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Literature summary for 1.8.4.12 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
Search for more literature for 1.8.4.12

Cloned(Commentary)

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

Localization

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

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining

Substrates and Products (Substrate)

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

Synonyms

Synonyms Comment Organism
methionine sulfoxide reductase B3
-
 Homo sapiens
MsrB3
-
 Homo sapiens

Cofactor

Cofactor Comment Organism Structure
thioredoxin
-
 Homo sapiens

General Information

General Information Comment Organism
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
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