Selenoprotein | Normal Functions | Clinical Features of Deficiency [ref] |
---|---|---|
Thioredoxin reductase | ▪ Disulfide reduction ▪ Maintenance of cellular redox homeostasis |
Dilated Cardiomyopathy in humans [5] |
Glutathione peroxidase 1 | ▪ H2O2 signaling ▪ Inactivation of hydroperoxides ▪ Maintenance of cellular redox homeostasis |
Larger myocardial infarct size in a mouse model [76] |
Methionine sulfoxide reductase A | ▪ Prevention of the buildup of oxidized methionine residues in proteins | Impaired myocardial contractility when stressed in a mouse model [77] |
deiodinases | ▪ Activation of T4 to T3 ▪ Degradation of T3 ▪ Regulation of catabolic homeostasis |
Restrictive cardiomyopathy in a mouse model [78] |
Selenophosphate Synthetase 2 | ▪ Synthesis of selenophosphate required for the synthesis of selenoproteins | No data on clinical features of deficiency [3] |
Selenoprotein I | ▪ Synthesis of phosphatidylcholine and phosphatidylethanolamine | No data on clinical features of deficiency [3] |
Selenoprotein M | ▪ Maintenance of the redox homeostasis in the ER ▪ Facilitation of protein folding in the ER |
No data on clinical features of deficiency [3] |
Selenoproteins K and S | ▪ Facilitating proteasome-mediated degradation of misfolded proteins in the ER | No data on clinical features of deficiency [3] |