Response to bistability in apoptosis: roles of bax, Bcl-2,and mitochondrial permeability transition pores
Eissing, T. and Waldherr, S. and Allgöwer, F. and Scheurich, P. and Bullinger, Eric (2007) Response to bistability in apoptosis: roles of bax, Bcl-2,and mitochondrial permeability transition pores. Biophysical Journal, 92 (9). pp. 3332-3334. ISSN 0006-3495 (https://doi.org/10.1529/biophysj.106.100362)
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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.
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Item type: Article ID code: 11997 Dates: DateEvent2007PublishedSubjects: Technology > Electrical engineering. Electronics Nuclear engineering Department: Faculty of Engineering > Electronic and Electrical Engineering Depositing user: Strathprints Administrator Date deposited: 28 Nov 2011 14:39 Last modified: 08 Apr 2024 16:48 URI: https://strathprints.strath.ac.uk/id/eprint/11997