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Literature summary extracted from

  • Esposito, G.; Vos, M.; Vilain, S.; Swerts, J.; De Sousa Valadas, J.; Van Meensel, S.; Schaap, O.; Verstreken, P.
    Aconitase causes iron toxicity in Drosophila pink1 mutants (2013), PLoS Genet., 9, e1003478.
    View publication on PubMedView publication on EuropePMC

Protein Variants

EC Number Protein Variants Comment Organism
4.2.1.3 C459S catalytically inactive mutant without its [4Fe-4S]-cluster. Mitochondrial morphological defects as a consequence of acon inactivation depend on its [4Fe-4S] cluster Drosophila melanogaster
4.2.1.3 S677A catalytically inactive mutant Drosophila melanogaster

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
4.2.1.3 mitochondrion
-
Drosophila melanogaster 5739
-

Metals/Ions

EC Number Metals/Ions Comment Organism Structure
4.2.1.3 [4Fe-4S] center acon harbors a single unligated iron atom in its [4Fe-4S], enzyme is in this respect unique in mitochondria Drosophila melanogaster

Organism

EC Number Organism UniProt Comment Textmining
4.2.1.3 Drosophila melanogaster
-
-
-

Synonyms

EC Number Synonyms Comment Organism
4.2.1.3 acon
-
Drosophila melanogaster
4.2.1.3 aconitase
-
Drosophila melanogaster

General Information

EC Number General Information Comment Organism
4.2.1.3 malfunction aconitase down-regulation suppresses pink1 mutant phenotypes. In contrast to partial loss of aconitase that rescues mitochondrial defects in pink1 mutants, overexpression of aconitase in transgenic mice causes mitochondrial morphological defects and swelling of mitochondria in dopaminergic neurons Drosophila melanogaster