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Literature summary extracted from

  • Kwak, G.H.; Lim, D.H.; Han, J.Y.; Lee, Y.S.; Kim, H.Y.
    Methionine sulfoxide reductase B3 protects from endoplasmic reticulum stress in Drosophila and in mammalian cells (2012), Biochem. Biophys. Res. Commun., 420, 130-135.
    View publication on PubMed

Cloned(Commentary)

EC Number Cloned (Comment) Organism
1.8.4.12 expressed in Drosophila melanogaster, in A-549 cells and human dermal fibroblasts Homo sapiens

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.8.4.12 endoplasmic reticulum
-
 Homo sapiens 5783
-

Organism

EC Number Organism UniProt Comment Textmining
1.8.4.12 Homo sapiens
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.8.4.12 dabsyl-L-methionine (R)-sulfoxide + dithiothreitol
-
 Homo sapiens dabsyl-L-methionine + dithiothreitol disulfide + H2O
-
 ?

Synonyms

EC Number Synonyms Comment Organism
1.8.4.12 methionine sulfoxide reductase B3
-
 Homo sapiens
1.8.4.12 MsrB3
-
 Homo sapiens

Cofactor

EC Number Cofactor Comment Organism Structure
1.8.4.12 thioredoxin
-
 Homo sapiens

General Information

EC Number General Information Comment Organism
1.8.4.12 malfunction knockdown of MsrB3A in mammalian cells leads to a significant decrease in the resistance to thapsigargin-induced endoplasmic reticulum (ER) stress, but had no effects on the resistance to either dithiothreitol- or tunicamycin-induced ER stress Homo sapiens
1.8.4.12 physiological function methionine sulfoxide reductase B3 protects from endoplasmic reticulum (ER) stress. Drosophila flies overexpressing human MsrB3A exhibit significantly increased resistance to ER stress induced by dithiothreitol (cell viability is enhanced by 40% and 30% in the treatment of 0.5 and 1 mM dithiothreitol, respectively). These flies also show slightly enhanced resistance to tunicamycin-induced ER stress. The enzyme may be involved in the regulation of ER homeostasis. Overexpression of MsrB3A in mammalian cells increases resistance to dithiothreitol- and thapsigargin-induced endoplasmic reticulum (ER) stresses. However, MsrB3A overexpression has no effect on the resistance to tunicamycin-induced ER stress Homo sapiens