- Author:
- pmr2.import <nobody@models.cellml.org>
- Date:
- 2009-06-17 15:05:11+12:00
- Desc:
- committing version01 of maly_wiley_lauffenburger_2004
- Permanent Source URI:
- https://models.cellml.org/workspace/maly_wiley_lauffenburger_2004/rawfile/a650bb380cacdc4313cda100ce7ebbd7928ac540/maly_wiley_lauffenburger_2004.cellml
<?xml version='1.0' encoding='utf-8'?>
<!-- FILE : maly_model_2004_raw.xml
CREATED : 26th February 2004
LAST MODIFIED : 26th February 2004
AUTHOR : Catherine Lloyd
The Bioengineering Institute
The University of Auckland
MODEL STATUS : This model conforms to the CellML 1.0 Specification released on
10th August 2001, and the 16/01/2002 CellML Metadata 1.0
Specification.
DESCRIPTION : This file contains a CellML description of Maly et al's 2004 computational model analysis of self-organisation of polarised cell signalling via autocrine circuits.
CHANGES:
--><model xmlns="http://www.cellml.org/cellml/1.0#" xmlns:cmeta="http://www.cellml.org/metadata/1.0#" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bqs="http://www.cellml.org/bqs/1.0#" xmlns:cellml="http://www.cellml.org/cellml/1.0#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:pathway_editor="http://www.physiome.com/pathway_editor/1.0#" xmlns:vCard="http://www.w3.org/2001/vcard-rdf/3.0#" pathway_editor:rendering_config_file="maly_model_2004_CellMLrender.xml" cmeta:id="maly_wiley_lauffenburger_2004_version01" name="maly_wiley_lauffenburger_2004_version01">
<documentation xmlns="http://cellml.org/tmp-documentation">
<article>
<articleinfo>
<title>A Computational Model Analysis of the Self-Organisation of Polarised Cell Signalling via Autocrine Circuits</title>
<author>
<firstname>Catherine</firstname>
<surname>Lloyd</surname>
<affiliation>
<shortaffil>Bioengineering Institute, University of Auckland</shortaffil>
</affiliation>
</author>
</articleinfo>
<section id="sec_status">
<title>Model Status</title>
<para>
This model contains partial differentials and as such can not currently be solved by existing CellML tools.
</para>
</section>
<sect1 id="sec_structure">
<title>Model Structure</title>
<para>
Autocrine cells both produce signalling modelcules and respond to them. AN example of an autocrine system is signalling through epidermal growth factor (EGF) receptor (EGFR). A cell releases EGFR ligands into its environment, and a fraction of the released ligand is recaptured by the receptors at the cell surface. The activated receptors then trigger a signal transduction cascade, whose effects range from cell proliferation to cell migration behaviour. An additional effect can be the further production of EGFR ligands, producing a positive feedback loop which results in a sustained activity of the autocrine signalling circuit. If, as hypothesised, this sustained autoendocrine circuit is localised within a defined domain of the cell, then it may contribute to the intrinsic cell polarity or assymmetry.
</para>
<para>
The difficulty associated with the experimental investigation of autoendocrine signalling makes computational modelling especially valuable when trying to deduce nature of the molecular mechanisms underlying signalling circuits. In the Maly <emphasis>et al.</emphasis> 2004 publication described here, the authors develop and analyse a dymanic computational model of autocrine EGFR signalling. Their description is based on integrating select elements from the models of <ulink url="${HTML_EXMPL_KHOLODENKO_MODEL}">Kholodenko <emphasis>et al.</emphasis>, Quantification of EGF Receptor Signalling, 1999</ulink>, and of <ulink url="${HTML_EXMPL_MAPK_CASCADE}">Huang and Ferrell, MAPK Cascade, 1996</ulink>, into the existing model of EGFR aurocrine signalling bt Shvartsman <emphasis>et al.</emphasis>, 2002.
</para>
<para>
It should be noted that although the original Maly <emphasis>et al.</emphasis> model is a spatially distributed dynamic computational model, the spatial parameters in this CellML description have been removed, as CellML is currently unable to handle spatial parameters. The model is still dynamic.
</para>
<para>
The complete original paper reference is cited below:
</para>
<para>
<ulink url="http://www.biophysj.org/cgi/content/abstract/86/1/10">Self-Organization of Polarized Cell Signaling via Autocrine Circuits: Computational Model Analysis</ulink>, Ivan V. Maly, H. Steven Wiley, and Douglas A. Lauffenburger, 2004, <ulink url="http://www.biophysj.org/">
<emphasis>Biophysical Journal</emphasis>
</ulink>, 86, 10-22. (<ulink url="http://www.biophysj.org/cgi/content/full/86/1/10">Full text (HTML)</ulink> and <ulink url="http://www.biophysj.org/cgi/reprint/86/1/10.pdf">PDF</ulink> versions of the article are available on the <emphasis>Biophysical Journal</emphasis> website.) <ulink url="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14695245&dopt=Abstract">PubMed ID: 14695245</ulink>
</para>
<informalfigure float="0" id="fig_reaction_diagram">
<mediaobject>
<imageobject>
<objectinfo>
<title>reaction diagram</title>
</objectinfo>
<imagedata fileref="maly_2004.png"/>
</imageobject>
</mediaobject>
<caption>Components of the autocrine EGFR signalling system and their interactions in the model. Transport, covalent modifications, and protein binding processes are shown by solid arrows. Catalysation is shown by a dashed arrow. EGFR is a receptor of ligand L; Gbr2 is an adaptor protein; Sos is an activator protein, Raf, MEK and ERK are protein kinases; p denotes the phosphorylated form of a protein and pp is a double-phosphorylated form.</caption>
</informalfigure>
<para>
Model siumulations supported the hypothesis that autocrine EGFR siganlling circuits could contribute to the generation and/or maintainance of intrinsic cell spatial polarity, possibly realted to migration as ell as tissue organisation.
</para>
</sect1>
</article>
</documentation>
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<unit units="mole"/>
<unit units="litre" exponent="-1"/>
</units>
<units name="flux">
<unit units="molar"/>
<unit units="second" exponent="-1"/>
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<dc:title>L</dc:title>
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</rdf:Description>
</rdf:RDF>
<variable units="molar" public_interface="out" name="L" initial_value="1.0E-9"/>
<variable units="m2_per_s" name="DL" initial_value="1.0E-12"/>
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</rdf:Description>
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<variable units="first_order_rate_constant" public_interface="in" name="kdgc"/>
<variable units="second_order_rate_constant" public_interface="in" name="kagsc"/>
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<rdf:RDF>
<rdf:Description rdf:about="CGrb">
<dc:title>CGrb</dc:title>
<dcterms:alternative>surface density of extracellular ligand-receptor-Grb2 complex</dcterms:alternative>
</rdf:Description>
</rdf:RDF>
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</rdf:Description>
</rdf:RDF>
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<dc:title>Grb</dc:title>
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</rdf:Description>
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<variable units="molar" public_interface="out" name="Grb" initial_value="5.0E-8"/>
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<rdf:RDF>
<rdf:Description rdf:about="Sos">
<dc:title>Sos</dc:title>
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</rdf:Description>
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<rdf:li>MAPK cascade</rdf:li>
<rdf:li>polarised signaling</rdf:li>
<rdf:li>autocrine</rdf:li>
<rdf:li>signal transduction</rdf:li>
<rdf:li>signal transductions</rdf:li>
<rdf:li>mapk</rdf:li>
<rdf:li>Autocrine Cell</rdf:li>
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Below is a CellML description of Maly et al's 2004 computational model analysis of self-organisation of polarised cell signalling via autocrine circuits.
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<vCard:Given>H</vCard:Given>
<vCard:Family>Wiley</vCard:Family>
<vCard:Other>Steven</vCard:Other>
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<dc:title>
Maly et al's 2004 computational model analysis of self-organisation of polarised cell signalling via autocrine circuits.
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<cmeta:bio_entity>Autocrine Cell</cmeta:bio_entity>
<cmeta:comment rdf:resource="rdf:#3040f478-acba-45d3-9174-e0a44399a927"/>
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<dc:creator rdf:resource="rdf:#1e7126c5-e667-4d7f-87a4-21913bed1616"/>
<dc:title>
Self-Organization of Polarized Cell Signaling via Autocrine Circuits: Computational Model Analysis
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<bqs:volume>86</bqs:volume>
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