Translation Control: A Multifaceted Regulator of Inflammatory Response

被引:63
作者
Mazumder, Barsanjit [1 ]
Li, Xiaoxia [2 ]
Barik, Sailen [3 ]
机构
[1] Cleveland State Univ, Dept Biol Geol & Environm Sci, Ctr Gene Regulat Hlth & Dis, Coll Sci, Cleveland, OH 44115 USA
[2] Cleveland Clin Fdn, Dept Immunol, Lerner Res Inst, Cleveland, OH 44195 USA
[3] Univ S Alabama, Coll Med, Dept Biochem & Mol Biol, Mobile, AL 36688 USA
基金
美国国家卫生研究院;
关键词
TUMOR-NECROSIS-FACTOR; RNA-BINDING PROTEIN; HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; RHEUMATOID-ARTHRITIS SYNOVIUM; SIGNAL-DEPENDENT TRANSLATION; 60S RIBOSOMAL-SUBUNIT; FACTOR-KAPPA-B; MESSENGER-RNA; INITIATION-FACTOR; GAMMA-INTERFERON;
D O I
10.4049/jimmunol.0903778
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
A robust innate immune response is essential to the protection of all vertebrates from infection, but it often comes with the price tag of acute inflammation. If unchecked, a runaway inflammatory response can cause significant tissue damage, resulting in myriad disorders, such as dermatitis, toxic shock, cardiovascular disease, acute pelvic and arthritic inflammatory diseases, and various infections. To prevent such pathologies, cells have evolved mechanisms to rapidly and specifically shut off these beneficial inflammatory activities before they become detrimental. Our review of recent literature, including our own work, reveals that the most dominant and common mechanism is translational silencing, in which specific regulatory proteins or complexes are recruited to cis-acting RNA structures in the untranslated regions of single or multiple mRNAs that code for the inflammatory protein(s). Enhancement of the silencing function may constitute a novel pharmacological approach to prevent immunity-related inflammation. The Journal of immunology, 2010, 184: 3311-3319.
引用
收藏
页码:3311 / 3319
页数:9
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