ArticlePLoS computational biology2017
Chemical Reaction Network Theory elucidates sources of multistability in interferon signaling.
Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- GenAI-Net: A generative AI framework for automated biomolecular network design.Science advances · 2026Article
- Biology-inspired graph neural network encodes reactome and reveals biochemical reactions of disease.Patterns (New York, N.Y.) · 2023Article
- Article
- A numerical approach for detecting switch-like bistability in mass action chemical reaction networks with conservation laws.BMC bioinformatics · 2022Article
- Computational quantification of global effects induced by mutations and drugs in signaling networks of colorectal cancer cells.Scientific reports · 2021Article
- Optimal ligand discrimination by asymmetric dimerization and turnover of interferon receptors.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Robustness and parameter geography in post-translational modification systems.PLoS computational biology · 2020Article
- Transient hysteresis and inherent stochasticity in gene regulatory networks.Nature communications · 2019Article
- Analyzing pharmacological intervention points: A method to calculate external stimuli to switch between steady states in regulatory networks.PLoS computational biology · 2019Article
- Identifying parameter regions for multistationarity.PLoS computational biology · 2017Article
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Authors and funding
3 authors.
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Abstract
Bistability has important implications in signaling pathways, since it indicates a potential cell decision between alternative outcomes. We present two approaches developed in the framework of the Chemical Reaction Network Theory for easy and efficient search of multiple steady state behavior in signaling networks (both with and without mass conservation), and apply them to search for sources of bistability at different levels of the interferon signaling pathway. Different type I interferon subtypes and/or doses are known to elicit differential bioactivities (ranging from antiviral, antiproliferative to immunomodulatory activities). How different signaling outcomes can be generated through the same receptor and activating the same JAK/STAT pathway is still an open question. Here, we detect bistability at the level of early STAT signaling, showing how two different cell outcomes are achieved under or above a threshold in ligand dose or ligand-receptor affinity. This finding could contribute to explain the differential signaling (antiviral vs apoptotic) depending on interferon dose and subtype (α vs β) observed in type I interferons.
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