Abstract
Studies of the full selenoproteome have found that five, four, and one of 24 rodent selenoprotein transcripts in liver, kidney, and muscle, respectively, decrease in Se deficiency to <40% of Se-adequate levels, but that the majority of selenoprotein mRNAs are not regulated by Se deficiency. These differences match with the hierarchy of selenoprotein expression, helping to explain this hierarchy, and also showing that selenoprotein transcripts can be used as molecular biomarkers for assessing Se status. The similarity of the response curves for regulated selenoproteins suggests one underlying mechanism is responsible for the downregulation of selenoprotein mRNAs in Se deficiency, but the heterogeneity of UGA position in regulated and nonregulated selenoprotein transcripts now indicates that current nonsense-mediated decay models cannot explain which transcripts are susceptible to mRNA decay in Se deficiency.
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Acknowledgements
This work was supported in part by NIH DK74184, by training grant T32-DK07665, and by UW Selenium Nutrition Research Fund.
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Sunde, R.A. (2011). Selenoproteins: Hierarchy, Requirements, and Biomarkers. In: Hatfield, D., Berry, M., Gladyshev, V. (eds) Selenium. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-1025-6_11
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