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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

Reaction

myo-inositol
+
O2
=
D-glucuronate
 +
H2O

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

ECTree

     1 Oxidoreductases
         1.13 Acting on single donors with incorporation of molecular oxygen (oxygenases)
             1.13.99 Miscellaneous
                1.13.99.1 inositol oxygenase

Expression

Expression on EC 1.13.99.1 - inositol oxygenase

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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
445.7fold gene induction in syncytia induced by nematode Heterodera schachtii
7.64fold gene induction in syncytia induced by nematode Heterodera schachtii
administration of high-fat diet to CD1 mice over a period of 2-6 weeks induces a tremendous increase in the expression of Miox, exclusively confined to the tubular compartment of the kidney cortex. Besides the increased expression in superficial cortical tubules, it also extends into the deeper cortex. Upregulation of Miox is accompanied by upregulation of mSrebp1 in kidney cells. Rapamycin reverses palmitate/bovine serum albumin-induced Miox, Srebp1, and p53 expression and apoptosis in renal tubular cells
all MIOX genes are strongly expressed in syncytia induced by the beet cyst nematode Heterodera schachtii in Arabidopsis thaliana roots
antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl hydroquinone reduces MIOX expression
-
cisplatin increases the enzyme expression via demethylation of its promoter
coexpression of the Pichia pastoris ppMIOX and the urinate dehydrogenase (Udh) from Pseudomonas putida KT2440 does not lead to accumulation of glucaric acid from myo-inositol or increased enzyme activity of neither MIOX nor Udh
diabetic, nephropathy
-
enzyme expression increases in HK-2 cells after 4 h of cisplatin treatment
-
enzyme expression is significantly up-regulated by heat (5fold), cold (7fold), and drought (5fold) stresses as compared to transgenic plants grown without stress-induced conditions
-
gene induction in syncytia induced by nematode Heterodera schachtii
genes encoding the enzyme are strongly expressed in syncytia induced by the beet cyst nematode Heterodera schachtii in Arabidopsis roots
-
GsMIOX1a is rapidly induced by alkaline stress. Under alkaline stress, GsMIOX1a expression levels increase and reach a maximum level at 6 h that is approximately 42fold higher than that at 0 h
high glucose levels, exposure of cells to oxidants H2O2 and methylglyoxal up-regulates MIOX expression
-
high-fat diet administration over a period of 6 weeks results in a marked time-dependent up-regulation of Miox
MIOX2 expression is suppressed by exogenous glucose addition in the shoot, but not in the root
-
MIOX4 expression is suppressed by exogenous glucose addition in the shoot,but not in the root
-
OsMIOX enzyme expression is highly enhanced in rice plants overexpressing the Alternaria tenuissima PeaT1 gene during drought stress, the plants show enhanced drought stress tolerance and increased the survival rate following a drought treatment
palmitate-conjugated bovine serum albumin causes a dose-dependent increase in Miox expression and activity in LLCPK-1 cells. Concomitant with Miox upregulation, a dose-dependent increased Bax protein expression is observed following palmitate/BSA treatment of LLCPK-1 cells. Concomitant treatment with palmitate/bovine serum albumin and activators of PKA (forskolin), PDK/PI3K (insulin), and PKC (TPA) further increase Miox activity
the concentration of the enzyme in serum is higher in the acute kidney injury group compared to the healthy control group
-
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
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
treatment of HK-2 cells with palmitate/bovine serum albumin for 24 h induces an increased Miox expression with a concomitant decrease in the membrane-bound precursor form of pre-Srebp1 in the cytoplasmic fraction. No change in the expression of beta-actin or laminB1 is observed. Miox is transcriptionally upregulated by high glucose ambience. A dose-dependent increase in the expression of Miox is observed following insulin treatment. At the same time, a dose-dependent increase in the mSrebp1 is observed. Rapamycin reverses palmitate/bovine serum albumin-induced Miox, Srebp1, and p53 expression and apoptosis in renal tubular cells
under high-glucose (30 mM) ambience, the enzyme expression increases compared with the control low-glucose (5 mM) ambience
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