EC Number   |
General Information |
Reference |
|---|
    1.6.1.2 | malfunction |
C57BL/6J mice, which have a deletion in the Nnt gene, exhibit greater resistance to acute pulmonary infection with Streptococcus pneumoniae. Macrophages from these mice generate more reactive oxygen species and establish a stronger inflammatory response to this pathogen |
-, 724953 |
| 1.6.1.2 | malfunction |
enzyme inhibition decreases NADPH levels, decreases thioredoxin and thioredoxin reductase activity, and increases toxicity to oxidative stress |
742857 |
| 1.6.1.2 | malfunction |
enzyme knockdown decreases reductive carboxylation and stimulates glucose catabolism in the tricarboxylic acid cycle |
742841 |
| 1.6.1.2 | malfunction |
gene disruption of pntA results in phenotypic growth defects observed under low light intensities in the presence of glucose, whereas under autotrophic conditions the mutant does not differ from the wild type strain |
743367 |
| 1.6.1.2 | malfunction |
knockdown of the enzyme inhibits the contribution of glutamine to the tricarbonic acid cycle and activates glucose catabolism in SkMel5 melanoma cells. The increase in glucose oxidation partially occurs through pyruvate carboxylase and renders NNT knockdown cells more sensitive to glucose deprivation. Importantly, knocking down NNT inhibits reductive carboxylation in SkMel5 and 786-O renal carcinoma cells. Overexpression of NNT is sufficient to stimulate glutamine oxidation and reductive carboxylation, whereas it inhibits glucose catabolism in the TCA cycle, with impairment of the NAD(P)H/NAD(P)+ ratios |
-, 725514 |
| 1.6.1.2 | malfunction |
lack of enzyme activity impairs peroxide metabolism in intact mitochondria |
742893 |
| 1.6.1.2 | malfunction |
small interfering RNA silencing of the enzyme in PC-12 cells results in decreased cellular NADPH levels, altered redox status of the cell in terms of decreased GSH/GSSG ratios and increased H2O2 levels, thus leading to an increased redox potential (a more oxidized redox state). NNT knockdown results in a decrease of oxidative phosphorylation while anaerobic glycolysis levels remain unchanged. Decreased oxidative phosphorylation was associated with 1. inhibition of mitochondrial pyruvate dehydrogenase and succinyl-CoA:3-oxoacid CoA transferase activity, 2. reduction of NADH availability, 3. decline of mitochondrial membrane potential, and 4. decrease of ATP levels |
724435 |
| 1.6.1.2 | malfunction |
spontaneous C57BL/6J(B6J-NntMUT) mutant mice show major redox alterations in respiring mitchondria, including an absence of transhydrogenation between NAD+ and NADP+, higher rates of H2O2 release, the spontaneous oxidation of NADPH,the poor ability to metabolize organic peroxide, and a higher susceptibility to undergo Ca2+-induced mitochondrial permeability transition. Liver mitochondria from B6J-NntMUT mice do not possess NNT activity. The mitochondria of mutant B6J-NntMUT mice exhibit increased oxidized/reduced glutathione ratios as compared to wild-type B6JUnib-NntW mice, phenotypes, overview |
-, 725068 |
| 1.6.1.2 | malfunction |
the absence of enzyme leads to variation in mitochondrial function and contributes to a unique mitochondrial redox phenotype that influences susceptibility to hypertension by contributing to endothelial and vascular dysfunction |
-, 742757 |
| 1.6.1.2 | metabolism |
the enzyme coordinates glutamine and glucose metabolism in the tricarboxylic acid cycle |
742841 |
