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Literature summary for 1.13.99.1 extracted from
- Disruption of renal tubular mitochondrial quality control by myo-inositol oxygenase in diabetic kidney disease (2015), J. Am. Soc. Nephrol., 26, 1304-1321 .
Application
| Application | Comment | Organism |
|---|---|---|
| medicine | the enzyme is a possible target for treatment of diabetic kidney disease. MIOX enzyme inhibitor D-glucarate might be a potential therapeutic agent for the amelioration of diabetic kidney disease | Mus musculus |
| medicine | the enzyme is a possible target for treatment of diabetic kidney disease. MIOX enzyme inhibitor D-glucarate might be a potential therapeutic agent for the amelioration of diabetic kidney disease | Homo sapiens |
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| gene MIOX, quantitative enzyme expression analysis | Mus musculus |
| gene MIOX, quantitative enzyme expression analysis | Homo sapiens |
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| D-glucarate | a MIOX inhibitor | Homo sapiens |  |
| D-glucarate | a MIOX inhibitor, D-glucarate normalizes reduced autophagy and mitophagy in tubules of STZ-induced diabetic mice | Mus musculus | |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| mitochondrion | - |
Mus musculus | 5739 | - |
| mitochondrion | - |
Homo sapiens | 5739 | - |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| myo-inositol + O2 | Mus musculus | - |
D-glucuronate + H2O | - |
? | |
| myo-inositol + O2 | Homo sapiens | - |
D-glucuronate + H2O | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | Q9UGB7 | - |
- |
| Mus musculus | Q9QXN5 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| HK-2 cell | - |
Homo sapiens | - |
| kidney | - |
Mus musculus | - |
| kidney | - |
Homo sapiens | - |
| renal tubule | MIOX is a tubular-specific enzyme | Mus musculus | - |
| renal tubule | MIOX is a tubular-specific enzyme | Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| myo-inositol + O2 | - |
Mus musculus | D-glucuronate + H2O | - |
? | |
| myo-inositol + O2 | - |
Homo sapiens | D-glucuronate + H2O | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| MIOX | - |
Mus musculus |
| MIOX | - |
Homo sapiens |
| Myo-inositol oxygenase | - |
Mus musculus |
| Myo-inositol oxygenase | - |
Homo sapiens |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Mus musculus | upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins under high-glucose ambience | up |
| Homo sapiens | upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins under high-glucose ambience | up |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins under high-glucose ambience. Additionally, dysfunctional mitochondria accumulate in the cytoplasm. Decreasing the expression of MIOX under high-glucose ambience increases PTEN-induced putative kinase 1 expression and the dependent mitofusin-2-Parkin interaction. Overexpression of MIOX in the cells enhances the effects of high-glucose, whereas MIOX siRNA or D-glucarate, an inhibitor of MIOX, partially reverse these perturbations | Homo sapiens |
| malfunction | upregulation of MIOX accompanied by mitochondrial fragmentation and depolarization, inhibition of autophagy/mitophagy, and altered expression of mitochondrial dynamic and mitophagic proteins under high-glucose ambience. Additionally, dysfunctional mitochondria accumulate in the cytoplasm. Decreasing the expression of MIOX under high-glucose ambience increases PTEN-induced putative kinase 1 expression and the dependent mitofusin-2-Parkin interaction. Overexpression of MIOX in the cells enhances the effects of high-glucose, whereas MIOX siRNA or D-glucarate, an inhibitor of MIOX, partially reverse these perturbations, D-glucarate normalizes reduced autophagy and mitophagy in tubules of STZ-induced diabetic mice | Mus musculus |
| metabolism | a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease | Mus musculus |
| metabolism | a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease | Homo sapiens |
| physiological function | myo-inositol oxygenase (MIOX) is a tubular-specific enzyme, that modulates redox imbalance and apoptosis in tubular cells in diabetes, role of MIOX in perturbation of mitochondrial quality control, including mitochondrial dynamics and autophagy/mitophagy, under high-glucose ambience or a diabetic state, overview | Mus musculus |
| physiological function | myo-inositol oxygenase (MIOX) is a tubular-specific enzyme, that modulates redox imbalance and apoptosis in tubular cells in diabetes, role of MIOX in perturbation of mitochondrial quality control, including mitochondrial dynamics and autophagy/mitophagy, under high-glucose ambience or a diabetic state, overview | Homo sapiens |
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Release 2023.1 (January 2023)
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