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Literature summary for 1.2.1.3 extracted from

  • Moon, K.H.; Lee, Y.M.; Song, B.J.
    Inhibition of hepatic mitochondrial aldehyde dehydrogenase by carbon tetrachloride through JNK-mediated phosphorylation (2010), Free Radic. Biol. Med., 48, 391-398.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 1.2.1.3

Inhibitors

Inhibitors Comment Organism Structure
c-Jun N-terminal protein kinase incubation with catalytically active JNK leads to significant inhibition of ALDH2 activity. CCl4 exposure activates JNK which translocates to mitochondria and phosphorylates ALDH2 contributing to inhibition of ALDH2 activity Rattus norvegicus

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion isoform ALDH2 Rattus norvegicus 5739
-

Organism

Organism UniProt Comment Textmining
Rattus norvegicus P11884
-
-

Posttranslational Modification

Posttranslational Modification Comment Organism
phosphoprotein CCl4 exposure activates JNK, which translocates to mitochondria and phosphorylates ALDH2 Rattus norvegicus

Source Tissue

Source Tissue Comment Organism Textmining
hepatocyte
-
 Rattus norvegicus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
propionaldehyde + NAD+ + H2O
-
 Rattus norvegicus propionate + NADH + H+
-
 ?

Synonyms

Synonyms Comment Organism
ALDH2 isoform Rattus norvegicus

Cofactor

Cofactor Comment Organism Structure
NAD+
-
 Rattus norvegicus

General Information

General Information Comment Organism
malfunction inhibition of ALDH2 leads to accumulation of cytotoxic 4-hydroxynonenal and malondialdehyde, which can cause cell death through activation of c-Jun N-terminal protein kinase and/or p38 kinase Rattus norvegicus