Models

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Legewie2006_apoptosis_NC


ABSTRACT: This model represents the non-competitive binding of XIAP to Casapase-3 and Caspase-9. In other words, XIAP mediated feedback is abolished in this model. The authors state that this leads to bistable-reversible behaviour as depicted in Fig 4C. The wild-type model displays a bistable-irreversible profile. This shows that irreversibility requires XIAP mediated feedback. The model was tested on MathSBML. However, please note that the paper does not contain any figure that corresponds to simulation of the Non-Competitive model. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

SUBMITTER: Nicolas Le Novère  

PROVIDER: BIOMD0000000103 | BioModels | 2006-04-20

REPOSITORIES: BioModels

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Publications

Mathematical modeling identifies inhibitors of apoptosis as mediators of positive feedback and bistability.

Legewie Stefan S   Blüthgen Nils N   Herzel Hanspeter H  

PLoS computational biology 20060728 9


The intrinsic, or mitochondrial, pathway of caspase activation is essential for apoptosis induction by various stimuli including cytotoxic stress. It depends on the cellular context, whether cytochrome c released from mitochondria induces caspase activation gradually or in an all-or-none fashion, and whether caspase activation irreversibly commits cells to apoptosis. By analyzing a quantitative kinetic model, we show that inhibition of caspase-3 (Casp3) and Casp9 by inhibitors of apoptosis (IAPs  ...[more]

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