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Literature summary for 4.2.1.3 extracted from

  • Goncalves, S.; Paupe, V.; Dassa, E.P.; Rustin, P.
    Deferiprone targets aconitase: implication for Friedreich's ataxia treatment (2008), BMC Neurol., 8, 20.
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine enzyme inhibition, e.g. by deferiprone, is helpful in Friedreich's ataxia treatment Homo sapiens

Inhibitors

Inhibitors Comment Organism Structure
deferiprone the loss of aconitase activity observed in cells should be ascribed to the chelation of available iron rather than to a direct effect of the chelator on the iron-sulfur clusters of the enzyme Homo sapiens

Localization

Localization Comment Organism GeneOntology No. Textmining
cytosol
-
Homo sapiens 5829
-
mitochondrion mitochondrial aconitase activity represents up to 80% of the total aconitase activity in skin fibroblasts Homo sapiens 5739
-

Metals/Ions

Metals/Ions Comment Organism Structure
Fe2+ required, the enzyme contains iron-sulfur clusters. Chelating mitochondrial free iron in various cell systems causes loss of aconitase activity Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
additional information Homo sapiens impairing aconitase activity precedes decreased cell proliferation ?
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
fibroblast
-
Homo sapiens
-
skin
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
additional information impairing aconitase activity precedes decreased cell proliferation Homo sapiens ?
-
?

Synonyms

Synonyms Comment Organism
aconitase
-
Homo sapiens