Reference : Response to bistability in apoptosis: Roles of Bax, Bcl-2, and mitochondrial permeabilit...
Scientific journals : Article
Engineering, computing & technology : Multidisciplinary, general & others
http://hdl.handle.net/2268/12476
Response to bistability in apoptosis: Roles of Bax, Bcl-2, and mitochondrial permeability transition pores
English
Eissing, Thomas [> > > >]
Waldherr, Steffen [> > > >]
Allgöwer, Frank [> > > >]
Scheurich, Peter [> > > >]
Bullinger, Eric mailto [Université de Liège - ULg > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Méthodes computationnelles pour la biologie systémique >]
2007
Biophysical Journal
Biophysical Society
92
9
3332-3334
Yes (verified by ORBi)
International
0006-3495
1542-0086
Bethesda
MD
[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.
Deutsche Forschungsgemeinschaft - DFG
Researchers
http://hdl.handle.net/2268/12476
10.1529/biophysj.106.100362

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