[en] Recently, a mathematical model of the mitochondrial apoptotic pathway was proposed. In that study, the robustness of different simplified signaling models with respect to parameter changes was also investigated. It was found that bistability achieved via cooperative ultrasensitivity is ‘‘much more robust’’ than other mechanisms such as inhibitor ultrasensitivity. We reinvestigate this interesting finding to reveal that it does not hold in such generality. Our results
indicate that mechanisms other than cooperative ultrasensitivity, such as inhibitor ultrasensitivity, can confer a similar robust bistable performance. Thereby, these findings are not restricted to apoptosis signaling, but relevant to bistable signaling in general. In addition, example calculations
indicate the potential practical relevance of inhibitor ultrasensitivity for generating robustness in apoptosis signaling.
Disciplines :
Engineering, computing & technology: Multidisciplinary, general & others
Author, co-author :
Eissing, Thomas
Waldherr, Steffen
Allgöwer, Frank
Scheurich, Peter
Bullinger, Eric ; Université de Liège - ULiège > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Méthodes computationnelles pour la biologie systémique
Language :
English
Title :
Response to bistability in apoptosis: Roles of Bax, Bcl-2, and mitochondrial permeability transition pores
Publication date :
2007
Journal title :
Biophysical Journal
ISSN :
0006-3495
eISSN :
1542-0086
Publisher :
Biophysical Society, Bethesda, United States - Maryland
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