DocumentCode
2645438
Title
Sensitivity analysis of programmed cell death and implications for crosstalk phenomena during Tumor Necrosis Factor stimulation
Author
Eissing, Thomas ; Waldherr, Steffen ; Gondro, Cedric ; Bullinger, Eric ; Sawodny, Oliver ; Allgöwer, Frank ; Scheurich, Peter ; Sauter, Thomas
Author_Institution
Institute for Systems Theory and Automatic Control, University of Stuttgart, Pfaffenwaldring 9, 70550, Germany
fYear
2006
fDate
4-6 Oct. 2006
Firstpage
1746
Lastpage
1752
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.
Keywords
Cancer; Crosstalk; Degradation; Inhibitors; Neoplasms; Organisms; Pharmaceuticals; Production; Sensitivity analysis; Signal analysis;
fLanguage
English
Publisher
ieee
Conference_Titel
Computer Aided Control System Design, 2006 IEEE International Conference on Control Applications, 2006 IEEE International Symposium on Intelligent Control, 2006 IEEE
Conference_Location
Munich, Germany
Print_ISBN
0-7803-9797-5
Electronic_ISBN
0-7803-9797-5
Type
conf
DOI
10.1109/CACSD-CCA-ISIC.2006.4776905
Filename
4776905
Link To Document