ArticleTheoretical biology & medical modelling2013
Boolean network-based model of the Bcl-2 family mediated MOMP regulation.
Article in Theoretical biology & medical modelling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 9 citations in OpenAlex.
- A Novel Data-Driven Boolean Model for Genetic Regulatory Networks.Frontiers in physiology · 2018Article
- Activation of Apoptotic Signal in Endothelial Cells through Intracellular Signaling Molecules Blockade in Tumor-Induced Angiogenesis.BioMed research international · 2015Article
- Sensitivity analysis of biological Boolean networks using information fusion based on nonadditive set functions.BMC systems biology · 2014Article
- SBML qualitative models: a model representation format and infrastructure to foster interactions between qualitative modelling formalisms and tools.BMC systems biology · 2013Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundMitochondrial outer membrane permeabilization (MOMP) is one of the most important points in the majority of apoptotic signaling cascades and it is controlled by a network of interactions between the members of the Bcl-2 family.
methodsTo understand the role of individual members of this family within the MOMP regulation, we have constructed a Boolean network-based model of interactions between the Bcl-2 proteins.
resultsComputational simulations have revealed the existence of trapping states which, independently from the incoming stimuli, block the occurrence of MOMP. Our results emphasize the role of the antiapoptotic protein Mcl-1 in the majority of these configurations. We demonstrate here the importance of the Bid and Bim for activation of effectors Bax and Bak, and the irreversibility of this activation. The model further points to the antiapoptotic protein Bcl-w as a key factor preventing Bax activation.
conclusionsIn spite of relative simplicity, the Boolean network-based model provides useful insight into main functioning logic of the Bcl-2 switch, consistent with experimental findings.
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