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Open Access Highly Accessed Research article

A metabolic model of the mitochondrion and its use in modelling diseases of the tricarboxylic acid cycle

Anthony C Smith and Alan J Robinson*

Author Affiliations

The Medical Research Council, Mitochondrial Biology Unit, Hills Road, Cambridge CB2 0XY, UK

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BMC Systems Biology 2011, 5:102  doi:10.1186/1752-0509-5-102

Published: 29 June 2011

Additional files

Additional file 1:

Reaction details. Excel file detailing the reactions included in the model including the applied directionality, evidence for mitochondrial localisation and corresponding KEGG identifier, where applicable.

Format: XLSX Size: 71KB Download file

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Additional file 2:

Metabolite details. Excel file detailing the metabolites included in the model, the assigned compartment and corresponding KEGG identifier.

Format: XLSX Size: 40KB Download file

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Additional file 3:

Applied constraints. Excel file detailing the constraints placed on the boundary conditions and the mitochondrial transport steps.

Format: XLSX Size: 47KB Download file

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Additional file 4:

iAS253 metabolic model in SBML format. XML file of the iAS253 model, in SBML format. Boundary constraints and biomass pseudo reactions are included.

Format: XML Size: 349KB Download file

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Additional file 5:

Supplementary Figures. Supplementary Figure S1. Graph of the effect of varying succinate dehydrogenase flux on maximum ATP production. Supplementary Figure S2. Effects of metabolites on maximum ATP production while succinate dehydrogenase deficiency flux is at 33% of its flux under normal conditions. Supplementary Figure S3. Effects of metabolites on maximum ATP production while succinate dehydrogenase deficiency flux is at 0% of its flux under normal conditions. Supplementary Figure S4. The active pathways (red) that contribute to ATP production during succinate dehydrogenase deficiency. Black dotted lines show pathways that are inactive.

Format: PDF Size: 2.1MB Download file

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