1.13.99.1: inositol oxygenase
This is an abbreviated version!
For detailed information about inositol oxygenase, go to the full flat file.
Word Map on EC 1.13.99.1
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1.13.99.1
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d-glucuronate
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glucaric
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diiron
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ambience
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mixed-valent
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four-electron
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glucuronate-xylulose
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medicine
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diagnostics
- 1.13.99.1
- d-glucuronate
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glucaric
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diiron
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ambience
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mixed-valent
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four-electron
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glucuronate-xylulose
- medicine
- diagnostics
Reaction
Synonyms
amyoinositol oxygenase, AtMIOX, EC 1.13.1.11, EC 1.99.2.6, GsMIOX1a, Inositol oxygenase, inositol oxygenase 1, InOx, Kidney-specific protein 32, meso-Inositol oxygenase, MIOX, MIOX1, MIOX2, MIOX4, MIOX5, mMIOX, MOO, Myo-inositol oxygenase, OsMIOX, Oxygenase, inositol, ppMIOX, Renal-specific oxidoreductase, renal-specific oxidoreductase/myo-inositol oxygenase, RSOR/MIOX
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General Information
General Information on EC 1.13.99.1 - inositol oxygenase
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evolution
malfunction
metabolism
physiological function
additional information
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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
MIOX proteins are highly conserved and present in nearly all eukaryotes
evolution
Glycine soja 07256
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MIOX proteins are highly conserved and present in nearly all eukaryotes
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increased expression in diabetic kidneys may contribute to tubulointerstitial injury and development of diabetic nephropathy
malfunction
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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
malfunction
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loss-of-function mutants in MIOX genes contain alterations in myo-inositol levels and growth changes in the root
malfunction
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loss-of-function mutants in MIOX genes contain alterations in myo-inositol levels and growth changes in the root. Miox2 mutants can be complemented with a MIOX2:green fluorescent protein fusion
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
malfunction
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. This reduction in susceptibility can also be achieved by exogenous application of galactinol to wild-type seedlings. Except for MIOX2, transcripts for the other three MIOX genes are still detected at a level of 2-14% of their abundance in the wild-type, the mutant does not show any visible phenotype and produced viable pollen, but the incorporation of myo-inositol-derived sugars into cell walls is strongly inhibited by over 90% with no change in the ultrastructure of syncytial cell walls
malfunction
the T-DNA insertion mutant atmiox1 is sensitive to alkaline stress, the phenotype can be complemented by expression of Glycine soja MIOX1 under constitutive CaMV35S promoter control
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
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
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
malfunction
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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. This reduction in susceptibility can also be achieved by exogenous application of galactinol to wild-type seedlings. Except for MIOX2, transcripts for the other three MIOX genes are still detected at a level of 2-14% of their abundance in the wild-type, the mutant does not show any visible phenotype and produced viable pollen, but the incorporation of myo-inositol-derived sugars into cell walls is strongly inhibited by over 90% with no change in the ultrastructure of syncytial cell walls
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MIOX is the first and rate-limiting enzyme in myo-inositol metabolism pathway
metabolism
a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease
metabolism
a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease
metabolism
the enzyme is important in the glucaric acid synthetic pathway
metabolism
the enzyme is important in the glucaric acid synthetic pathway
metabolism
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the enzyme is important in the glucaric acid synthetic pathway
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physiological function
control level of myoinositol, no influence on ascorbic acid
physiological function
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start of catabolism of carbon skeleton of cell-signaling inositol polyphosphates and phosphoinositides
physiological function
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start of catabolism of carbon skeleton of cell-signaling inositol polyphosphates and phosphoinositides
physiological function
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the importance of MIOX in syncytium development is the removal of excess myo-inositol from syncytia
physiological function
kidney-specific expression of myo-inositol oxygenase in acute kidney injury
physiological function
MIOX is a renal specific, proximal tubule protein that is increased in plasma ofanimals and critically ill patients with acute kidney injury, AKI. MIOX preceds the elevation in SCr by approximately two days in human patients
physiological function
myo-inositol oxygenase (MIOX) is a tubular enzyme that catabolizes myo-inositol to D-glucuronate via the glucuronate-xylulose pathway
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
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
physiological function
overexpression of the PeaT1 elicitor gene from Alternaria tenuissima in Oryza sativa improves drought tolerance in rice plants via interaction with a myo-inositol oxygenase. In PeaT1-overexpressing (PeaT1OE) plants, abscisic acid and chlorophyll contents significantly increase, while the malondialdehyde (MDA) content decreases compared with the wild-type plants. Transcript levels of drought-responsive genes, including OsAM1, OsLP2, and OsDST, are prominently lower in the PeaT1OE plants. In contrast, expression levels of genes encoding positive drought stress regulators including OsSKIPa, OsCPK9, OsNAC9, OSEREBP1, and OsTPKb are upregulated in PeaT1OE plants. OsMIOX is highly expressed in PeaT1OE plants during the drought treatment
physiological function
positive function of enzyme GsMIOX1a in the alkaline response in Glycine soja plants, GsMIOX1a gene positively regulates plant tolerance to alkaline stress. Other soybean varieties, including Glycine soja 07256, Glycine soja 50109, Glycine max Suinong 28 and Glycine max Hefeng 55. Glycine max Suinong 28 and Glycine max Hefeng 55 are Chinese soybean cultivars that exhibit much lower adaptability to stress compared to Glycine soja 07256. Glycine soja 50109 is also a kind of wild soybean but is not reported to be alkaline resistant
physiological function
the enzyme myo-inositol oxygenase is the key enzyme of a pathway leading from myo-inositol to UDP-glucuronic acid. The primary function of myo-inositol oxygenase for syncytium development after infection with Heterodera schachtii is probably not the production of UDP-glucuronic acid as a precursor for cell wall polysaccharides, but the reduction of myo-inositol levels and thereby a reduction in the galactinol level to avoid the induction of defence-related genes
physiological function
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enzyme overexpression accentuates the cellular injury related to endoplasmic reticulum stress and accentuates tunicamycin-induced generation of reactive oxygen species
physiological function
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enzyme overexpression accentuates the cellular injury related to endoplasmic reticulum stress and accentuates tunicamycin-induced generation of reactive oxygen species
physiological function
enzyme overexpression accentuates the cellular injury related to endoplasmic reticulum stress and accentuates tunicamycin-induced generation of reactive oxygen species
physiological function
enzyme overexpression exacerbates cisplatin-induced acute kidney injury by accentuating renal tubular cell apoptosis and modulating the expression of inflammatory cytokines
physiological function
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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
physiological function
Glycine soja 07256
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positive function of enzyme GsMIOX1a in the alkaline response in Glycine soja plants, GsMIOX1a gene positively regulates plant tolerance to alkaline stress. Other soybean varieties, including Glycine soja 07256, Glycine soja 50109, Glycine max Suinong 28 and Glycine max Hefeng 55. Glycine max Suinong 28 and Glycine max Hefeng 55 are Chinese soybean cultivars that exhibit much lower adaptability to stress compared to Glycine soja 07256. Glycine soja 50109 is also a kind of wild soybean but is not reported to be alkaline resistant
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physiological function
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the enzyme myo-inositol oxygenase is the key enzyme of a pathway leading from myo-inositol to UDP-glucuronic acid. The primary function of myo-inositol oxygenase for syncytium development after infection with Heterodera schachtii is probably not the production of UDP-glucuronic acid as a precursor for cell wall polysaccharides, but the reduction of myo-inositol levels and thereby a reduction in the galactinol level to avoid the induction of defence-related genes
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physiological function
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kidney-specific expression of myo-inositol oxygenase in acute kidney injury
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