Please use this identifier to cite or link to this item:
Title: Emerging roles of endoplasmic reticulum-resident selenoproteins in the regulation of cellular stress responses and the implications for metabolic disease.
Austin Authors: Addinsall, Alex B;Wright, Craig R;Andrikopoulos, Sofianos;van der Poel, Chris;Stupka, Nicole
Affiliation: Centre for Molecular and Medical Research, School of Medicine, Deakin University, Waurn Ponds, Victoria, Australia
Institute for Physical Activity and Nutrition (IPAN), School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Physiology, Anatomy & Microbiology, School of Life Sciences, La Trobe University, Bundoora, Victoria, Australia
Issue Date: 2018 2018-03-20
Publication information: The Biochemical journal 2018; 475(6): 1037-1057
Abstract: Chronic metabolic stress leads to cellular dysfunction, characterized by excessive reactive oxygen species, endoplasmic reticulum (ER) stress and inflammation, which has been implicated in the pathogenesis of obesity, type 2 diabetes and cardiovascular disease. The ER is gaining recognition as a key organelle in integrating cellular stress responses. ER homeostasis is tightly regulated by a complex antioxidant system, which includes the seven ER-resident selenoproteins - 15 kDa selenoprotein, type 2 iodothyronine deiodinase and selenoproteins S, N, K, M and T. Here, the findings from biochemical, cell-based and mouse studies investigating the function of ER-resident selenoproteins are reviewed. Human experimental and genetic studies are drawn upon to highlight the relevance of these selenoproteins to the pathogenesis of metabolic disease. ER-resident selenoproteins have discrete roles in the regulation of oxidative, ER and inflammatory stress responses, as well as intracellular calcium homeostasis. To date, only two of these ER-resident selenoproteins, selenoproteins S and N have been implicated in human disease. Nonetheless, the potential of all seven ER-resident selenoproteins to ameliorate metabolic dysfunction warrants further investigation.
DOI: 10.1042/BCJ20170920
ORCID: 0000-0001-9142-0841
PubMed URL: 29559580
Type: Journal Article
Subjects: SEPS1
cellular stress
endoplasmic reticulum
metabolic disease
Appears in Collections:Journal articles

Show full item record

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.