Post-transcriptional regulons coordinate the initiation and resolution of inflammation

被引：220

作者：

Anderson, Paul ^{[1
]}

机构：

[1] Brigham & Womens Hosp, Dept Med, Div Rheumatol, Boston, MA 02115 USA

来源：

NATURE REVIEWS IMMUNOLOGY | 2010年 / 10卷 / 01期

基金：

美国国家卫生研究院;

关键词：

TUMOR-NECROSIS-FACTOR; MESSENGER-RNA STABILITY; AU-RICH-ELEMENT; T-CELL-ACTIVATION; CD40 LIGAND EXPRESSION; 60S RIBOSOMAL-SUBUNIT; IL-2; GENE-EXPRESSION; BINDING PROTEIN HUR; FACTOR-ALPHA; TNF-ALPHA;

D O I：

10.1038/nri2685

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Transcriptional control mechanisms chart the course of the inflammatory response by synthesizing mRNAs encoding proteins that promote or inhibit inflammation. Because these mRNAs can be long-lived, turning off their synthesis does not rapidly stop or change the direction of inflammation. Post-transcriptional mechanisms that modify mRNA stability and/or translation provide more rapid and flexible control of this process and are particularly important in coordinating the initiation and resolution of inflammation. Here, I review the surprising variety of post-transcriptional control mechanisms that regulate the initiation and resolution of inflammation and discuss how these mechanisms are integrated to coordinate this essential process.

引用

页码：24 / 35

页数：12

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