ArticleSystems and synthetic biology2014
Death ligand concentration and the membrane proximal signaling module regulate the type 1/type 2 choice in apoptotic death signaling.
Article in Systems and synthetic biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Gasdermin pores permeabilize mitochondria to augment caspase-3 activation during apoptosis and inflammasome activation.Nature communications · 2019Article
- Clinical perspectives of TRAIL: insights into central nervous system disorders.Cellular and molecular life sciences : CMLS · 2016Review
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Authors and funding
2 authors at 1 institution in 2 countries.
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Abstract
Apoptotic death pathways are frequently activated by death ligand induction and subsequent activation of the membrane proximal signaling module. Death receptors cluster upon binding to death ligands, leading to formation of a membrane proximal death-inducing-signaling-complex (DISC). In this membrane proximal signalosome, initiator caspases (caspase 8) are processed resulting in activation of both type 1 and type 2 pathways of apoptosis signaling. How the type 1/type 2 choice is made is an important question in the systems biology of apoptosis signaling. In this study, we utilize a Monte Carlo based in silico approach to elucidate the role of membrane proximal signaling module in the type 1/type 2 choice of apoptosis signaling. Our results provide crucial mechanistic insights into the formation of DISC signalosome and caspase 8 activation. Increased concentration of death ligands was shown to correlate with increased type 1 activation. We also study the caspase 6 mediated system level feedback activation of apoptosis signaling and its role in the type 1/type 2 choice. Our results clarify the basis of cell-to-cell stochastic variability in apoptosis activation and ramifications of this issue is further discussed in the context of therapies for cancer and neurodegenerative disorders.
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