BioModels

This the model used in the article:
Quantitative analysis of pathways controlling extrinsic apoptosis in single cells.
Albeck JG, Burke JM, Aldridge BB, Zhang M, Lauffenburger DA, Sorger PK. Mol Cell. 2008 Apr 11;30(1):11-25. PMID: 18406323 , doi: 10.1016/j.molcel.2008.02.012
Abstract:
Apoptosis in response to TRAIL or TNF requires the activation of initiator caspases, which then activate the effector caspases that dismantle cells and cause death. However, little is known about the dynamics and regulatory logic linking initiators and effectors. Using a combination of live-cell reporters, flow cytometry, and immunoblotting, we find that initiator caspases are active during the long and variable delay that precedes mitochondrial outer membrane permeabilization (MOMP) and effector caspase activation. When combined with a mathematical model of core apoptosis pathways, experimental perturbation of regulatory links between initiator and effector caspases reveals that XIAP and proteasome-dependent degradation of effector caspases are important in restraining activity during the pre-MOMP delay. We identify conditions in which restraint is impaired, creating a physiologically indeterminate state of partial cell death with the potential to generate genomic instability. Together, these findings provide a quantitative picture of caspase regulatory networks and their failure modes.
The mitochondrial compartment is just added as a logical partition and its volume is not used in the mathematical formulas, to stick closer to the expressions used in the matlab files distributed with the original publication. There only the rate constants for bimolecular reactions are adapted by division by v , the ration of the volumes of the mitochondrial compartment and the total cell.
For BCL2 overexpression in figure 5, the initial BCL2 amount was increased by a factor 12 to 2.4*10 ⁵ . For siRNA downregulation of XIAP its amount was multiplied by 0.13 to 1.3*10 ⁴ .

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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.