ABSTRACT:
This a model from the article:
Oxidative ATP synthesis in skeletal muscle is controlled by substrate feedback.
Wu F, Jeneson JA, Beard DA. Am J Physiol Cell Physiol
2007 Jan;292(1):C115-24 16837647
,
Abstract:
Data from (31)P-nuclear magnetic resonance spectroscopy of human forearm flexor
muscle were analyzed based on a previously developed model of mitochondrial
oxidative phosphorylation (PLoS Comp Bio 1: e36, 2005) to test the hypothesis
that substrate level (concentrations of ADP and inorganic phosphate) represents
the primary signal governing the rate of mitochondrial ATP synthesis and
maintaining the cellular ATP hydrolysis potential in skeletal muscle.
Model-based predictions of cytoplasmic concentrations of phosphate metabolites
(ATP, ADP, and P(i)) matched data obtained from 20 healthy volunteers and
indicated that as work rate is varied from rest to submaximal exercise
commensurate increases in the rate of mitochondrial ATP synthesis are effected
by changes in concentrations of available ADP and P(i). Additional data from
patients with a defect of complex I of the respiratory chain and a patient with
a deficiency in the mitochondrial adenine nucleotide translocase were also
predicted the by the model by making the appropriate adjustments to the
activities of the affected proteins associates with the defects, providing both
further validation of the biophysical model of the control of oxidative
phosphorylation and insight into the impact of these diseases on the ability of
the cell to maintain its energetic state.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wu F, Jeneson JA, Beard DA. (2006) - version=1.0
The original CellML model was created by:
Geoffrey Nunns
gnunns1@jhu.edu
The University of Auckland
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Camille Laibe 