Response to bistability in apoptosis: roles of bax, Bcl-2,and mitochondrial permeability transition pores

T. Eissing, S. Waldherr, F. Allgöwer, P. Scheurich, Eric Bullinger

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)3332-3334
Number of pages3
JournalBiophysical Journal
Volume92
Issue number9
DOIs
Publication statusPublished - 2007

Keywords

  • apoptosis
  • mitochondrial permeability transition pores
  • apoptosis signaling
  • signaling models

Cite this