Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary extracted from

  • Seale, L.A.; Hashimoto, A.C.; Kurokawa, S.; Gilman, C.L.; Seyedali, A.; Bellinger, F.P.; Raman, A.V.; Berry, M.J.
    Disruption of the selenocysteine lyase-mediated selenium recycling pathway leads to metabolic syndrome in mice (2012), Mol. Cell. Biol., 32, 4141-4154.
    View publication on PubMedView publication on EuropePMC

Protein Variants

EC Number Protein Variants Comment Organism
4.4.1.16 additional information construction of enzyme knockout mice, phenotype, overview Mus musculus

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
4.4.1.16 L-selenocysteine + reduced acceptor Mus musculus
-
 selenide + L-alanine + acceptor
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
4.4.1.16 Mus musculus
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
4.4.1.16 kidney
-
 Mus musculus
-
4.4.1.16 liver
-
 Mus musculus
-
4.4.1.16 testis
-
 Mus musculus
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
4.4.1.16 L-selenocysteine + reduced acceptor
-
 Mus musculus selenide + L-alanine + acceptor
-
 ?

Synonyms

EC Number Synonyms Comment Organism
4.4.1.16 SCL
-
 Mus musculus
4.4.1.16 Scly
-
 Mus musculus

General Information

EC Number General Information Comment Organism
4.4.1.16 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
4.4.1.16 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