EC Number   |
General Information |
Reference |
|---|
   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 | malfunction |
a quadruple (miox1/2/4/5) mutant that incorporates T-DNA insertions in all four MIOX genes is generated. This mutant shows a severe reduction in transcripts for all four MIOX genes. The quadruple myo-inositol oxygenase mutant shows a significant reduction in susceptibility to Heterodera schachtii, and syncytia have elevated myo-inositol and galactinol levels and an elevated expression level of the antimicrobial thionin gene Thi2.1 |
728381 |
| 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 |
| 1.13.99.1 | malfunction |
following increased expression of MIOX in tubular cells under high glucose ambience, there is an accentuated perturbation in cellular redox and mitochondrial homeostasis, leading to cellular apoptosis. In addition, there is an increased synthesis of extracellular matrix proteins, reflective of tubulo-interstitial injury in diabetic nephropathy |
745357 |
| 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 | malfunction |
increased expression in diabetic kidneys may contribute to tubulointerstitial injury and development of diabetic nephropathy |
697793 |
