The Abramson Family Cancer Research Institute, Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Trends Biochem Sci. 2013 Sep;38(9):447-52. doi: 10.1016/j.tibs.2013.06.012. Epub 2013 Jul 29.
The endoplasmic reticulum (ER) senses both extracellular and intracellular stresses that can disrupt its ability to facilitate the maturation of proteins destined for secretory pathways. The accumulation of misfolded proteins within the ER triggers an adaptive signaling pathway coined the unfolded protein response (UPR). UPR activation contributes to cell adaptation by reducing the rate of protein translation while increasing the synthesis of chaperones. Although we have gained considerable insight into the mechanisms that regulate gene expression and certain aspects of protein translation, the contribution of miRNAs to UPR-dependent activities has only recently been investigated. Here we highlight recent insights into the contribution of miRNAs to UPR-dependent cellular adaptive responses.
内质网 (ER) 能感知细胞外和细胞内的应激，这些应激会破坏其促进蛋白质向分泌途径成熟的能力。错误折叠的蛋白质在内质网中的积累会引发一种适应性信号通路，称为未折叠蛋白反应 (UPR)。UPR 的激活通过降低蛋白质翻译的速率，同时增加伴侣蛋白的合成，有助于细胞适应。尽管我们已经深入了解了调节基因表达和某些蛋白质翻译方面的机制，但 miRNA 对 UPR 依赖性活性的贡献最近才被研究。在这里，我们强调了 miRNA 对 UPR 依赖性细胞适应性反应的贡献的最新见解。
