Eissing, Thomas and Waldherr, Steffen and Gondro, Cedric and Bullinger, Eric and Sawodny, Oliver and Allgöwer, Frank and Scheurich, Peter and Sauter, Thomas (2006) Sensitivity analysis of programmed cell death and implications for crosstalk phenomena during Tumor Necrosis Factor stimulation. In: Proceedings of the 2006 IEEE International Conference on Control Applications Munich, Germany, October 4-6, 2006. IEEE, pp. 1746-1752. ISBN 0-7803-9797-5

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Abstract

Different methods for analyzing the sensitivity of the direct signal transduction pathway of receptor-induced apoptosis to parameter changes are presented. Apoptosis is a form of programmed cell death, removing unwanted cells within multicellular organisms to maintain a proper balance between cell reproduction and death. The results indicate the importance of controlling activated caspases by direct inhibition to prevent apoptosis. A misregulation of IAP molecules, one of the main inhibitors, appears to be especially critical. The results indicate how an increased production of this molecule promotes survival and might promote cancer progression, while a reduced degradation might not, thereby providing insight of potential pharmaceutical relevance and also stimulating experimental verification. The different engineering methods applied, nicely complement each other to provide valuable insight into this important process. Because IAPs, among others, are also an important connection to other signaling pathways, the results will enable a more efficient extension of the current model. This is outlined at the example of Tumor Necrosis Factor induced signaling pathways.

Item Type:	Book Section
Additional Information:	©2006 IEEE. Reprinted from Proceedings of the 2006 IEEE International Conference on Control Applications Munich, Germany, October 4-6, 2006. Personal use of this material is permitted. However, permission to reprint/republish this material for advertising or promotional purposes or for creating new collective works for resale or redistribution to servers or lists, or to reuse any copyrighted component of this work in other works must be obtained from the IEEE. http://ieeexplore.ieee.org/stamp/stamp.jsp?tp=&arnumber=4776905&isnumber=4776587
Keywords:	Tumor Necrosis Factor; Apoptosis; Sensitivity analysis; Hamilton Institute.
Academic Unit:	Faculty of Science and Engineering > Biology Faculty of Science and Engineering > Mathematics and Statistics
Item ID:	1761
Identification Number:	https://doi.org/10.1109/CACSD-CCA-ISIC.2006.4776905
Depositing User:	Hamilton Editor
Date Deposited:	22 Dec 2009 13:59
Publisher:	IEEE
Refereed:	Yes
URI:
Use Licence:	This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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