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 5
Akt activation by EGF, IGF, and PMA is reduced in cells lacking PDGFR. (AC) Immunoblots of cell lysates. Each set of 3 lanes in A consists of lysates from PDGFRα/β double-null, Pdgfra–/–, and Pdgfrb–/– MEFs. All cells were serum starved for 48 hours and then stimulated with 50 ng/ml PDGFbb, 50 ng/ml EGF, 50 ng/ml IGF, or 10% serum for 10 minutes; or 200 nM PMA for 30 minutes. p-Akt levels were markedly reduced in PDGFRα/β double-null cells in response to all stimuli. (D) Immunoblots of WT or Egfr–/– MEFs. Cells were serum starved for 24 hours and stimulated with 50 ng/ml EGF (E), 50 ng/ml TGF-α (T), 50 ng/ml PDGF (P), 50 ng/ml IGF (I), or 0.2 nM insulin (In) for 10 minutes. Note that phosphorylation of Akt, S6, and ERK in response to PDGF, IGF, and insulin was similar in Egfr–/– and control MEFs.