Expression of a familial amyotrophic lateral sclerosis-associated mutant human superoxide dismutase in yeast leads to decreased mitochondrial electron transport.

@article{Gunther2004ExpressionOA,
  title={Expression of a familial amyotrophic lateral sclerosis-associated mutant human superoxide dismutase in yeast leads to decreased mitochondrial electron transport.},
  author={Michael R. Gunther and Reyna L. Vangilder and Jing Fang and Diana S. Beattie},
  journal={Archives of biochemistry and biophysics},
  year={2004},
  volume={431 2},
  pages={207-14}
}
Strains of Saccharomyces cerevisiae that express either the wild type or the amyotrophic lateral sclerosis-associated mutant human copper-zinc superoxide dismutase (SOD1) proteins A4V and G93A, respectively, in a yeast SOD1-deficient parent strain were used to investigate the hypothesis that expression of a mutant SOD1 protein causes deficient mitochondrial electron transport as a possible mechanism for disease induction. Mitochondria isolated from the wild type SOD1-expressing yeast were… CONTINUE READING