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dc.contributor.authorAddinsall, Alex B-
dc.contributor.authorWright, Craig R-
dc.contributor.authorAndrikopoulos, Sofianos-
dc.contributor.authorvan der Poel, Chris-
dc.contributor.authorStupka, Nicole-
dc.identifier.citationThe Biochemical journal 2018; 475(6): 1037-1057-
dc.description.abstractChronic 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.-
dc.subjectcellular stress-
dc.subjectendoplasmic reticulum-
dc.subjectmetabolic disease-
dc.titleEmerging roles of endoplasmic reticulum-resident selenoproteins in the regulation of cellular stress responses and the implications for metabolic disease.-
dc.typeJournal Article-
dc.identifier.journaltitleThe Biochemical journal-
dc.identifier.affiliationCentre for Molecular and Medical Research, School of Medicine, Deakin University, Waurn Ponds, Victoria, Australia-
dc.identifier.affiliationInstitute for Physical Activity and Nutrition (IPAN), School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia-
dc.identifier.affiliationDepartment of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia-
dc.identifier.affiliationDepartment of Physiology, Anatomy & Microbiology, School of Life Sciences, La Trobe University, Bundoora, Victoria, Australia-
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