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MODEL1106160000 - Smith2011_HumanHeartMitochondrian_MetabolicModel

 

The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.


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Reference Publication
Publication ID: 21714867
Smith AC, Robinson AJ.
A metabolic model of the mitochondrion and its use in modelling diseases of the tricarboxylic acid cycle.
BMC Syst Biol 2011; 5: 102
The Medical Research Council, Mitochondrial Biology Unit, Hills Road, Cambridge CB2 0XY, UK.  [more]
Model
Original Model: MODEL1106160000.origin
Submitter: Anthony Smith
Submission Date: 16 Jun 2011 11:38:49 UTC
Last Modification Date: 18 Jul 2011 17:29:39 UTC
Creation Date: 18 Jul 2011 17:29:39 UTC
Non kinetic model: network icon.
Encoders:
bqbiol:isVersionOf Gene Ontology glycolytic process
bqbiol:hasTaxon Taxonomy Eukaryota
Notes

This model is from the article:
A metabolic model of the mitochondrion and its use in modelling diseases of the tricarboxylic acid cycle.
Smith AC, Robinson AJ. BMC Syst Biol. 2011 Jun 29;5(1):102. 21714867 ,
Abstract:
BACKGROUND:Mitochondria are a vital component of eukaryotic cells and their dysfunction is implicated in a large number of metabolic, degenerative and age-related human diseases. The mechanism or these disorders can be difficult to elucidate due to the inherent complexity of mitochondrial metabolism. To understand how mitochondrial metabolic dysfunction contributes to these diseases, a metabolic model of a human heart mitochondrion was created. RESULTS: A new model of mitochondrial metabolism was built on the principle of metabolite availability using MitoMiner, a mitochondrial proteomics database, to evaluate the subcellular localisation of reactions that have evidence for mitochondrial localisation. Extensive curation and manual refinement was used to create a model called iAS253, containing 253 reactions, 245 metabolites and 89 transport steps across the inner mitochondrial membrane. To demonstrate the predictive abilities of the model, flux balance analysis was used to calculate metabolite fluxes under normal conditions and to simulate three metabolic disorders that affect the TCA cycle: fumarase deficiency, succinate dehydrogenase deficiency and alpha-ketoglutarate dehydrogenase deficiency. CONCLUSION: The results of simulations using the new model corresponded closely with phenotypic data under normal conditions and provided insight into the complicated and unintuitive phenotypes of the three disorders, including the effect of interventions that may be of therapeutic benefit, such as low glucose diets or amino acid supplements. The model offers the ability to investigate other mitochondrial disorders and can provide the framework for the integration of experimental data in future studies.

Created by Anthony C. Smith (Mon Mar 14 11:03:11 2011) MRC - Mitochondrial Biology Unit, Cambridge, UK. acs@mrc-mbu.cam.ac.uk

This metabolic network is a stocihiometric model of a human heart mitochondrion. Identifiers are KEGG Ids.

This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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