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Literature summary extracted from

  • Hanssen, N.M.; Stehouwer, C.D.; Schalkwijk, C.G.
    Methylglyoxal and glyoxalase I in atherosclerosis (2014), Biochem. Soc. Trans., 42, 443-449.
    View publication on PubMed

Inhibitors

EC Number Inhibitors Comment Organism Structure
4.4.1.5 additional information posttranslational modification of Glo1 by oxidized glutathione (GSSG) and nitrosylation strongly inhibits Glo1 activity Homo sapiens

Organism

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

Posttranslational Modification

EC Number Posttranslational Modification Comment Organism
4.4.1.5 phosphoprotein the enzyme is susceptible to post-translational modifications, in particular phosphorylation in response to TNFalpha, a key mediator of inflammation Homo sapiens
4.4.1.5 side-chain modification posttranslational modification of Glo1 by oxidized glutathione (GSSG) and nitrosylation strongly inhibits Glo1 activity Homo sapiens

Source Tissue

EC Number Source Tissue Comment Organism Textmining
4.4.1.5 blood vessel the enzyme is absent from the necrotic core of atherosclerotic plaques Homo sapiens
-
4.4.1.5 endothelial cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
4.4.1.5 glutathione + methylglyoxal
-
 Homo sapiens (R)-S-lactoylglutathione
-
 ?

Synonyms

EC Number Synonyms Comment Organism
4.4.1.5 Glo1
-
 Homo sapiens
4.4.1.5 glyoxalase I
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
4.4.1.5 Homo sapiens the promoter of Glo1 harbours an nuclear factor kappaB-responsive element, indicating a link between inflammation and reduced Glo1 expression down

General Information

EC Number General Information Comment Organism
4.4.1.5 metabolism rate-limiting enzyme in the glyoxalase system Homo sapiens
4.4.1.5 physiological function methylglyoxal is a key player in vascular dysfunction, particularly due to its capacity to induce the formation of oxidative stress, cell death andendothelial dysfunction, glyoxylase I is the rate-limiting enzyme in the glyoxalase system for detoxifcation of methylglyoxal, accumulation of methylglyoxal and methylglyoxal-derived advanced glycation end-products may be a major contributing factor to atherosclerotic plaque rupture. Intracellular accumulation of methylglyoxal in endothelial cells causes dysfunction as indicated by expression of adhesion molecules such as vascular cell adhesion molecule 1 expression, which can be prevented by Glo1 overexpression Homo sapiens