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- W2379931407 endingPage "1246" @default.
- W2379931407 startingPage "1238" @default.
- W2379931407 abstract "The endoplasmic reticulum (ER) is most notable for its central roles in calcium ion storage, lipid biosynthesis, and protein sorting and processing. By virtue of its extensive membrane contact sites that connect the ER to most other organelles and to the plasma membrane, the ER can also regulate diverse cellular processes including inflammatory and insulin signaling, nutrient metabolism, and cell proliferation and death via a signaling pathway called the unfolded protein response (UPR). Chronic UPR activation has been observed in liver and/or adipose tissue of dietary and genetic murine models of obesity, and in human obesity and non-alcoholic fatty liver disease (NAFLD). Activation of the UPR in obesity and obesity-related disorders likely has two origins. One linked to classic ER stress involving the ER lumen and one linked to alterations to the ER membrane environment. This review discusses both of these origins and also considers the role of post-translational protein modifications, such as acetylation and palmitoylation, and ER-mitochondrial interactions to obesity-mediated impairments in the ER and activation of the UPR." @default.
- W2379931407 created "2016-06-24" @default.
- W2379931407 creator A5027969739 @default.
- W2379931407 creator A5031410582 @default.
- W2379931407 creator A5038162906 @default.
- W2379931407 creator A5049347827 @default.
- W2379931407 creator A5066924487 @default.
- W2379931407 date "2016-09-01" @default.
- W2379931407 modified "2023-10-13" @default.
- W2379931407 title "Endoplasmic reticulum stress in obesity and obesity-related disorders: An expanded view" @default.
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