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Gene Information
Gene symbol: MIOX
Gene name: myo-inositol oxygenase
HGNC ID: 14522
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | ACOT2 | 1 hits |
| 2 | GREM1 | 1 hits |
| 3 | HSD17B3 | 1 hits |
| 4 | NFE2L2 | 1 hits |
| 5 | PRKAR2A | 1 hits |
| 6 | PTDSS1 | 1 hits |
| 7 | RAF1 | 1 hits |
| 8 | RAP1B | 1 hits |
| 9 | SPP1 | 1 hits |
| 10 | SST | 1 hits |
| 11 | SULT2A1 | 1 hits |
| 12 | TGFB1 | 1 hits |
| 13 | TIMM44 | 1 hits |
| 14 | UBA52 | 1 hits |
| 15 | VIM | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 20335317 | The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation. |
| 2 | 20335317 | These changes were significantly reduced by the inhibitors of PKC, aldose reductase, Ras farnesylation, and MEK1. |
| 3 | 20335317 | Expression of E-cadherin and vimentin paralleled in cells overexpressing RSOR/MIOX or subjected to high-glucose ambience. |
| 4 | 20335317 | The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation. |
| 5 | 20335317 | These changes were significantly reduced by the inhibitors of PKC, aldose reductase, Ras farnesylation, and MEK1. |
| 6 | 20335317 | Expression of E-cadherin and vimentin paralleled in cells overexpressing RSOR/MIOX or subjected to high-glucose ambience. |
| 7 | 21252517 | Several genes, such as Tim44 (translocase of inner mitochondrial membrane- 44), RSOR/MIOX (renal specific oxidoreductase/myo-inositol oxygenase), UbA52, Rap1b (Ras-related GTPase), gremlin, osteopontin, hydroxysteroid dehydrogenase- 3β isotype 4 and those of the Wnt signaling pathway, were identified as differentially expressed genes in kidneys of diabetic rodents. |
| 8 | 21652700 | Using phosphothreonine, protein kinase A (PKA), and PKC substrate antibodies, analyses of kidney lysates of diabetic animals and LLC-PK1/HK-2 cells subjected to HG ambience indicated MIOX to be a phosphoprotein. |
| 9 | 21652700 | Treatment with HG or oxidants or overexpression of MIOX induced nuclear translocation of redox-sensitive transcription factor Nrf2, which binds to antioxidant response elements of various promoters. |
| 10 | 21652700 | Using phosphothreonine, protein kinase A (PKA), and PKC substrate antibodies, analyses of kidney lysates of diabetic animals and LLC-PK1/HK-2 cells subjected to HG ambience indicated MIOX to be a phosphoprotein. |
| 11 | 21652700 | Treatment with HG or oxidants or overexpression of MIOX induced nuclear translocation of redox-sensitive transcription factor Nrf2, which binds to antioxidant response elements of various promoters. |
| 12 | 22707198 | Microarray data demonstrated for the first time that overexpression of the genes encoding IL-1 receptor, lipid metabolic enzymes (e.g. |
| 13 | 22707198 | Mte1, Ptdss1, and Sult2a1), myo-inositol oxygenase, glucagon, and somatostatin as well as down-regulation of olfactory receptor 984 and mitochondrial ribosomal protein, which are highly linked to T1DM etiology. |
| 14 | 22707198 | The results of the microarray analysis revealed that up-regulation of IL-2, IL12a, and leptin receptor and down-regulation of PIK3 played important physiological roles in the onset of T2DM. |