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Jaruszewicz-Blonska, J.

Publications and source records attributed to Jaruszewicz-Blonska, J..

2 recordsLinked to original sources

A plausible identifiable model of the canonicalNF-kB signaling pathway

An overwhelming majority of mathematical models of regulatory pathways, including intensively studied NF-{kappa}B pathway, remains non-identifiable meaning that their parameters may not be determined by existing data. The existing NF-{kappa}B models that are capable to reproduce experimental data, contain non-identifiable parameters, while simplified models with a smaller number of parameters exhibit dynamics that significantly differs from that observed in experiments. Here, we reduce an existing model of the canonical NF-{kappa}B pathway by decreasing the number of equations from 15 to 6 in a way that the resulting model exhibits dynamics closely following that of the original model, both for the nominal and the randomly selected parameters. We carried out the sensitivity-based linear analysis and Monte Carlo-based analysis to demonstrate that the resulting model is structurally and practically identifiable based on a simple TNF stimulation protocol in which 5 model variables are measured. The reduced model is capable to reproduce different types of responses characteristic to regulatory motives controlled by negative feedback loops: nearly-perfect adaptation, damped and sustained oscillations. It can serve as a building block of more comprehensive models of immune responses and cancer, where NF-{kappa}B plays a decisive role. Our approach, although may not be automatically generalized, suggests that other regulatory pathways models can be transformed to identifiable, while retaining their dynamical features.

systems biology↗

Non-self RNA rewires IFNβ signaling: A mathematical model of the innate immune response

Type I interferons (IFNs) are key coordinators of the innate immune response to viral infection, which through activation of STAT1/2 in bystander cells induce the expression of IFN-stimulated genes (ISGs). The complex system-level mechanisms of IFN signaling are however not well understood. Here, we show that in cells transfected with an analog of viral RNA, poly(I:C), transcriptional activity of STAT1/2 is terminated due to depletion of the interferon {beta} (IFN{beta}) receptor, IFNAR. Two ISGs, RNase L and PKR, not only hinder replenishment of IFNAR, but also suppress negative regulators of IRF3 and NF-{kappa}B, consequently promoting IFN{beta} transcription. We incorporated these findings into a comprehensive mathematical model of innate immunity. By coupling signaling through the IRF3/NF-{kappa}B and STAT1/2 pathways with the activity of RNase L and PKR, the model explains how poly(I:C) switches the transcriptional program from STAT1/2-induced to IRF3/NF-{kappa}B-induced, turning IFN{beta}-responding cells to IFN{beta}-secreting cells. One-sentence summaryA computational model explains how non-self RNA turns cells from IFN{beta}- responders to IFN{beta}-producers.

immunology↗