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EC Number
General Information
Commentary
Reference
evolution
MIOX proteins are highly conserved and present in nearly all eukaryotes
malfunction
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
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; 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
increased expression in diabetic kidneys may contribute to tubulointerstitial injury and development of diabetic nephropathy
malfunction
loss-of-function mutants in MIOX genes contain alterations in myo-inositol levels and growth changes in the root; 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
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; 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; 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; 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
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
metabolism
a mechanism links MIOX to impaired mitochondrial quality control during tubular injury in the pathogenesis of diabetic kidney disease
Results 1 - 10 of 24 > >>