Computational modeling of the dynamics of the MAP kinase cascade activated by surface and internalized EGF receptors
By Birgit Schoeberl, Claudia Eichler-Jonsson, Ernst Dieter Gilles, G. Müller. Nature Biotechnology, 2002
1,048 citations recorded by the source corpus.
Subfields: Computational Theory and Mathematics, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/509f1971d67425c00eb55f435cf67274acb0fe25
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In Computational Theory and Mathematics
- Chris J. Oates
- Vincent Danos
- Jean-Louis Krivine
- Aik Choon Tan
- Karen A. Ryall
- Sach Mukherjee
- Jane Hillston
- Federica Ciocchetta
In Molecular Biology
- Chris J. Oates
- Jason A. Papin
- Walter Kolch
- Bernhard O. Palsson
- Sach Mukherjee
- C. Hill
- Bernhard Schmierer
- Boris N. Kholodenko
In Oncology
- Sach Mukherjee
- Chris J. Oates
- Jane Hillston
- Federica Ciocchetta
- Walter Kolch
- P. Bastiaens
- T. Hunter
- Silvia D. M. Santos
Citations in the corpus
- Cancer: a Systems Biology disease. (2006, background): “Several detailed kinetic models ('computer replica') of metabolic systems , such as glycolysis (Schuster and Holzhütter, 1995; Teusink et al., 2000), provide rather accurate descriptions of their in vivo counterparts.”
- A methodology for the structural and functional analysis of signaling and regulatory networks (2006, neutral): “[3-6]).”
- Rule-Based Modelling of Cellular Signalling (2007, positive): “The rule set itself was mainly obtained from refactoring two existing ordinary differential equations (ODE) models [11,12] treating two different aspects of EGFEGFR signalling: down-regulation of Erk activity through a negative feedback and down-regulation of the signal through internalization.”
- Complex N-glycan number and degree of branching cooperate to regulate cell proliferation and differentiation. (2007, background): “Downstream intracellular signaling does not appear to be a confounding factor as both ERK and SMAD activation increase hyperbolically with increasing surface receptor when stimulated by excess ligand, based on computational models (Figures S4E and S4F; Schoeberl et al., 2002; Vilar et al., 2006) and”
- Input–output behavior of ErbB signaling pathways as revealed by a mass action model trained against dynamic data (2009, methodology): “To construct a computational model of ErbB-mediated signaling, we extended our previous model (Schoeberl et al , 2002), which contained only the ErbB1 receptor, using information from models of other mammalian signal-transduction cascades and a large body of newly published data (Yarden and…”
- Systems biology approaches for advancing the discovery of effective drug combinations (2015, background): “…kinetic models that typically represent interactions between molecular species in the signaling network as ordinary differential equations (ODEs) and require selection of parameter values for concentrations of species in the network and rate constants controlling protein-protein associations [23].”
- Computational modeling of the EGF-receptor system: a paradigm for systems biology. (2003, background): “The model of Schoeberl et al. is the most comprehensive in that it includes the fullest range of dynamic processes and makes several interesting and significant predictions that can be validated by experimental tests [ 39 ].”
- Reconstruction of cellular signalling networks and analysis of their properties (2005, background): “However, this maximum value is reasonable considering that some cells are estimated to contain 10 4 –10 5 of each type of recepto”
- A quantitative protein interaction network for the ErbB receptors using protein microarrays (2006, background): “Whereas our arrays provide a list of previously unrecognized bio-chemical interactions, as well as data that can fuel efforts to build computational models of signal transduction 14 , they also offer an unbiased, system-level view of the ErbB receptors that was previously unavailable.”
- Network Inference and Biological Dynamics (2011, methodology): “Kinetic models have been described for many cellular processes [Cantone et al. (2009); Schoeberl et al. (2002); Swat, Kel and Herzel (2004); Wilkinson (2009)].”
- Cell-signalling dynamics in time and space (2006, background): “…small GTPases Ras and Rap1) to various growth factors 32,41,49 , the nonlinear dependences of the amplitude of MAPK activation on the EGFR numbers 34 , autocrine positive-feedback loops 50 , the cross-talk between the MAPK and AKT/PKB pathways 37 , and the integration of EGFR signalling from the…”
- Bio-PEPA: A framework for the modelling and analysis of biological systems (2009, methodology): “A first study concerns the influence of the Raf Kinase Inhibitor Protein (RKIP) on the Extracellular signal Regulated Kinase (ERK) [11], whereas in [12] the PEPA system for Schoeberl’s model [34] involving the MAP kinase and EFG receptors is reported.”