TLRs: differential adapter utilization by toll-like receptors mediates TLR-specific patterns of gene expression.
TLRs: differential adapter utilization by toll-like receptors mediates TLR-specific patterns of gene expression.
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DOI：
10.1124/mi.3.8.466
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发表时间：
2003-12-01
影响因子：
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通讯作者：
Fenton, Matthew J
中科院分区：
文献类型：
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作者：
Vogel, Stefanie N;Fitzgerald, Katherine A;Fenton, Matthew J
在响应微生物或环境的“危险”信号，代表的结构基序通常不表达的细胞，Toll样受体介导的细胞内信号，导致炎症基因的表达。响应于激动剂，TLR聚集使得能够募集和/或激活TLR特异性衔接子分子。迄今为止，已经鉴定了四种衔接蛋白：MyD 88、TIRAP/Mal、TRIF/TICAM-1和TIRP/TRAM/TICAM-2。不同的TLR与衔接分子的不同组合的相互作用产生了一个平台，额外的激酶，反式作用因子和可能的其他分子被招募，最终导致基因表达的事件。鉴于这种相互作用已经描述的速度，我们试图总结我们目前对TLR信号传导至关重要的适配器的理解，并为未来的研究提供一个工作模型。
In response to microbial or environmental "danger" signals, represented by structural motifs not normally expressed by cells, Toll-like receptors mediate intracellular signaling that leads to inflammatory gene expression. In response to agonists, TLR aggregation enables the recruitment and/or activation of TLR-specific adapter molecules. To date, four adapter proteins have been identified: MyD88, TIRAP/Mal, TRIF/TICAM-1, and TIRP/TRAM/TICAM-2. The interaction of the different TLRs with distinct combinations of adapter molecules creates a platform to which additional kinases, transacting factors, and possibly other molecules are recruited, events that lead, ultimately, to gene expression. Given the rapidity with which such interactions have been described, we have attempted to summarize our current understanding of the adapters that are so essential for TLR signaling and provide a working model for future studies.