低剂量IL-1刺激后NFκB信号通路的建模时间延迟。

Johannes Witt, Sandra Barisic, Oliver Sawodny, Michael Ederer, Dagmar Kulms, Thomas Sauter
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引用次数: 5

摘要

IL-1 (10 ng/ml) + UVB辐射刺激人上皮细胞可导致IKKβ持续磷酸化引起的nf - κ b持续活化。我们最近发表了一个严格简化的常微分方程模型,阐明了所涉及的机制。在这里,我们比较了低IL-1剂量(0.5 ng/ml)的模型扩展,其中观察到延迟的IKKβ磷酸化。扩展模型包括一个正调控元件,最有可能是TRAF6的自泛素化,最令人信服地再现了观察到的实验数据。扩展显示与原始模型一致,并且包含可能作为潜在干预目标的非常敏感的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Modeling time delay in the NFκB signaling pathway following low dose IL-1 stimulation.

Stimulation of human epithelial cells with IL-1 (10 ng/ml) + UVB radiation results in sustained NFκB activation caused by continuous IKKβ phosphorylation. We have recently published a strictly reduced ordinary differential equation model elucidating the involved mechanisms. Here, we compare model extensions for low IL-1 doses (0.5 ng/ml), where delayed IKKβ phosphorylation is observed. The extended model including a positive regulatory element, most likely auto-ubiquitination of TRAF6, reproduces the observed experimental data most convincingly. The extension is shown to be consistent with the original model and contains very sensitive processes which may serve as potential intervention targets.

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