Background and objective

NF-κB can be activated by the canonical and non-canonical pathways. These two pathways interplay via the TRAF1|NIK complex after stimulation by TNF. However existing mathematical models of two pathways are inadequate. In this context, an improved mathematical model is constructed to simulate these two pathways and their coupling stimulated by TNF.

Methods

A schematic description of two NF-κB pathways and their relation after TNF stimulation is constructed at first. Then twenty-eight ordinary differential equations are utilized to build the mathematical model. Model equations are solved via the ordinary differential equation solver (ode23).

Results

The proposed model firstly reconstructs the changes in concentrations of NF-κB pathway related biochemical factors with time, and further investigates the underlying mechanism of interaction between two pathways through the TRAF1|NIK complex after stimulation.

Conclusions

The model is validated through good agreement between simulation results and published experimental observations. This study helps to well understand the canonical and non-canonical pathways and their interaction. It also provides a potential tool to investigate how the dysregulated pathways act in pathological conditions.

中文翻译：

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TNF刺激中典型和非典型NF-κB途径的数学模型。

背景和目标

NF-κB可以通过规范和非规范途径激活。TNF刺激后，这两个途径通过TRAF1 | NIK复合体相互作用。但是，现有的两种途径的数学模型是不充分的。在这种情况下，构建了改进的数学模型来模拟这两个途径及其受TNF刺激的偶联。

方法

首先构建两个NF-κB通路及其在TNF刺激后的关系的示意图。然后利用二十八个常微分方程建立数学模型。通过普通的微分方程求解器（ode23）求解模型方程。

结果

该模型首先重建了NF-κB途径相关生化因子的浓度随时间的变化，并进一步研究了刺激后通过TRAF1 | NIK复合物的两种途径之间相互作用的潜在机制。

结论

通过仿真结果与已发表的实验观察之间的良好一致性来验证该模型。这项研究有助于很好地理解规范和非规范途径及其相互作用。它还提供了潜在的工具，以研究失调的途径如何在病理条件下起作用。