MyD88: a central player in innate immune signaling.
MyD88: a central player in innate immune signaling.
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DOI：
10.12703/p6-97
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Barton GM
中科院分区：
文献类型：
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作者：
Deguine J;Barton GM
MyD88是toll样受体（TLR）和白细胞介素-1 （IL-1）受体家族下游炎症信号通路的典型接头。MyD88通过同型蛋白相互作用将IL-1受体（IL-1R）或TLR家族成员与IL-1R相关激酶（IRAK）家族激酶连接起来。IRAK家族激酶的激活导致多种功能输出，包括核因子κB （NFκB）、丝裂原活化蛋白激酶和激活蛋白1的激活，使MyD88成为炎症通路的中心节点。随着myd88依赖性信号的更多细节被阐明，这一关键信号组件的功能可以受到不同亚细胞区室中多个相互作用伙伴的影响，这一点已经变得很清楚。在这篇综述中，我们将重点关注MyD88信号复合物组装的最新进展以及导致MyD88信号多样化的机制。
MyD88 is the canonical adaptor for inflammatory signaling pathways downstream of members of the Toll-like receptor (TLR) and interleukin-1 (IL-1) receptor families. MyD88 links IL-1 receptor (IL-1R) or TLR family members to IL-1R-associated kinase (IRAK) family kinases via homotypic protein-protein interaction. Activation of IRAK family kinases leads to a variety of functional outputs, including the activation of nuclear factor-kappa B (NFκB), mitogen-activated protein kinases, and activator protein 1, making MyD88 a central node of inflammatory pathways. As more details of MyD88-dependent signaling have been elucidated, it has become clear that the functions of this critical signaling component can be influenced by multiple interaction partners in distinct subcellular compartments. In this review, we will focus on recent developments in the understanding of the assembly of MyD88 signaling complexes and the mechanisms leading to the diversification of MyD88-based signaling.