Response to Bistability in Apoptosis: Roles of Bax, Bcl-2, and Mitochondrial Permeability Transition Pores
- 1 May 2007
- journal article
- other
- Published by Elsevier in Biophysical Journal
- Vol. 92 (9) , 3332-3334
- https://doi.org/10.1529/biophysj.106.100362
Abstract
No abstract availableThis publication has 22 references indexed in Scilit:
- Steady state and (bi-) stability evaluation of simple protease signalling networksBiosystems, 2007
- Mathematical Modeling Identifies Inhibitors of Apoptosis as Mediators of Positive Feedback and BistabilityPLoS Computational Biology, 2006
- Systems analysis of effector caspase activation and its control by X-linked inhibitor of apoptosis proteinThe EMBO Journal, 2006
- Identification of a ‘genuine’ mammalian homolog of nematodal CED-4: is the hunt over or do we need better guns?Cell Death & Differentiation, 2006
- Bistability in Apoptosis: Roles of Bax, Bcl-2, and Mitochondrial Permeability Transition PoresBiophysical Journal, 2006
- Robustness properties of circadian clock architecturesProceedings of the National Academy of Sciences, 2004
- Cell Death: Critical Control PointsPublished by Elsevier ,2004
- Quantifying robustness of biochemical network modelsBMC Bioinformatics, 2002
- Bistability in cell signaling: How to make continuous processes discontinuous, and reversible processes irreversibleChaos: An Interdisciplinary Journal of Nonlinear Science, 2001
- Caspase inhibitorsCell Death & Differentiation, 1999