinases are found in neural stem cells and their progeny (neurons, astrocytes and oligodendrocytes), this has significant implication.
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Lee and States, MCB 20:6779,2000