8.3 Modeling of Electron Transport: Implications to Mitochondrial Diseases
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Springer US
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http://link.springer.com/content/pdf/10.1007/978-0-387-30411-3_32.pdf
Reference75 articles.
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2. Beziat F, Morel F, Volz-Lingenhol A, Saint Paul N, Alziari S. 1993. Mitochondrial genome expression in a mutant strain of D. subobscura, an animal model for large-scale mtDNA deletion. Nucleic Acids Res 21: 387–392.
3. Bohnensack R. 1981. Control of energy transformation of mitochondria. Analysis by a quantitative model. Biochim Biophys Acta 634: 203–218.
4. Bohnensack R, Küster U, Letko G. 1982. Rate-controlling steps of oxidative phosphorylation in rat liver mitochondria. A synoptic approach of model and experiment. Biochim Biophys Acta 680: 271–280. The use of MCA to demonstrate for the first time that the control of oxidative phosphorylation is shared, ending in this way a long-standing riddle concerning the determination of the “controlling step”; see also Groen et al. (1982), who were very active in this field. These two articles profoundly changed the way to apprehend the regulation of oxidative phosphorylation and even the design of experiments in this field.
5. Chance B, Williams GR. 1955. Respiration enzymes in oxidative phosphorylation. 1. Kinetics of oxygen utilization. J Biol Chem 217: 383–393.
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