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. 2013 Apr 18;4(4):e602. doi: 10.1038/cddis.2013.99

Figure 5.

Figure 5

Ack1 modulates Akt1 and MAPK pathways. (a) Starved PC12 cells lines (wild-type PC12 cells, lanes 1–4, PC12 cells stably transfected with an empty vector, lanes 5–8; PC12 cells overexpressing Ack1i, lanes 9–12) were treated for 5, 15, 30, and 60 min with NGF (50 ng/ml) or left untreated (t=0) (lanes 1, 5, and 9). Overexpression of Ack1 enhanced the NGF-induced phosphorylation of Akt (panel 1, lanes 9–12) and ERK 1/2 (panel 3, lanes 9–12). Loading controls are in panels 2 and 4. (b) Starved PC12 cells lines (PC12 wild type, lanes 1–4; PC12 expressing two shRNAs against Ack1, lanes 5–12) were treated for 5, 15, 30, and 60 min with NGF (50 ng/ml) or left untreated (t=0) (lanes 1, 5, and 9). Ack1 knock-down counteracted the NGF-induced phosphorylation of Akt (panel 1, lanes 5–8 and 9–12) and ERK 1/2 (panel 3, lanes 5–8 and 9–12). Loading controls are in panels 2 and 4. Quantification of NGF-induced phospho-Akt levels (c) and phospho-ERK (d) is illustrated. The mean data ±S.E.M. of 3–6 separate experiments are shown. Data were normalized to control t=0. Groups compared with the T-test are indicated (*P<0.01; ***P<0.001)