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. 2020 Sep 25;11(9):802. doi: 10.1038/s41419-020-03003-w

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — ER stress signalling involves three main protein sensors, PRKR-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme-1α (IRE1α) and activating transcription factor-6 (ATF6). These proteins remain inactive while are bound to the intraluminal chaperone glucose-regulated protein 78 (GRP78), also named Binding Protein (BiP). In response to ER stress, these mediators become activated and released, thereby triggering molecular cascades that activate the unfolded protein response (UPR). Overall, activation of each sensor promotes ATF4, XBP1s and ATF6 translocation to the nucleus to induce the expression of their relevant target genes associated with apoptosis, inflammation, antioxidant response and protein folding mechanisms, among others, to restore ER homeostasis.