Protein Variants | Comment | Organism |
---|---|---|
additional information | construction of enzyme knockout mice, phenotype, overview | Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-selenocysteine + reduced acceptor | Mus musculus | - |
selenide + L-alanine + acceptor | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
kidney | - |
Mus musculus | - |
liver | - |
Mus musculus | - |
testis | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
L-selenocysteine + reduced acceptor | - |
Mus musculus | selenide + L-alanine + acceptor | - |
? |
Synonyms | Comment | Organism |
---|---|---|
SCL | - |
Mus musculus |
Scly | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
malfunction | disruption of the selenocysteine lyase-mediated selenium recycling pathway leads to metabolic syndrome in mice affecting hepatic glucose and lipid homeostasis. Mice lacking the enzyme and raised on an Se-adequate diet exhibit hyperinsulinemia, hyperleptinemia, glucose intolerance, and hepatic steatosis, with increased hepatic oxidative stress, but maintain selenoprotein levels and circulating Se status. Insulin challenge of enyme KO mice results in attenuated Akt phosphorylation but does not decrease phosphorylation levels of AMP kinase alpha. Upon dietary Se restriction, enzyme KO animals develop several characteristics of metabolic syndrome, such as obesity, fatty liver, and hypercholesterolemia, with aggravated hyperleptinemia, hyperinsulinemia, and glucose intolerance. Hepatic glutathione peroxidase 1 and selenoprotein S production and circulating selenoprotein P levels are significantly diminished. Enzyme disruption increases the levels of insulin-signaling inhibitor insulin signaling inhibitor protein phosphatase 1B | Mus musculus |
physiological function | the enzyme is involved in Sec decomposition to salvage Se, e.g. from plasma glutathione peroxidase 3 and Sepp1 proteins, for selenoprotein production. Because insulin signaling inhibitor protein phosphatase 1B expression is regulated by Se levels, it is also possible that the hepatic Se decline in enzyme KO mice is driving the expression of insulin signaling inhibitor protein phosphatase 1B, suggesting that Se derived from Sec decomposition participates in insulin signaling inhibitor protein phosphatase 1B regulation | Mus musculus |