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MODEL0848279215 - Hornberg2005_MAPKsignalling


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Reference Publication
Publication ID: 16007170
Hornberg JJ, Binder B, Bruggeman FJ, Schoeberl B, Heinrich R, Westerhoff HV.
Control of MAPK signalling: from complexity to what really matters.
Oncogene 2005 Aug; 24(36): 5533-5542
Department of Molecular Cell Physiology, Institute of Molecular Cell Biology, Faculty of Earth and Life Sciences, Vrije Universiteit, Amsterdam, The Netherlands.  [more]
Original Model: CellML logo
Submitter: Vijayalakshmi Chelliah
Submission Date: 28 Apr 2009 13:25:23 UTC
Last Modification Date: 28 Apr 2009 13:25:23 UTC
Creation Date: 28 Apr 2009 13:25:23 UTC
bqmodel:isDerivedFrom PubMed 11923843
PubMed 10514507
bqbiol:isVersionOf Gene Ontology regulation of MAPK cascade
bqbiol:hasTaxon Taxonomy Homo sapiens

This a model from the article:
Control of MAPK signalling: from complexity to what really matters.
Hornberg JJ, Binder B, Bruggeman FJ, Schoeberl B, Heinrich R, Westerhoff HV. Oncogene 2005 Aug 25;24(36):5533-42 16007170 ,
Oncogenesis results from changes in kinetics or in abundance of proteins in signal transduction networks. Recently, it was shown that control of signalling cannot reside in a single gene product, and might well be dispersed over many components. Which of the reactions in these complex networks are most important, and how can the existing molecular information be used to understand why particular genes are oncogenes whereas others are not? We implement a new method to help address such questions. We apply control analysis to a detailed kinetic model of the epidermal growth factor-induced mitogen-activated protein kinase network. We determine the control of each reaction with respect to three biologically relevant characteristics of the output of this network: the amplitude, duration and integrated output of the transient phosphorylation of extracellular signal-regulated kinase (ERK). We confirm that control is distributed, but far from randomly: a small proportion of reactions substantially control signalling. In particular, the activity of Raf is in control of all characteristics of the transient profile of ERK phosphorylation, which may clarify why Raf is an oncogene. Most reactions that really matter for one signalling characteristic are also important for the other characteristics. Our analysis also predicts the effects of mutations and changes in gene expression.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Hornberg JJ, Binder B, Bruggeman FJ, Schoeberl B, Heinrich R, Westerhoff HV. (2005) - version02
The original CellML model was created by:
Lloyd, Catherine, May
The University of Auckland
The Bioengineering Institute

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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.