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. 2012 Jun 7;21(17):3910–3917. doi: 10.1093/hmg/dds219

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© The Author 2012. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Loss of E2f1 in mdx male mice increases oxidative metabolic gene expression, mitochondrial activity, muscle contraction and endurance capacity. (A) Quantification of the expression by Q-PCR of relevant genes involved in mitochondrial biogenesis and function in GN of E2f1+/+;mdx and −/−;mdx mice. Results were normalized by the expression of mouse 18S RNA. n = 6 animals/group. (B) O₂ consumption was measured before and after the addition of succinate in isolated mitochondria from E2f1+/+, E2f1−/−, E2f1+/+;mdx and E2f1−/−;mdx GN muscle. n = 4 animals/group. (C) Isometric force production was measured in diaphragm muscle in 12-week-old mice of the indicated genotypes. n = 9 animals/group. (D) Twelve-week-old control E2f1−/−, E2f1+/+;mdx and −/−;mdx mice were run for 1 h on a treadmill with a 15° incline. The average distance run is represented. Values in A to D represent means ± SEM. *P < 0.05; **P < 0.01.