EC Number   |
General Information |
Reference |
|---|
   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 |
745184 |
| 1.13.99.1 | metabolism |
a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease |
745184 |
| 1.13.99.1 | metabolism |
MIOX is the first and rate-limiting enzyme in myo-inositol metabolism pathway |
712593 |
| 1.13.99.1 | metabolism |
the enzyme is important in the glucaric acid synthetic pathway |
-, 744811 |
| 1.13.99.1 | more |
increase in MIOX enzyme activity is in proportion to serum glucose concentrations and may be responsible for the myo-inositol depletion found in the type I diabetes mellitus complications, detailed phenotype analysis of 130 Caucasian patients, overview |
712593 |
| 1.13.99.1 | physiological function |
biological production of glucaric acid |
695783 |
| 1.13.99.1 | physiological function |
control level of myoinositol, no influence on ascorbic acid |
700818 |
| 1.13.99.1 | physiological function |
enzyme overexpression accentuates the cellular injury related to endoplasmic reticulum stress and accentuates tunicamycin-induced generation of reactive oxygen species |
763868 |
| 1.13.99.1 | physiological function |
enzyme overexpression exacerbates cisplatin-induced acute kidney injury by accentuating renal tubular cell apoptosis and modulating the expression of inflammatory cytokines |
764984 |
| 1.13.99.1 | physiological function |
ferroptosis, an integral process in the pathogenesis of cisplatin-induced acute kidney injury, is modulated by the expression profile of the enzyme. Overexpression of the enzyme promotes cisplatin-induced cell death and RSL3-induced ferroptosis in HK-2 cells |
765142 |
