Bagci2006_ApoptoticStimuli

This a model from the article:
Bistability in apoptosis: roles of bax, bcl-2, and mitochondrial permeability
transition pores.

Bagci EZ, Vodovotz Y, Billiar TR, Ermentrout GB, Bahar I. Biophys J
2006 Mar 1;90(5):1546-59 16339882
,
Abstract:

We propose a mathematical model for mitochondria-dependent apoptosis, in which
kinetic cooperativity in formation of the apoptosome is a key element ensuring
bistability. We examine the role of Bax and Bcl-2 synthesis and degradation
rates, as well as the number of mitochondrial permeability transition pores
(MPTPs), on the cell response to apoptotic stimuli. Our analysis suggests that
cooperative apoptosome formation is a mechanism for inducing bistability, much
more robust than that induced by other mechanisms, such as inhibition of
caspase-3 by the inhibitor of apoptosis (IAP). Simulations predict a
pathological state in which cells will exhibit a monostable cell survival if Bax
degradation rate is above a threshold value, or if Bax expression rate is below
a threshold value. Otherwise, cell death or survival occur depending on initial
caspase-3 levels. We show that high expression rates of Bcl-2 can counteract the
effects of Bax. Our simulations also demonstrate a monostable (pathological)
apoptotic response if the number of MPTPs exceeds a threshold value. This study
supports our contention, based on mathematical modeling, that cooperativity in
apoptosome formation is critically important for determining the healthy
responses to apoptotic stimuli, and helps define the roles of Bax, Bcl-2, and
MPTP vis-a-vis apoptosome formation.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Bagci EZ, Vodovotz Y, Billiar TR, Ermentrout GB, Bahar I. (2006) - version=1.0

The original CellML model was created by:
Wendy Kang

[e-mail]
The University of Auckland
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