nicotinamide adenine dinucleotide kinases are attractive for inhibitor development, since they catalyze the phosphorylation of NAD to NADP, which is an essential step of NADP metabolism
nicotinamide adenine dinucleotide kinases are attractive for inhibitor development, since they catalyze the phosphorylation of NAD to NADP, which is an essential step of NADP metabolism
nicotinamide adenine dinucleotide kinases are attractive for inhibitor development, since they catalyze the phosphorylation of NAD to NADP, which is an essential step of NADP metabolism
the reduction of the NADP(H) level in the sll1415 mutant leads to a significant accumulation of glucose-6-phosphate and a loss of photoheterotrophic growth
slr0400-deficient mutant possesses a metabolic profile differed from that of wild-type. It shows metabolic changes in the levels of sugar phosphates (glucose-6-phosphate, ribulose-5-phosphate, 6-phosphogluconate, and fructose-6-phosphate), implying that the upper parts of the glycolytic pathway, the oxidative pentose phosphate pathway, and the Calvin cycle are affected by the disruption of slr0400
the mutant plant osnadk1 in which OsNADK1 is knocked out is a dwarf at the heading stage and has decreased NADP(H)/NAD(H), ascorbic acid (ASA)/dehydroascorbate (DHA) and reduced glutathione (GSH)/oxidized glutathione (GSSG) ratios, which leads to increased oxidation states in the rice cells and sensitivity to drought. Certain stress-related genes show differential expression patterns in osnadk1 under both normal growth and drought-stress conditions compared with wild-type. Compared with the wild-type plants, osnadk1 has a reduced height, smaller flag-leaf dimensions and lower chlorophyll contents at the early filling stage of plant growth
the enzyme regulates the size of the NADPH pool and insulin secretion in pancreatic beta-cells. Enzyme overexpression also protects beta-cells against oxidative damage by the redox cycling agent menadione and reverses menadione-mediated inhibition of glucose-stimulated insulin secretion
the enzyme regulates the size of the NADPH pool and insulin secretion in pancreatic beta-cells. Enzyme overexpression also protects beta-cells against oxidative damage by the redox cycling agent menadione and reverses menadione-mediated inhibition of glucose-stimulated insulin secretion
the NAD kinase gene sll1415 inhibits the transcription of genes involved in redox homeostasis and exerts stronger effects on methyl viologen tolerance than NAD kinase gene slr0040
the enzyme is required for the de novo synthesis of NADP+ from NAD+. In neutrophils, the enzyme plays an essential role by providing sufficient levels of NADPH to support a robust oxidative burst