Application | Comment | Organism |
---|---|---|
medicine | it is shown that the cytosolic aconitase defect and consequent IRP1 activation occurring in Friedreich's Ataxia (FRDA) cells are reversed by the action of extramitochondrial frataxin | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | Homo sapiens | it is demonstrated that the extramitochondrial form of frataxin directly interacts with cytosolic aconitase/iron regulatory protein-1 (IRP1). The inability to produce normal levels of the mitochondrial protein frataxin causes the hereditary degenerative disorder Friedreichs Ataxia (FRDA) | ? | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
additional information | it is demonstrated that the extramitochondrial form of frataxin directly interacts with cytosolic aconitase/iron regulatory protein-1 (IRP1). The inability to produce normal levels of the mitochondrial protein frataxin causes the hereditary degenerative disorder Friedreichs Ataxia (FRDA) | Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
aconitase | - |
Homo sapiens |