MFN2 mediates ER-mitochondrial coupling during ER stress through specialized stable contact sites.
ER stress
mitochondria
mitochondria-associated membranes (MAM)
mitochondrial Ca2+
mitofusin 2
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2022
2022
Historique:
received:
12
04
2022
accepted:
29
07
2022
entrez:
26
9
2022
pubmed:
27
9
2022
medline:
27
9
2022
Statut:
epublish
Résumé
Endoplasmic reticulum (ER) functions critically depend on a suitable ATP supply to fuel ER chaperons and protein trafficking. A disruption of the ability of the ER to traffic and fold proteins leads to ER stress and the unfolded protein response (UPR). Using structured illumination super-resolution microscopy, we revealed increased stability and lifetime of mitochondrial associated ER membranes (MAM) during ER stress. The consequent increase of basal mitochondrial Ca
Identifiants
pubmed: 36158213
doi: 10.3389/fcell.2022.918691
pii: 918691
pmc: PMC9493370
doi:
Types de publication
Journal Article
Langues
eng
Pagination
918691Informations de copyright
Copyright © 2022 Gottschalk, Koshenov, Bachkoenig, Rost, Malli and Graier.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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