Attention: As this model cannot be encoded in SBML at this time, the SBML file contains the whole model in GINML , a different XML model description language, in its main annotation element. Still, the model can be loaded by GINsim as it is by just ignoring the error messages. Alternatively, you can remove the surrounding SBML elements in a text editor and save the remaining GINsim file with the suffix .ginml . To do this keep the first line with the xml declaration and all lines starting from <gxl xmlns="http://gin.univ-mrs.fr/GINsim/" xmlns:xlink="http://www.w3.org/1999/xlink"> until </glx> and delete or comment out all others. This is the master model described in: Mathematical Modelling of Cell-Fate Decision in Response to Death Receptor Engagement Calzone L, Tournier L, Fourquet S, Thieffry D, Zhivotovsky B, Barillot E and Zinovyev A.; PLoS Comput Biol. 2010 Mar 5; 6(3) :e1000702. PubmedID: 20221256 ; doi: 10.1371/journal.pcbi.1000702 ; Abstract: Cytokines such as TNF and FASL can trigger death or survival depending on cell lines and cellular conditions. The mechanistic details of how a cell chooses among these cell fates are still unclear. The understanding of these processes is important since they are altered in many diseases, including cancer and AIDS. Using a discrete modelling formalism, we present a mathematical model of cell fate decision recapitulating and integrating the most consistent facts extracted from the literature. This model provides a generic high-level view of the interplays between NFkappaB pro-survival pathway, RIP1-dependent necrosis, and the apoptosis pathway in response to death receptor-mediated signals. Wild type simulations demonstrate robust segregation of cellular responses to receptor engagement. Model simulations recapitulate documented phenotypes of protein knockdowns and enable the prediction of the effects of novel knockdowns. In silico experiments simulate the outcomes following ligand removal at different stages, and suggest experimental approaches to further validate and specialise the model for particular cell types. We also propose a reduced conceptual model implementing the logic of the decision process. This analysis gives specific predictions regarding cross-talks between the three pathways, as well as the transient role of RIP1 protein in necrosis, and confirms the phenotypes of novel perturbations. Our wild type and mutant simulations provide novel insights to restore apoptosis in defective cells. The model analysis expands our understanding of how cell fate decision is made. Moreover, our current model can be used to assess contradictory or controversial data from the literature. Ultimately, it constitutes a valuable reasoning tool to delineate novel experiments. This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. 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.