Diminished Exercise Capacity and Mitochondrial bc1 Complex Deficiency in Tafazzin-Knockdown Mice

@inproceedings{Powers2013DiminishedEC,
  title={Diminished Exercise Capacity and Mitochondrial bc1 Complex Deficiency in Tafazzin-Knockdown Mice},
  author={Corey Powers and Yan Huang and Arnold Strauss and Zaza Khuchua},
  booktitle={Front. Physiol.},
  year={2013}
}
The phospholipid, cardiolipin, is essential for maintaining mitochondrial structure and optimal function. Cardiolipin-deficiency in humans, Barth syndrome, is characterized by exercise intolerance, dilated cardiomyopathy, neutropenia, and 3-methyl-glutaconic aciduria. The causative gene is the mitochondrial acyl-transferase, tafazzin, that is essential for remodeling acyl chains of cardiolipin. We sought to determine metabolic rates in tafazzin-deficient mice during resting and exercise, and… CONTINUE READING
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Diminished exercise capacity and mitochondrial bc1 complex deficiency in tafazzinknockdown mice

C Citation Powers, Y Huang, A Strauss, Z Khuchua
2013

This is an openaccess article distributed under the terms of the Creative Commons Attribution

Powers, Huang, Strauss, Khuchua
2013

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