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Literature summary extracted from

  • Zhan, M.; Usman, I.M.; Sun, L.; Kanwar, Y.S.
    Disruption of renal tubular mitochondrial quality control by myo-inositol oxygenase in diabetic kidney disease (2015), J. Am. Soc. Nephrol., 26, 1304-1321 .
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
1.13.99.1 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
1.13.99.1 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)

EC Number Cloned (Comment) Organism
1.13.99.1 gene MIOX, quantitative enzyme expression analysis Mus musculus
1.13.99.1 gene MIOX, quantitative enzyme expression analysis Homo sapiens

Inhibitors

EC Number Inhibitors Comment Organism Structure
1.13.99.1 D-glucarate a MIOX inhibitor Homo sapiens
1.13.99.1 D-glucarate a MIOX inhibitor, D-glucarate normalizes reduced autophagy and mitophagy in tubules of STZ-induced diabetic mice Mus musculus

Localization

EC Number Localization Comment Organism GeneOntology No. Textmining
1.13.99.1 mitochondrion
-
 Mus musculus 5739
-
1.13.99.1 mitochondrion
-
 Homo sapiens 5739
-

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1.13.99.1 myo-inositol + O2 Mus musculus
-
 D-glucuronate + H2O
-
 ?
1.13.99.1 myo-inositol + O2 Homo sapiens
-
 D-glucuronate + H2O
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
1.13.99.1 Homo sapiens Q9UGB7
-
-
1.13.99.1 Mus musculus Q9QXN5
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.13.99.1 HK-2 cell
-
 Homo sapiens
-
1.13.99.1 kidney
-
 Mus musculus
-
1.13.99.1 kidney
-
 Homo sapiens
-
1.13.99.1 renal tubule MIOX is a tubular-specific enzyme Mus musculus
-
1.13.99.1 renal tubule MIOX is a tubular-specific enzyme Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.13.99.1 myo-inositol + O2
-
 Mus musculus D-glucuronate + H2O
-
 ?
1.13.99.1 myo-inositol + O2
-
 Homo sapiens D-glucuronate + H2O
-
 ?

Synonyms

EC Number Synonyms Comment Organism
1.13.99.1 MIOX
-
 Mus musculus
1.13.99.1 MIOX
-
 Homo sapiens
1.13.99.1 Myo-inositol oxygenase
-
 Mus musculus
1.13.99.1 Myo-inositol oxygenase
-
 Homo sapiens

Expression

EC Number Organism Comment Expression
1.13.99.1 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
1.13.99.1 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

EC Number General Information Comment Organism
1.13.99.1 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
1.13.99.1 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
1.13.99.1 metabolism a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease Mus musculus
1.13.99.1 metabolism a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease Homo sapiens
1.13.99.1 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
1.13.99.1 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