The model reproduces Fig 3a of the paper. Please note that the authors mention that they used a value of 2 for n, n being the power in the positive feedback function for kinase autocatalysis, however the model here has n=1.95 because this results in a simulation that is identical to Fig 3a. The model was successfully tested on MathSBML.
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- Feedback control of T-cell receptor activation.
- Chan C, Stark J, George AJ
- Proceedings. Biological sciences , 5/ 2004 , Volume 271 , pages: 931-939
- Department of Immunology, Division of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 ONN, UK.
- The specificity and sensitivity of T-cell recognition is vital to the immune response. Ligand engagement with the T-cell receptor (TCR) results in the activation of a complex sequence of signalling events, both on the cell membrane and intracellularly. Feedback is an integral part of these signalling pathways, yet is often ignored in standard accounts of T-cell signalling. Here we show, using a mathematical model, that these feedback loops can explain the ability of the TCR to discriminate between ligands with high specificity and sensitivity, as well as provide a mechanism for sustained signalling. The model also explains the recent counter-intuitive observation that endogenous 'null' ligands can significantly enhance T-cell signalling. Finally, the model may provide an archetype for receptor switching based on kinase-phosphatase switches, and thus be of interest to the wider signalling community.
Gene Ontology regulation of T cell receptor signaling pathway
- Model originally submitted by : Harish Dharuri
- Submitted: 22-Jun-2007 14:02:10
- Last Modified: 08-Apr-2016 16:36:48
(added: 22 Jun 2007, 13:20:12, updated: 22 Jun 2007, 13:20:12)