ABSTRACT:
This a model from the article:
Mathematical model of human growth hormone (hGH)-stimulated cell proliferation
explains the efficacy of hGH variants as receptor agonists or antagonists.
Haugh JM. Biotechnol Prog
2004 Sep-Oct;20(5):1337-44 15458315
,
Abstract:
Human growth hormone (hGH) is a therapeutically important endocrine factor that
signals various cell types. Structurally and functionally, the interactions of
hGH with its receptor have been resolved in fine detail, such that hGH and hGH
receptor variants can be practically engineered by either random or rational
approaches to achieve significant changes in the free energies of binding. A
somewhat unique feature of hGH action is its homodimerization of two hGH
receptors, which is required for intracellular signaling and stimulation of cell
proliferation, yet the potencies of hGH mutants in cell-based assays rarely
correlate with their overall receptor-binding avidities. Here, a mathematical
model of hGH-stimulated cell signaling is posed, accounting not only for binding
interactions at the cell surface but induction of receptor endocytosis and
downregulation as well. Receptor internalization affects ligand potency by
imposing a limit on the lifetime of an active receptor complex, irrespective of
ligand-receptor binding properties. The model thus explains, in quantitative
terms, the numerous published observations regarding hGH receptor agonism and
antagonism and challenges the interpretations of previous studies that have not
considered receptor trafficking as a central regulatory mechanism in hGH
signaling.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Haugh JM. (2004) - version02
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
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.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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.