Crosstalk via the NF-κB signaling system
Crosstalk via the NF-κB signaling system
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DOI：
10.1016/j.cytogfr.2008.04.005
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发表时间：
2008-06-01
影响因子：
13
通讯作者：
Hoffmann, Alexander
中科院分区：
文献类型：
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作者：
Basak, Soumen;Hoffmann, Alexander
核因子 kappaB (NF-kappa B) 转录因子家族由 15 种可能的二聚体组成，其活性由称为 I kappa B 的抑制剂蛋白家族控制。多种细胞刺激（其中许多由肿瘤坏死因子受体 (TNFR) 超家族成员转导）诱导 I kappa B 降解，从而激活 NF-kappa B 二聚体的重叠子集。然而，NF-κ B 二聚体的产生和刺激响应激活通过各种交叉调节机制密切相关，这些机制允许通过 NF-κ B 信号系统在不同信号通路之间进行串扰。在这篇综述中，我们总结了这些机制，并讨论了明显不同的炎症和发育信号之间串扰的生理和病理后果。我们认为，系统方法对于理解高度网络化的细胞信号系统的特异性和新兴特性问题非常有价值。 (c) 2008 Elsevier Ltd. 保留所有权利。
The nuclear factor kappaB (NF-kappa B) family of transcription factors consists of 15 possible dimers whose activity is controlled by a family of inhibitor proteins, known as I kappa Bs. A variety of cellular stimuli, many of them transduced by members of the tumor necrosis factor receptor (TNFR) superfamily, induce degradation of I kappa Bs to activate an overlapping subset of NF-kappa B dimers. However, generation and stimulus-responsive activation of NF-kappa B dimers are intimately linked via various cross-regulatory mechanisms that allow crosstalk between different signaling pathways through the NF-kappa B signaling system. In this review, we summarize these mechanisms and discuss physiological and pathological consequences of crosstalk between apparently distinct inflammatory and developmental signals. We argue that a systems approach will be valuable for understanding questions of specificity and emergent properties of highly networked cellular signaling systems. (c) 2008 Elsevier Ltd. All rights reserved.