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. 2012 Apr 16;109(18):6975–6980. doi: 10.1073/pnas.1120043109

Fig. 6.

Fig. 6.

MFN2 restores the mitochondrial respiratory capacity in C2C12 cells stably expressing ALCAT1. C2C12 cells stably expressing ALCAT1 were transiently transfected with expression vectors for MFN2 or EGFP and were compared with vector control for changes in OCR in response to treatment with various mitochondrial inhibitors, including: FCCP, an mitochondrial uncoupler (A); rotenone, a complex I inhibitor (B); antimycin, a complex III inhibitor (C); and oligomycin, an ATPase inhibitor (D). The exogenous and endogenous MFN2 protein levels were analyzed by Western blot analysis using MFN2 antibodies, as shown in A. OCR was analyzed by Seahorse X-24 analyzer and calculated from at least three independent measurements for each chemical treatment. *P < 0.05 compared with control; #P < 0.05 and ##P < 0.01 compared with nontransfected ALCAT1-expressing cells.