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Literature summary for 4.2.1.3 extracted from

  • Talib, J.; Cook, N.; Pattison, D.; Davies, M.
    Disruption of the iron-sulfur cluster of aconitase by myeloperoxidase-derived oxidants (2014), Free Radic. Biol. Med., 75 Suppl 1, S27-S28 .
    View publication on PubMed
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Inhibitors

Inhibitors Comment Organism Structure
HOCl exposure of human coronary artery endothelial cells to 0-50 microM HOCl or 0-150 microM HOSCN results in an increase in intracellular iron, loss of aconitase activity and a loss of mitochondrial aconitase protein. Cytosolic aconitase is not affected Homo sapiens
HOSCN exposure of human coronary artery endothelial cells to 0-50 microM HOCl or 0-150 microM HOSCN results in an increase in intracellular iron, loss of aconitase activity and a loss of mitochondrial aconitase protein. Cytosolic aconitase is not affected. HOSCN induces rapid and efficient release of iron from aconitase. Blocking the [4Fe-4 S] cluster inhibits HOSCN-mediated inactivation Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
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-
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Source Tissue

Source Tissue Comment Organism Textmining
artery coronary artery endothelial cells Homo sapiens
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endothelium coronary artery endothelial cells Homo sapiens
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Cofactor

Cofactor Comment Organism Structure
[4Fe-4S]-center HOSCN induces rapid and efficient release of iron from aconitase. Blocking the [4Fe-4 S] cluster inhibits HOSCN-mediated inactivation Homo sapiens