Models

Despite the crucial role of the liver in glucose homeostasis, a detailed mathematical
model of human hepatic glucose metabolism is lacking so far. Here we present a
detailed kinetic model of glycolysis, gluconeogenesis and glycogen metabolism in
human hepatocytes integrated with the hormonal control of these pathways by insulin,
glucagon and epinephrine. Model simulations are in good agreement with experimental
data on (i) the quantitative contributions of glycolysis, gluconeogenesis, and glycogen
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This is HepatoNet1 including MIRIAM annotations.

supplementary information for L. O. Schwen, A. Schenk, C. Kreutz, J. Timmer, M. M. Bartolomé-Rodriguez, L. Kuepfer, and T. Preusser: Representative Sinusoids For Hepatic Four-Scale Pharmacokinetics Simulations, PLoS ONE, 10(7):e0133653, 1-39, 2015, DOI 10.1371/journal.pone.0133653

For detailed description see:
Biomech Model Mechanobiol. 2015 Jun;14(3):515-36. doi: 10.1007/s10237-014-0619-z. Epub 2014 Sep 19.
Modeling function-perfusion behavior in liver lobules including tissue, blood, glucose, lactate and glycogen by use of a coupled two-scale PDE-ODE approach.
Ricken T1, Werner D, Holzhütter HG, König M, Dahmen U, Dirsch O.
http://www.ncbi.nlm.nih.gov/pubmed/25236798

JSBML is a community-driven project to create a free, open-source, pure Java library for reading, writing, and manipulating SBML files and data streams. It is an alternative to the mixed Java/native code-based interface provided in libSBML.

It is a link to a supplementary information from a publication: Benary, U., Kofahl, B., Hecht, A. and Wolf, J. (2015), Mathematical modelling suggests a differential impact of β-transducin repeat-containing protein paralogues on Wnt/β-catenin signalling dynamics. FEBS Journal, 282: 1080–1096. doi: 10.1111/febs.13204

http://onlinelibrary.wiley.com/doi/10.1111/febs.13204/suppinfo

The Wnt/β-catenin signalling pathway is involved in the regulation of a multitude of cellular processes by controlling
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Mobi PBPK Models of Paracetamol, Ammonia and Allopurinol, relating to Publication Krauss et al (2012) in PLoS Comp Biol

Model has been published in Hohmann et al., PLoS ONE 9(4): e93207 (2014), doi: 10.1371/journal.pone.0093207

used for the publication "Spatio-Temporal Simulation of First Pass Drug Perfusion in the Liver"

Rabs constitute a group of small GTPases that confer directionality to intracellular vesicle transport by promoting on the membrane of transport vesicles in the formation of specific protein complexes allowing for efficient fusion with a selected set of target organelles. The molecular mechanism controlling recruitment of the correct Rab at the right time is not fully understood. We propose a model according to which the residence time of a given Rab on the membrane of an organelle is determined
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Formation, degradation and renewal of cellular organelles is a dynamic process based on permanent budding, fusion and inter-organelle traffic of vesicles.

Morpheus model of Smo regulation in response to Hh

As used in refereence:
A.P. Kupinski, I. Raabe, M. Michel, D. Ail, L. Brusch, T. Weidemann, C. Bökel (2013) Phosphorylation of the Smo tail is controlled by membrane localization and is dispensable for clustering, J. Cell Sci., 126, 20, 4684-4697 doi: 10.1242/​jcs.128926

SBML model of Smo regulation in response to Hh

As used in refereence:
A.P. Kupinski, I. Raabe, M. Michel, D. Ail, L. Brusch, T. Weidemann, C. Bökel (2013) Phosphorylation of the Smo tail is controlled by membrane localization and is dispensable for clustering, J. Cell Sci., 126, 20, 4684-4697 doi: 10.1242/​jcs.128926

Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven, consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared with its predecessors, the reconstruction has improved topological and functional features, including ∼2× more reactions and ∼1.7× more unique metabolites. Using Recon 2 we predicted
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Transforming growth factor β (TGF-β) ligands activate a signaling cascade with multiple cell context dependent outcomes. Disruption or disturbance leads to variant clinical disorders. To develop strategies for disease intervention, delineation of the pathway in further detail is required. Current theoretical models of this pathway describe production and degradation of signal mediating proteins and signal transduction from the cell surface into the nucleus, whereas feedback loops have not
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We created an ODE-based model of TNFalpha-induced NFkappaB signalling in primary hepatocytes.