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Literature summary for 4.2.1.3 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

Protein Variants Comment Organism
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
S677A catalytically inactive mutant Drosophila melanogaster

Localization

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

Metals/Ions

Metals/Ions Comment Organism Structure
[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

Organism UniProt Comment Textmining
Drosophila melanogaster
-
-
-

Synonyms

Synonyms Comment Organism
acon
-
Drosophila melanogaster
aconitase
-
Drosophila melanogaster

General Information

General Information Comment Organism
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