Rab32 connects ER stress to mitochondrial defects in multiple sclerosis.

2.50
Hdl Handle:
http://hdl.handle.net/11287/620203
Title:
Rab32 connects ER stress to mitochondrial defects in multiple sclerosis.
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; Giuliani, F.; Simmen, T.
Abstract:
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
Publisher:
BioMed Central
Journal:
Journal of Neuroinflammation
Issue Date:
23-Jan-2017
URI:
http://hdl.handle.net/11287/620203
DOI:
10.1186/s12974-016-0788-z
PubMed ID:
28115010
Additional Links:
https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0788-z
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.
Type:
Journal Article
Language:
en
ISSN:
1742-2094
Appears in Collections:
Neurology; 2017 RD&E publications

Full metadata record

DC FieldValue Language
dc.contributor.authorHaile, Y.en
dc.contributor.authorDeng, X.en
dc.contributor.authorOrtiz-Sandoval, C.en
dc.contributor.authorTahbaz, N.en
dc.contributor.authorJanowicz, A.en
dc.contributor.authorLu, J-Qen
dc.contributor.authorKerr, B. J.en
dc.contributor.authorGutowski, Nicholas J.en
dc.contributor.authorHolley, Janet E.en
dc.contributor.authorEggleton, Paulen
dc.contributor.authorGiuliani, F.en
dc.contributor.authorSimmen, T.en
dc.date.accessioned2017-02-01T15:09:38Z-
dc.date.available2017-02-01T15:09:38Z-
dc.date.issued2017-01-23-
dc.identifier.citationRab32 connects ER stress to mitochondrial defects in multiple sclerosis. 2017, 14 (1):19 J Neuroinflammationen
dc.identifier.issn1742-2094-
dc.identifier.pmid28115010-
dc.identifier.doi10.1186/s12974-016-0788-z-
dc.identifier.urihttp://hdl.handle.net/11287/620203-
dc.description.abstractEndoplasmic 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.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttps://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-016-0788-zen
dc.rightsArchived 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.en
dc.subjectWessex Classification Subject Headings::Neurologyen
dc.titleRab32 connects ER stress to mitochondrial defects in multiple sclerosis.en
dc.typeJournal Articleen
dc.identifier.journalJournal of Neuroinflammationen
dc.description.noteThis article is freely available via Open Access. Click on the Additional Link above to access the full-text via the publisher's site.en
dc.type.versionPublisheden

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