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Literature summary for 1.13.99.1 extracted from

  • Sun, L.; Dutta, R.K.; Xie, P.; Kanwar, Y.S.
    myo-Inositol oxygenase overexpression accentuates generation of reactive oxygen species and exacerbates cellular injury following high glucose ambience a new mechanism relevant to the pathogenesis of diabetic nephropathy (2016), J. Biol. Chem., 291, 5688-5707 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 1.13.99.1

Cloned(Commentary)

Cloned (Comment) Organism
gene MIOX, quantitative real-time PCR enzyme expression analysis, overexpression of MIOX in LLC-PK1 cells boosts the generation of H2O2 Sus scrofa

Protein Variants

Protein Variants Comment Organism
additional information under high-glucose ambience, MIOX overexpression accentuates redox imbalance, perturbed NAD+/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes are also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of diabetic nephropathy. These perturbations are largely blocked by various reactive oxygen species inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA, overview. Cells under high glucose ambience or transfected with MIOX-pcDNA show increased expression of apoptogenic protein Bax. The expression is further increased following concomitant treatment with HG and MIOX transfection. Treatment with N-acetylcysteine reduces the expression of Bax Sus scrofa

Localization

Localization Comment Organism GeneOntology No. Textmining
mitochondrion
-
 Sus scrofa 5739
-

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
myo-inositol + O2 Sus scrofa
-
 D-glucuronate + H2O
-
 ?

Organism

Organism UniProt Comment Textmining
Sus scrofa Q8WN98
-
-

Source Tissue

Source Tissue Comment Organism Textmining
kidney
-
 Sus scrofa
-
LLC-PK1 cell
-
 Sus scrofa
-
additional information immunohistochemic analysis Sus scrofa
-
renal tubule MIOX is a tubular-specific enzyme Sus scrofa
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
myo-inositol + O2
-
 Sus scrofa D-glucuronate + H2O
-
 ?

Synonyms

Synonyms Comment Organism
MIOX
-
 Sus scrofa
Myo-inositol oxygenase
-
 Sus scrofa

Temperature Optimum [°C]

Temperature Optimum [°C] Temperature Optimum Maximum [°C] Comment Organism
37
-
 assay at Sus scrofa

pH Optimum

pH Optimum Minimum pH Optimum Maximum Comment Organism
8
-
 assay at Sus scrofa

Expression

Organism Comment Expression
Sus scrofa the enzyme expression is upregulated under high glucose treatment in LLC-PK1 cells, a tubular cell line. Under high-glucose ambience, MIOX overexpression accentuates redox imbalance, perturbed NAD+/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes are also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of diabetic nephropathy. These perturbations are largely blocked by various reactive oxygen species inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA, overview up

General Information

General Information Comment Organism
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 Sus scrofa
malfunction under high-glucose ambience, MIOX overexpression accentuates redox imbalance, perturbed NAD+/NADH ratios, increased ROS generation, depleted reduced glutathione, reduced GSH/GSSG ratio, and enhanced adaptive changes in the profile of the antioxidant defense system. These changes are also accompanied by mitochondrial dysfunctions, DNA damage and induction of apoptosis, accentuated activity of profibrogenic cytokine, and expression of fibronectin, the latter two being the major hallmarks of diabetic nephropathy. These perturbations are largely blocked by various reactive oxygen species inhibitors (Mito Q, diphenyleneiodonium chloride, and N-acetylcysteine) and MIOX/NOX4 siRNA Sus scrofa
physiological function myo-inositol oxygenase (MIOX) is a tubular enzyme that catabolizes myo-inositol to D-glucuronate via the glucuronate-xylulose pathway Sus scrofa