| First Author | Hüttemann M | Year | 2012 |
| Journal | Mitochondrion | Volume | 12 |
| Issue | 2 | Pages | 294-304 |
| PubMed ID | 22119795 | Mgi Jnum | J:192141 |
| Mgi Id | MGI:5464081 | Doi | 10.1016/j.mito.2011.11.002 |
| Citation | Huttemann M, et al. (2012) Mice deleted for heart-type cytochrome c oxidase subunit 7a1 develop dilated cardiomyopathy. Mitochondrion 12(2):294-304 |
| abstractText | Subunit 7a of mouse cytochrome c oxidase (Cox) displays a contractile muscle-specific isoform, Cox7a1, that is the major cardiac form. To gain insight into the role of this isoform, we have produced a new knockout mouse line that lacks Cox7a1. We show that homozygous and heterozygous Cox7a1 knockout mice, although viable, have reduced Cox activity and develop a dilated cardiomyopathy at 6 weeks of age. Surprisingly, the cardiomyopathy improves and stabilizes by 6 months of age. Cox7a1 knockout mice incorporate more of the "liver-type" isoform Cox7a2 into the cardiac Cox holoenzyme and, also surprisingly, have higher tissue ATP levels. |
