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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
evolution
MIOX proteins are highly conserved and present in nearly all eukaryotes
evolution
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MIOX proteins are highly conserved and present in nearly all eukaryotes
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malfunction
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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
-
loss-of-function mutants in MIOX genes contain alterations in myo-inositol levels and growth changes in the root
malfunction
-
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
-
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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metabolism
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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
biological production of glucaric acid
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
-
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
-
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 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
-
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
-
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
-
kidney-specific expression of myo-inositol oxygenase in acute kidney injury
-
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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
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
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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
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
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
all MIOX genes are strongly expressed in syncytia induced by the beet cyst nematode Heterodera schachtii in Arabidopsis thaliana roots
-
-
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
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
-
-
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
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
-
-
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids, overview
-
-
under high-glucose (30 mM) ambience, the enzyme expression increases compared with the control low-glucose (5 mM) ambience
-
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
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
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Charalampous, F.C.
Biochemical studies on inositol. V. Purification and properties of the enzyme that cleaves inositol to D-glucuronic acid
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Mammalia, Mus musculus
brenda
Lu, Y.; Liu, C.; Miao, X.; Xu, K.; Wu, X.; Liu, C.
Increased expression of myo-inositol oxygenase is involved in the tubulointerstitial injury of diabetic nephropathy
Exp. Clin. Endocrinol. Diabetes
117
257-265
2009
Rattus norvegicus
brenda
Siddique, S.; Endres, S.; Atkins, J.M.; Szakasits, D.; Wieczorek, K.; Hofmann, J.; Blaukopf, C.; Urwin, P.E.; Tenhaken, R.; Grundler, F.M.; Kreil, D.P.; Bohlmann, H.
Myo-inositol oxygenase genes are involved in the development of syncytia induced by Heterodera schachtii in Arabidopsis roots
New Phytol.
184
457-472
2009
Arabidopsis thaliana (O82200), Arabidopsis thaliana (Q8H1S0), Arabidopsis thaliana (Q8L799), Arabidopsis thaliana (Q9FJU4)
brenda
Endres, S.; Tenhaken, R.
Myoinositol oxygenase controls the level of myoinositol in Arabidopsis, but does not increase ascorbic acid
Plant Physiol.
149
1042-1049
2009
Arabidopsis thaliana (O82200), Arabidopsis thaliana (Q8H1S0), Arabidopsis thaliana (Q8L799), Arabidopsis thaliana (Q9FJU4)
brenda
Yang, B.; Hodgkinson, A.; Millward, B.; Demaine, A.
Polymorphisms of myo-inositol oxygenase gene are associated with type 1 diabetes mellitus
J. Diabetes Complicat.
24
404-408
2010
Homo sapiens
brenda
Alford, S.R.; Rangarajan, P.; Williams, P.; Gillaspy, G.E.
myo-Inositol oxygenase is required for responses to low energy conditions in Arabidopsis thaliana
Front. Plant Sci.
3
69
2012
Arabidopsis thaliana
brenda
Senthilraja, P.; Paul Aime, N.; Manikandaprabhu, S.; Prakash, M.
Computational screening and docking analysis of natural compounds derived from mangrove plant against type-2 diabetes, myo-inositol oxygenase enzyme (MIOX)
Int. J. Pharm. Sci. Rev. Res.
20
158-161
2013
Homo sapiens
-
brenda
Nayak, B.; Kondeti, V.K.; Xie, P.; Lin, S.; Viswakarma, N.; Raparia, K.; Kanwar, Y.S.
Transcriptional and post-translational modulation of myo-inositol oxygenase by high glucose and related pathobiological stresses
J. Biol. Chem.
286
27594-27611
2011
Mus musculus
brenda
Siddique, S.; Endres, S.; Sobczak, M.; Radakovic, Z.; Fragner, L.; Grundler, F.; Weckwerth, W.; Tenhaken, R.; Bohlmann, H.
Myo-inositol oxygenase is important for the removal of excess myo-inositol from syncytia induced by Heterodera schachtii in Arabidopsis roots
New Phytol.
201
476-85
2014
Arabidopsis thaliana
brenda
Gaut, J.P.; Crimmins, D.L.; Ohlendorf, M.F.; Lockwood, C.M.; Griest, T.A.; Brada, N.A.; Hoshi, M.; Sato, B.; Hotchkiss, R.S.; Jain, S.; Ladenson, J.H.
Development of an immunoassay for the kidney-specific protein myo-inositol oxygenase, a potential biomarker of acute kidney injury
Clin. Chem.
60
747-757
2014
Homo sapiens (Q9UGB7), Homo sapiens, Mus musculus (Q9QXN5), Mus musculus, Mus musculus C57BL/6 (Q9QXN5)
brenda
Liu, Y.; Gong, X.; Wang, C.; Du, G.; Chen, J.; Kang, Z.
Production of glucaric acid from myo-inositol in engineered Pichia pastoris
Enzyme Microb. Technol.
91
8-16
2016
Komagataella phaffii (C4QZH8), Komagataella phaffii GS115 (C4QZH8), Mus musculus (Q9QXN5), Mus musculus
brenda
Shi, F.; Dong, Y.; Zhang, Y.; Yang, X.; Qiu, D.
Overexpression of the PeaT1 elicitor gene from Alternaria tenuissima improves drought tolerance in rice plants via interaction with a myo-inositol oxygenase
Front. Plant Sci.
8
970
2017
Oryza sativa (Q5Z8T3), Oryza sativa
brenda
Zhan, M.; Usman, I.M.; Sun, L.; Kanwar, Y.S.
Disruption of renal tubular mitochondrial quality control by myo-inositol oxygenase in diabetic kidney disease
J. Am. Soc. Nephrol.
26
1304-1321
2015
Mus musculus (Q9QXN5), Homo sapiens (Q9UGB7)
brenda
Tominaga, T.; Dutta, R.K.; Joladarashi, D.; Doi, T.; Reddy, J.K.; Kanwar, Y.S.
Transcriptional and translational modulation of myo-inositol oxygenase (Miox) by fatty acids implications in renal tubular injury induced in obesity and diabetes
J. Biol. Chem.
291
1348-1367
2016
Homo sapiens (Q9UGB7), Mus musculus (Q9QXN5), Mus musculus CD1 (Q9QXN5), Rattus norvegicus (Q9QXN4), Sus scrofa (Q8WN98)
brenda
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
J. Biol. Chem.
291
5688-5707
2016
Sus scrofa (Q8WN98)
brenda
Siddique, S.; Endres, S.; Sobczak, M.; Radakovic, Z.; Fragner, L.; Grundler, F.; Weckwerth, W.; Tenhaken, R.; Bohlmann, H.
Myo-inositol oxygenase is important for the removal of excess myo-inositol from syncytia induced by Heterodera schachtii in Arabidopsis roots
New Phytol.
201
476-485
2014
Arabidopsis thaliana (O82200), Arabidopsis thaliana (Q8H1S0), Arabidopsis thaliana (Q8L799), Arabidopsis thaliana (Q9FJU4), Arabidopsis thaliana Col-0 (O82200), Arabidopsis thaliana Col-0 (Q8H1S0), Arabidopsis thaliana Col-0 (Q8L799), Arabidopsis thaliana Col-0 (Q9FJU4)
brenda
Chen, C.; Sun, X.; Duanmu, H.; Yu, Y.; Liu, A.; Xiao, J.; Zhu, Y.
Ectopic expression of a Glycine soja myo-inositol oxygenase gene (GsMIOX1a) in Arabidopsis enhances tolerance to alkaline stress
PLoS ONE
10
e0129998
2015
Arabidopsis thaliana (Q8L799), Glycine soja (A0A0B2PCG9), Glycine soja, Glycine soja 07256 (A0A0B2PCG9)
brenda
Sharma, I.; Dutta, R.K.; Singh, N.K.; Kanwar, Y.S.
High glucose-induced hypomethylation promotes binding of Sp-1 to myo-inositol oxygenase implication in the pathobiology of diabetic tubulopathy
Am. J. Pathol.
187
724-739
2017
Homo sapiens, Mus musculus (Q9QXN5), Mus musculus
brenda
Tominaga, T.; Sharma, I.; Fujita, Y.; Doi, T.; Wallner, A.K.; Kanwar, Y.S.
Myo-inositol oxygenase accentuates renal tubular injury initiated by endoplasmic reticulum stress
Am. J. Physiol. Renal Physiol.
316
F301-F315
2019
Homo sapiens, Mus musculus (Q9QXN5), Sus scrofa
brenda
Alok, A.; Kaur, J.; Tiwari, S.
Functional characterization of wheat myo-inositol oxygenase promoter under different abiotic stress conditions in Arabidopsis thaliana
Biotechnol. Lett.
42
2035-2047
2020
Triticum aestivum
brenda
Teng, F.; You, R.; Hu, M.; Liu, W.; Wang, L.; Tao, Y.
Production of D-glucuronic acid from myo-inositol using Escherichia coli whole-cell biocatalyst overexpressing a novel myo-inositol oxygenase from Thermothelomyces thermophile
Enzyme Microb. Technol.
127
70-74
2019
Arabidopsis thaliana (A0A178V136), Arabidopsis thaliana, Mus musculus (Q9QXN5), Mus musculus, Thermothelomyces thermophilus (G2QA66), Thermothelomyces thermophilus, Thermothelomyces thermophilus ATCC 42464 (G2QA66)
brenda
Dutta, R.K.; Kondeti, V.K.; Sharma, I.; Chandel, N.S.; Quaggin, S.E.; Kanwar, Y.S.
Beneficial effects of myo-inositol oxygenase deficiency in cisplatin-induced AKI
J. Am. Soc. Nephrol.
28
1421-1436.
2017
Mus musculus (Q9QXN5)
brenda
Deng, F.; Sharma, I.; Dai, Y.; Yang, M.; Kanwar, Y.S.
Myo-inositol oxygenase expression profile modulates pathogenic ferroptosis in the renal proximal tubule
J. Clin. Invest.
129
5033-5049
2019
Homo sapiens
brenda
Mertoglu, C.; Gunay, M.; Gurel, A.; Gungor, M.
Myo-inositol oxygenase as a novel marker in the diagnosis of acute kidney injury
J. Med. Biochem.
37
1-6.
2018
Homo sapiens
brenda
Zheng, S.; Hou, J.; Zhou, Y.; Fang, H.; Wang, T.T.; Liu, F.; Wang, F.S.; Sheng, J.Z.
One-pot two-strain system based on glucaric acid biosensor for rapid screening of myo-inositol oxygenase mutations and glucaric acid production in recombinant cells
Metab. Eng.
49
212-219
2018
Mus musculus (Q9QXN5)
brenda