PDGFRs are critical for PI3K/Akt activation and negatively regulated by mTOR
J. Clin. Invest. Hongbing Zhang, et al. 117:730 doi:10.1172/JCI28984 [Go to this article.]

Figure 7
Restoration of PDGFR/Akt signaling potentiates the tumorigenicity of Tsc1-null and Tsc2-null cells. (A) myr-Akt expression restores p-Akt levels in Tsc2^–/– MEFs (left); markedly accelerates tumor formation (middle); and reduces survival (right) of immunodeficient nude mice injected with these cells in comparison to controls treated with vector alone. (B and C) PDGFRβ expression increases serum-induced p-Akt levels in Tsc1^–/– (B) and Tsc2^–/– (C) MEFs (left); accelerates tumor formation (middle); and reduces survival (right) of immunodeficient nude mice injected with these cells in comparison to controls treated with vector alone.