Literature DB >> 20304832

Translation control: a multifaceted regulator of inflammatory response.

Barsanjit Mazumder1, Xiaoxia Li, Sailen Barik.   

Abstract

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.

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Year:  2010        PMID: 20304832      PMCID: PMC2860598          DOI: 10.4049/jimmunol.0903778

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  98 in total

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  41 in total

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7.  Posttranscriptional silencing of effector cytokine mRNA underlies the anergic phenotype of self-reactive T cells.

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9.  Ribosomal protein L13a deficiency in macrophages promotes atherosclerosis by limiting translation control-dependent retardation of inflammation.

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10.  Insights into the mechanism of ribosomal incorporation of mammalian L13a protein during ribosome biogenesis.

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