ArticleBiophysical journal2006
Bistability in apoptosis: roles of bax, bcl-2, and mitochondrial permeability transition pores.
Article in Biophysical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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Who cites it
154 citing papers in PubMed, 1 synthesis or guideline pooled it.
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- Astrocytic Mitochondria Transplantation Rescues Neuron Loss and Dendritic Injuries in Acute Cerebral Ischemic Stroke Mouse Model by Flexibly Regulating Mitochondria Dynamics.Annals of neurology · 2026Article
- Stochasticity contributes to explaining minority and majority MOMP during apoptosis.Cell death & disease · 2025Article
- Optogenetic engineering of BAX to control mitochondrial permeabilization and attenuate apoptosis in cells.Experimental & molecular medicine · 2025Article
- Dynamical analysis of a model of BCL-2-dependent cellular decision making.NPJ systems biology and applications · 2025Article
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- The role of chloride intracellular channel 4 in tumors.Cancer cell international · 2025Review
- Effects of Nicotinamide Riboside Supplementation on Postmortem Mitochondrial Functionality and Apoptotic Activation.Metabolites · 2025Article
- Basal State Calibration of a Chemical Reaction Network Model for Autophagy.International journal of molecular sciences · 2024Article
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- Rotenone and Its Derivative, Rotenoisin A, Induce Neurodegeneration Differentially in SH-SY5Y Cells.Biomedicines · 2024Article
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- Chemotherapy-initiated cysteine-rich protein 61 decreases acute B-lymphoblastic leukemia chemosensitivity.Journal of cancer research and clinical oncology · 2024Article
94 more citing papers are in PubMed but not listed here.
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5 authors.
Funding
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-à-vis apoptosome formation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.