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. 2018 Oct 18;19(10):3215. doi: 10.3390/ijms19103215

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic describing the formation of mitochondria-associated endoplasmic reticulum (ER) membrane (MAM) and the unfolded protein response (UPR). The UPR induces the expression of MAM connectors, Rab32 and sigma 1 receptor (Sig1R), followed by fine-tuning of calcium signaling, calcium shuttling, mitochondrial dynamics, reactive oxygen species (ROS) production, and neurite outgrowth through the formation of MAM. The stability of inositol-requiring kinase 1 (IRE1) is regulated by Sig1R binding. The binding of Sig1R to IRE1 leads to long-lasting activation of IRE1, which promotes cellular survival under ER stress conditions. A second MAM connector, mitofusin 2 (MFN2), interacts with protein kinase R-like ER kinase (PERK) to inhibit its activity for regulating ROS production, calcium shuttling, and mitochondrial morphology.