Abstract | ||
---|---|---|
The transcription factor NF-κB is a biological component that is central to the regulation of genes involved in the innate immune system. Dysregulation of the pathway is known to be involved in a large number of inflammatory diseases. Although considerable research has been performed since its discovery in 1986, we are still not in a position to control the signalling pathway, and thus limit the effects of NF-κB within promotion of inflammatory diseases. We have developed an agent-based model of the IL-1 stimulated NF-κB signalling pathway, which has been calibrated to wet-lab data at the single-cell level. Through rigorous software engineering, we believe our model provides an abstracted view of the underlying real-world system, and can be used in a predictive capacity through in silico experimentation. In this study, we have focused on the dynamics of the IKK complex and its activation of NF-κB. Our agent-based model suggests that the pathway is sensitive to: variations in the binding probability of IKK to the inhibited NF-κB-IκBα complex; and variations in the temporal rebinding delay of IKK. |
Year | DOI | Venue |
---|---|---|
2017 | 10.1109/CEC.2017.7969320 | 2017 IEEE Congress on Evolutionary Computation (CEC) |
Keywords | Field | DocType |
IKK dynamics,IL-1 stimulated NF-κB signalling pathway,X-machines,NF-κB transcription factor,biological component,gene regulation,innate immune system,pathway dysregulation,inflammatory diseases,agent-based model,software engineering,binding probability,temporal rebinding delay | NF-κB,IκB kinase,Gene,Computer science,Artificial intelligence,Immune system,Computational biology,Transcription factor,In silico,Innate immune system,Hedgehog signaling pathway,Bioinformatics,Machine learning | Conference |
ISBN | Citations | PageRank |
978-1-5090-4602-7 | 1 | 0.35 |
References | Authors | |
8 | 3 |
Name | Order | Citations | PageRank |
---|---|---|---|
Richard A. Williams | 1 | 7 | 1.81 |
Jonathan Timmis | 2 | 339 | 33.03 |
Eva E Qwarnstrom | 3 | 3 | 1.41 |