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Results 1 - 10 of 14 > >>
EC Number General Information Commentary Reference
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1metabolism proton translocation and nucleotide exchange are tightly coupled by direct interactions between residue H664 and NADP(H), the attachment and detachment of NADP(H)-bound domain dIII is strictly dependent on the protonation state of H664 and opens the proton channel to the opposite sides of the membrane. The forward reaction occurs under a high proton motive force and an excess of NADP+. After hydride transfer, dIII-NADPH swivels down and attaches to dII-H664, opening it to the P side. This enables the protonation of H664 from the P side. Nucleotide exchange then follows. dIII-NADP+ detaches from dII-H664+, this opens dII to the N side where H664+ is deprotonated. Domain dIII-NADP+ then associates with dI, allowing for hydride transfer. All the steps can be easily reversed in the appropriate conditions 765468
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1metabolism transhydrogenase PntAB is a major source of NADPH that is required for biosynthesis in Escherichia coli 659437
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function disruption of subunit PntA results in phenotypic growth defects observed under low light intensities in the presence of glucose. Under autotrophic conditions the disruption mutant does not differ from the wild-type strain. The phenotypic defects of the mutant are accompanied by significant malfunction and damage of the photosynthetic machinery 743367
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function in a congenic mouse model carrying a mutated NNT gene, the absence of NNT activity results in lower total NADPH sources activity in the brain mitochondria of young mice, which is partially compensated in aged mice. Nonsynaptic mitochondria show higher NNT activity than synaptic mitochondria. In the absence of NNT, an increased release of H2O2 from mitochondria is observed when the metabolism of respiratory substrates occurs with restricted flux through relevant mitochondrial NADPH sources or when respiratory complex I is inhibited. Mitochondria from Nnt-/- brains are unable to sustain NADP in its reduced state when energized in the absence of carbon substrates 765255
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function in cardiac mitochondria from NNT-competent mice, H2O2 emission is equally low with pyruvate/malate or 2-oxoglutarate as substrates. In NNT-deficient mitochondria, H2O2 emission is higher with 2-oxoglutarate than with pyruvate/malate as substrate, and further potentiated by complex I blockade. NADH from 2-oxoglutarate dehydrogenase selectively shuttles to NNT for NADPH formation rather than to complex I of the respiratory chain for ATP production. In heart failure, 2-oxoglutarate dehydrogenase/NNT-dependent NADPH formation ameliorates oxidative stress imposed by complex I blockade 764052
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function NNT expression and activity are elevated in response to the mitochondrial dysfunction and oxidative stress associated with angiotensin II treatment. Knockdown of NNT leads to a significant elevation of mitochondrial ROS production and impaired glutathione peroxidase and glutathione reductase activities associated with a reduction in the NADPH/NADP+ ratio. Loss of NNT also promotes mitochondrial dysfunction, disruption of the mitochondrial membrane potential, and impaired ATP production in response to angiotensin II. The loss of NNT augments endothelial nitric oxide synthase phosphorylation at Ser1177, but neither endothelial nitric oxide synthase activity nor nitric oxide production are similarly increased 765744
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function NNT is largely responsible for the acute glucose-induced rise in pancreatic islet NADPH/NADP+ ratio and decrease in mitochondrial glutathione oxidation, with a small impact on cytosolic glutathione. These effects results from a glucose-dependent reduction in NADPH consumption by NNT reverse mode of operation, rather than from a stimulation of its forward mode of operation. Lack of NNT in islets decreases their sensitivity to exogenous H2O2 at non-stimulating glucose. The lack of NNT does not alter the glucose-stimulation of Ca2+ influx and upstream mitochondrial events, but it markedly reduces both phases of glucose stimulation of insulin secretion by altering Ca2+-induced exocytosis and its metabolic amplification 765394
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function NNT loss does not compromise the mitochondrial thioredoxin antioxidant system but compromises mitochondrial oxidative capacity. The activity of complex I-III is significantly reduced following NNT knockdown. NNT loss does not disrupt Fe-S cluster biosynthesis but is associated with decreases in mitochondrial Fe-S protein function and disrupts fatty acid metabolism 765163
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function NTH has an essential structural role in crystalloid biogenesis, whilst its enzymatic activity is required for sporozoite development. An enzyme null mutant develops normally in the mouse. NTH-KO parasites display normal gametocyte development, gametogenesis, and form ookinetes of normal size and shape. Pigment in these ookinetes is more dispersed and not found in clusters that surround and highlight the crystalloids. Absence of these pigment clusters is caused by loss of crystalloid formation. NTH-KO parasites developed oocyst numbers comparable to wild-type, but these oocysts fail to produce sporozoites 764573
Display the word mapDisplay the reaction diagram Show all sequences 7.1.1.1physiological function overexpression of pyridine nucleotide transhydrogenase, PntAB, results in a significant increase in biomass and glycolic acid titer and yield. Improved redox homeostasis resulting from PntAB overexpression positively affects the anabolic rate of the cell. PntAB overexpression result in 154 and 37% increase in NAD+/NADH ratio, at 48 and 72 h, respectively, while the NADP+ concentrations are 70 and 30% lower at 24 and 72 h. Expression of PntAB in an optimized glycolic acid-producing strain improves the growth and product titer significantly 765193
Results 1 - 10 of 14 > >>