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Stress HypERactivation in the Beta Cell

Fonseca, Sonya and Urano, Fumihiko and Burcin, Mark and Gromada, Jesper (2011) Stress HypERactivation in the Beta Cell. Islets, 2 (1). pp. 1-9. ISSN 1938-2014

Abstract

In pancreatic beta cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the beta cell, such as a high demand for insulin secretion, can lead to an imbalance in protein homeostasis and lead to ER stress. This stress can be mitigated by an adaptive, cellular response, the Unfolded Protein Response (UPR). UPR activation is vital to the survival of beta cells, as these cells represent one of the most susceptible tissues for ER stress, due to their highly secretory function. However, in some cases, this response is not sufficient to relieve stress, leading to apoptosis and contributing to the pathogenesis of diabetes. Recent evidence shows that ER stress plays a significant role in both type 1 and type 2 diabetes. In this review, we outline the mechanisms of ER stress-mediated beta cell death and focus on the role of ER stress in various forms of diabetes, particularly a genetic form of diabetes called Wolfram syndrome.

Item Type: Article
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Date Deposited: 13 Oct 2015 13:17
Last Modified: 13 Oct 2015 13:17
URI: https://oak.novartis.com/id/eprint/1446

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