Physiological roles of regulated Ire1 dependent decay.
Physiological roles of regulated Ire1 dependent decay.
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DOI：
10.3389/fgene.2014.00076
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发表时间：
2014
影响因子：
3.7
通讯作者：
Domingos PM
中科院分区：
文献类型：
--
作者：
Coelho DS;Domingos PM
肌醇要求酶1 （Ire1）是未折叠蛋白反应（UPR）的重要换能器，UPR是由内质网（ER应激）中错误折叠蛋白的积累激活的。激活的Ire1介导Xbp1 mRNA的内含子剪接，在翻译过程中引起帧移位，并在Xbp1蛋白中引入一个新的羧基结构域，然后才成为一个功能齐全的转录因子。利用细胞培养系统进行的研究表明，Ire1还能促进编码ER靶向蛋白的mrna的降解，从而在ER应激期间减少传入ER“客户”蛋白的负荷。这一过程被称为RIDD (regulated ire1 dependent decay)，但其生理意义在细胞培养系统之外仍然缺乏表征。在此，我们回顾了最近的几项研究，这些研究强调了RIDD在特定生物学范式中的生理作用，例如果蝇或哺乳动物肝脏的光感受器分化和内分泌胰腺功能。这些研究证明了RIDD在具有强烈分泌功能的组织中的重要性，并强调了RIDD在细胞和生物体中UPR激活过程中的生理作用。
Inositol-requiring enzyme 1 (Ire1) is an important transducer of the unfolded protein response (UPR) that is activated by the accumulation of misfolded proteins in the endoplamic reticulum (ER stress). Activated Ire1 mediates the splicing of an intron from the mRNA of Xbp1, causing a frame-shift during translation and introducing a new carboxyl domain in the Xbp1 protein, which only then becomes a fully functional transcription factor. Studies using cell culture systems demonstrated that Ire1 also promotes the degradation of mRNAs encoding mostly ER-targeted proteins, to reduce the load of incoming ER “client” proteins during ER stress. This process was called RIDD (regulated Ire1-dependent decay), but its physiological significance remained poorly characterized beyond cell culture systems. Here we review several recent studies that have highlighted the physiological roles of RIDD in specific biological paradigms, such as photoreceptor differentiation in Drosophila or mammalian liver and endocrine pancreas function. These studies demonstrate the importance of RIDD in tissues undergoing intense secretory function and highlight the physiologic role of RIDD during UPR activation in cells and organisms.
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影响因子：
30.3
作者：
Cho JA;Lee AH;Platzer B;Cross BCS;Gardner BM;De Luca H;Luong P;Harding HP;Glimcher LH;Walter P;Fiebiger E;Ron D;Kagan JC;Lencer WI
通讯作者：
Lencer WI
DOI：
10.1016/j.bbamcr.2013.01.016
发表时间：
2013-11-01
影响因子：
5.1
作者：
Hollien, Julie
通讯作者：
Hollien, Julie
影响因子：
64.8
作者：
Calfon, M;Zeng, HQ;Ron, D
通讯作者：
Ron, D
影响因子：
29
作者：
Iqbal, Jahangir;Dai, Kezhi;Hussain, M. Mahmood
通讯作者：
Hussain, M. Mahmood
DOI：
10.1073/pnas.1115623109
发表时间：
2012-04-10
影响因子：
11.1
作者：
Cross, Benedict C. S.;Bond, Peter J.;Harding, Heather P.
通讯作者：
Harding, Heather P.