EC Number   |
General Information |
Reference |
|---|
    1.1.1.39 | malfunction |
dme mutants of the broad-host-range Sinorhizobium sp. strain NGR234 form nodules whose level of N2 fixation vary from 27 to 83% (plant dry weight) of the wild-type level, depending on the host plant inoculated. The single dme mutant fixes N2 at reduced rate. A pckA dme double mutant has no N2-fixing activity, PCK is phosphoenolpyruvate carboxykinase. Symbiotic phenotypes of NGR234 and NGR234 dme mutants on different host plants, overview |
-, 721353 |
| 1.1.1.39 | malfunction |
knockdown of ME1 does not inhibit insulin release stimulated by glucose, pyruvate or 2-aminobicyclo [2,2,1]heptane-2-carboxylic acid-plus-glutamine |
741010 |
| 1.1.1.39 | malfunction |
the single Sco2951 and the double Sco2951 Sco5261 mutants, deficient in ME-NAD and ME-NADP, EC 1.1.1.40, activity, display a strong reduction in the production of the polyketide antibiotic actinorhodin. Additionally, the Sco2951/Sco5261 mutant shows a decrease in stored triacylglycerides during exponential growth |
-, 721357 |
| 1.1.1.39 | metabolism |
fish spermatozoa contain a glycolytic pathway, tricarboxylic acid cycle and oxidative phosphorylation system, all of which are key pathways contributing to ATP synthesis, involving the enzyme |
722082 |
| 1.1.1.39 | metabolism |
the citrate-malate-pyruvate cycle serves to regenerate NAD+ and maintain glycolytic flux. Pyruvate cycles all lead to the exchange of reducing equivalents from mitochondrial NADH to cytosolic NADPH. Malic enzyme is integral to the coupling of metabolism with insulin secretion |
712942 |
| 1.1.1.39 | metabolism |
the malic enzyme is involved in the (S)-malate catabolic pathways and the putative gluconeogenic pathways, overview |
-, 710948 |
| 1.1.1.39 | more |
deletion of either the gene encoding the histidine kinase or the response regulator of the TC system results in the loss of the ability to grow on L-malic acid, thus indicating that the cognate TC system regulates and is essential for the expression of malic enzyme. Expression of maeE is induced in the presence of L-malic acid and repressed by glucose, whereas TC system expression is induced by L-malic acid and is not repressed by glucose |
-, 710948 |
| 1.1.1.39 | more |
enzyme activity is allosterically regulated by acetyl-CoA |
-, 711524 |
| 1.1.1.39 | more |
higher expression of ME2 correlates with the degree of cell de-differentiation. Knockdown of ME2 leads to induction of erythroid differentiation, and diminished proliferation of tumor cells and increased apoptosis in vitro. ME2 knockdown also totally abolishes growth of K562 cells in nude mice. Depletion of endogenous ME2 levels enhances reactive oxygen species, increases NAD+/NADH and NADP+/NADPH ratio and inhibits ATP production in K562 cells. ME2 depletion resulted in high orotate levels, suggesting potential impairment of pyrimidine metabolism |
713373 |
| 1.1.1.39 | more |
identification of specific domains of the primary structure, which are involved in the differential allosteric regulation. Different properties of NAD-ME1, -2, and -H, mitochondrial NAD-ME activity may be regulated by varying native association in vivo, rendering enzymatic entities with distinct allosteric regulation to fulfill specific roles, overview |
712417 |
