Regulation of the transcriptome by ER stress: non-canonical mechanisms and physiological consequences.
Regulation of the transcriptome by ER stress: non-canonical mechanisms and physiological consequences.
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DOI：
10.3389/fgene.2013.00256
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发表时间：
2013-12-02
影响因子：
3.7
通讯作者：
Rutkowski DT
中科院分区：
文献类型：
--
作者：
Arensdorf AM;Diedrichs D;Rutkowski DT
哺乳动物的未折叠蛋白反应（UPR）是由三个ER驻留跨膜蛋白，其中每一个启动信号级联，最终在生产的转录激活剂达到高潮。UPR最初被表征为上调ER分子伴侣的途径，并且随后的工作的综合体已经表明，蛋白质合成、折叠、氧化、运输和降解都通过UPR在转录上增强。然而，UPR的全球范围延伸到参与各种生理过程的基因，这些基因似乎与ER蛋白折叠没有什么关系，这包括大量被应激抑制而不是刺激的mRNA。通过来自每个UPR途径的多个非经典机制，细胞动态调节转录和mRNA降解。在这里，我们强调这些机制及其对生理过程日益受到重视的影响。
The mammalian unfolded protein response (UPR) is propagated by three ER-resident transmembrane proteins, each of which initiates a signaling cascade that ultimately culminates in production of a transcriptional activator. The UPR was originally characterized as a pathway for upregulating ER chaperones, and a comprehensive body of subsequent work has shown that protein synthesis, folding, oxidation, trafficking, and degradation are all transcriptionally enhanced by the UPR. However, the global reach of the UPR extends to genes involved in diverse physiological processes having seemingly little to do with ER protein folding, and this includes a substantial number of mRNAs that are suppressed by stress rather than stimulated. Through multiple non-canonical mechanisms emanating from each of the UPR pathways, the cell dynamically regulates transcription and mRNA degradation. Here we highlight these mechanisms and their increasingly appreciated impact on physiological processes.
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影响因子：
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作者：
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通讯作者：
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影响因子：
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