Bistability Analyses of a Caspase Activation Model for Receptor-induced Apoptosis *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 279, Issue: 35, Page: 36892-36897
2004
- 256Citations
- 175Captures
- 1Mentions
Metric Options: Counts1 Year3 YearSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations256
- Citation Indexes256
- 256
- CrossRef226
- Captures175
- Readers175
- 175
- Mentions1
- References1
- 1
Article Description
Apoptosis is an important physiological process crucially involved in development and homeostasis of multicellular organisms. Although the major signaling pathways have been unraveled, a detailed mechanistic understanding of the complex underlying network remains elusive. We have translated here the current knowledge of the molecular mechanisms of the death-receptor-activated caspase cascade into a mathematical model. A reduction down to the apoptotic core machinery enables the application of analytical mathematical methods to evaluate the system behavior within a wide range of parameters. Using parameter values from the literature, the model reveals an unstable status of survival indicating the need for further control. Based on recent publications we tested one additional regulatory mechanism at the level of initiator caspase activation and demonstrated that the resulting system displays desired characteristics such as bistability. In addition, the results from our model studies allowed us to reconcile the fast kinetics of caspase 3 activation observed at the single cell level with the much slower kinetics found at the level of a cell population.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925820859419; http://dx.doi.org/10.1074/jbc.m404893200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=4344674786&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15208304; https://linkinghub.elsevier.com/retrieve/pii/S0021925820859419; http://www.jbc.org/lookup/doi/10.1074/jbc.M404893200; https://syndication.highwire.org/content/doi/10.1074/jbc.M404893200; https://dx.doi.org/10.1074/jbc.m404893200
Elsevier BV
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