The Function of KDEL Receptors as UPR Genes in Disease.

The Function of KDEL Receptors as UPR Genes in Disease.
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DOI:
10.3390/ijms22115436
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发表时间:
2021-05-21
影响因子:
5.6
通讯作者:
Harvey BK
Harvey BK
中科院分区:
生物学2区
文献类型:
--
作者:
Wires ES;Trychta KA;Kennedy LM;Harvey BK

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KDEL受体修复途径对于维持内质网(ER)腔中的驻留蛋白是必需的。ER驻留蛋白具有多种功能,包括蛋白质折叠和成熟。内腔ER微环境的扰动,如钙耗竭,可导致蛋白质错误折叠和未折叠蛋白反应(UPR)的激活。此外,ER驻留蛋白通过压倒KDEL受体修复途径从细胞分泌。最近的数据表明,KDEL受体也通过IRE 1/XBP 1信号通路在UPR期间被激活,作为对细胞应激的适应性反应,以减少ER驻留蛋白的损失。这篇综述将讨论UPR激活和KDEL受体之间的新兴联系,因为它涉及到ER蛋白稳态和疾病状态。
The KDEL receptor retrieval pathway is essential for maintaining resident proteins in the endoplasmic reticulum (ER) lumen. ER resident proteins serve a variety of functions, including protein folding and maturation. Perturbations to the lumenal ER microenvironment, such as calcium depletion, can cause protein misfolding and activation of the unfolded protein response (UPR). Additionally, ER resident proteins are secreted from the cell by overwhelming the KDEL receptor retrieval pathway. Recent data show that KDEL receptors are also activated during the UPR through the IRE1/XBP1 signaling pathway as an adaptive response to cellular stress set forth to reduce the loss of ER resident proteins. This review will discuss the emerging connection between UPR activation and KDEL receptors as it pertains to ER proteostasis and disease states.
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