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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Perturbation of PI3K/Akt signaling affected autophagy modulation in dystrophin-deficient myoblasts

Fig. 1Fig. 1

Dystrophin-deficient myoblasts have impaired differentiation capacity. Approximately 1.5 × 104 of both C2C12 (non-dystrophic) and dfd13 (dystrophin-deficient) myoblasts were cultured in GM (on the acid-etched coverslip) before being transferred to DM and allowed to differentiate for 10. Immunofluorescence analysis of F-MyHC in (a) C2C12 and (b) dfd13 cells during the non-differentiated stage and after 10 days of differentiation. c Percentage myotube formation was calculated by counting the nuclei (DAPI) present in myotubes (myonuclei) per total nuclei from 10 random microscope fields. d Representative immunoblot of the proteins during myoblast differentiation with the α-tubulin expression as a loading control. Densitometry analyses of (e) F-MyHC (MY-32), f pan-myosin (MF20), and g desmin expression. The graphs represent an average of three repeats from different samples. All data are presented as mean ± S.D. ND: non-differentiated; D10: day 10 of differentiation; **: significantly different (p < 0.01) compared to C2C12 myoblasts. *: significantly different (p < 0.05) compared to C2C12 myoblasts GM: growth medium (DMEM + 10% FCS); DM: differentiation medium (DMEM + 2% horse serum)

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