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. 2016 Feb 17;5(2):e002701. doi: 10.1161/JAHA.115.002701

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© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Molecular analyses of brains of all strains at 6 weeks of age. A through C, Brains of heterozygous SHR‐Ndufc2 ^em2Mcwi showed significantly lower amount of Ndufc2 mRNA and protein expression, as compared to both parental SHRSR and SHR‐Ndufc2 ^em1Mcwi. ^Δ P<0.01 versus SHRSR; *P<0.0001 versus all other samples (n=6 for each group). D through G, Representative western blot of BNG (n=3) showing defective complex I assembly only in heterozygous SHR‐Ndufc2 ^em2Mcwi rats. Corresponding densitometric analyses are shown on the right side of each blot. *P<0.0001 versus all other samples. H, Complex I activity and (I) ATP levels were comparable among all strains at this age (n=3). Values are expressed as means±SD. Ctrl indicates control; het, heterozygous; Hsp60, heat shock protein 60; SHRSP, stroke‐prone spontaneously hypertensive rat; SHRSR, stroke‐resistant SHR; wt, wild type.