Fig. 3
From: Perturbation of PI3K/Akt signaling affected autophagy modulation in dystrophin-deficient myoblasts
Akt is not/less activated in dystrophin-deficient myoblasts. Myoblasts were cultured in GM until 80–90% confluent and culturing in DM for 10 days before total protein extraction and immunoblot analysis. Untreated- and PDGF-treated MEF cells were used as a control for Akt phosphorylation at both Ser473 and Thr308. a Immunoblot analysis during myoblast differentiation with α-tubulin expression as a loading control. Densitometry analysis of (b) Akt expression and (c) Akt activation at Ser473. The graphs represent an average of three repeats from different samples. All data are presented as mean ± S.D