Rab32 connects ER stress to mitochondrial defects in multiple sclerosis.

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Authors
Haile, Y.
Deng, X.
Ortiz-Sandoval, C.
Tahbaz, N.
Janowicz, A.
Lu, J-Q
Kerr, B. J.
Gutowski, Nicholas J.
Holley, Janet E.
Eggleton, Paul
Journal
Journal of Neuroinflammation
Type
Journal Article
Publisher
BioMed Central
Rights
Archived with thanks to Journal of Neuroinflammation. s This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Endoplasmic reticulum (ER) stress is a hallmark of neurodegenerative diseases such as multiple sclerosis (MS). However, this physiological mechanism has multiple manifestations that range from impaired clearance of unfolded proteins to altered mitochondrial dynamics and apoptosis. While connections between the triggering of the unfolded protein response (UPR) and downstream mitochondrial dysfunction are poorly understood, the membranous contacts between the ER and mitochondria, called the mitochondria-associated membrane (MAM), could provide a functional link between these two mechanisms. Therefore, we investigated whether the guanosine triphosphatase (GTPase) Rab32, a known regulator of the MAM, mitochondrial dynamics, and apoptosis, could be associated with ER stress as well as mitochondrial dysfunction.
Citation
Rab32 connects ER stress to mitochondrial defects in multiple sclerosis. 2017, 14 (1):19 J Neuroinflammation
Note
This article is freely available via Open Access. Click on the Additional Link above to access the full-text via the publisher's site.