Markov Modelling of Mitochondrial BAK Activation Kinetics during Apoptosis

DOI10.1007/978-3-642-04944-6_16MaRDI QIDQ3646133zbMATH OpenOpenAlexFDO

Authors C. Grills, D. A. Fennell, S. F. C. Shearer

Publication date 19 November 2009

Published in Stochastic Algorithms: Foundations and Applications (Search for Journal in Brave)

Full work available at URL https://doi.org/10.1007/978-3-642-04944-6_16

zbMATH Keywords

agonism modelBAK activation kineticsBCL-2 family proteinsBH3-only proteinsderepressor model

Mathematics Subject Classification ID

Applications of Markov chains and discrete-time Markov processes on general state spaces (social mobility, learning theory, industrial processes, etc.) (60J20) Biochemistry, molecular biology (92C40)

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Cited in

(5)

• The Bcl-2-associated death promoter (BAD) lowers the threshold at which the Bcl-2-interacting domain death agonist (BID) triggers mitochondria disintegration
• Nuclear apoptotic volume decrease in individual cells: confocal microscopy imaging and kinetic modeling
• Molecular modeling of BAD complex resided in a mitochondrion integrating glycolysis and apoptosis
• Mathematical modeling of the regulation of caspase-3 activation and degradation
• Mitochondrial outer membrane permeabilization and inner membrane permeabilization in regulating apoptosis and inflammation

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