|Reference : Response to bistability in apoptosis: Roles of Bax, Bcl-2, and mitochondrial permeabi...|
|Scientific journals : Article|
|Engineering, computing & technology : Multidisciplinary, general & others|
|Response to bistability in apoptosis: Roles of Bax, Bcl-2, and mitochondrial permeability transition pores|
|Eissing, Thomas [> > > >]|
|Waldherr, Steffen [> > > >]|
|Allgöwer, Frank [> > > >]|
|Scheurich, Peter [> > > >]|
|Bullinger, Eric [Université de Liège - ULg > Dép. d'électric., électron. et informat. (Inst.Montefiore) > Méthodes computationnelles pour la biologie systémique >]|
|Yes (verified by ORBi)|
|[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|
|File(s) associated to this reference|
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