EC Number   |
General Information |
Reference |
|---|
    1.1.1.40 | evolution |
the enzyme belongs to the malic superfamily and the NAD_bind_amino_acid_DH superfamily which is a member of the Rossmann fold superfamily |
-, 739641 |
| 1.1.1.40 | evolution |
the five PtNADP-ME isoforms cluster in a phylogenetic tree constructed with the whole set of plant NADP-ME sequences, classification into four groups. PtNADP-ME2 and PtNADPME3 cluster with the cytosolic dicot NADP-ME group (group II), while PtNADP-ME4 and PtNADP-ME5 are included in the plastidic dicot NADP-ME group (group III). The group IV comprises both monocot and dicot enzymes, including PtNADP-ME1. Neither of the PtNADP-ME isoforms is included in the monocot NADPMEs (group I) |
723150 |
| 1.1.1.40 | malfunction |
antisense reduction of NADP-ME alters C3-C4 cycle coordination. Increase in Rubisco and phosphoenolpyruvate carboxylase activity and leaf nitrogen in low-NADP-ME antisense plants |
723474 |
| 1.1.1.40 | malfunction |
deletion of the enzyme gene in a Magnaporthe oryzae-resistant rice cultivar disrupts innate immunity against the rice blast fungus |
739074 |
| 1.1.1.40 | malfunction |
down-regulation of isoform ME2 reciprocally activates p53 through distinct Mdm2 and AMP-activated kinase -mediated mechanisms in a feed-forward manner, bolstering this pathway and enhancing p53 activation. Down-regulation of isoform ME2 also modulates the outcome of p53 activation leading to strong induction of senescence, but not apoptosis |
739163 |
| 1.1.1.40 | malfunction |
enzyme inactivation improves the anaerobic production of four-carbon dicarboxylic acids by recombinant Escherichia coli strains expressing oxaloacetate-forming pyruvate carboxylase |
760378 |
| 1.1.1.40 | malfunction |
knockdown of malic enzyme 2 suppresses lung tumor growth, induces differentiation and impacts PI3K/AKT signaling. In the A-549 non-small cell lung cancer cell line, ME2 depletion inhibits cell proliferation and induces cell death and differentiation, accompanied by increased reactive oxygen species (ROS) and NADP1/NADPH ratio, a drop in ATP, and increased sensitivity to cisplatin. ME2 knockdown impacts phosphoinositide-dependent protein kinase 1 (PDK1) and phosphatase and tensin homolog (PTEN) expression, leading to AKT inhibition. Depletion of ME2 leads to malate accumulation and pyruvate decrease, and exogenous cell permeable dimethyl-malate mimics the ME2 knockdown phenotype. Both ME2 knockdown and dimethyl-malate treatment reduce A-549 cell growth in vivo. Survival of ME2 knockdown cells is exquisitely dependent on glucose. Phenotype, overview |
741406 |
| 1.1.1.40 | malfunction |
knockdown of ME3, but not ME1 or ME2 (both EC 1.1.1.39) alone or together, inhibits insulin release stimulated by glucose, pyruvate or 2-aminobicyclo [2,2,1]heptane-2-carboxylic acid-plus-glutamine |
741010 |
| 1.1.1.40 | malfunction |
loss of cytosolic NADP-malic enzyme 2 in Arabidopsis thaliana is associated with enhanced susceptibility to Colletotrichum higginsianum, transient apoplastic reactive oxygen species production after elicitation and callose papilla formation after infection are dampened in mutant nadp-me2 |
723277 |
| 1.1.1.40 | malfunction |
seeds of Arabidopsis thaliana lacking a functional enzyme isoform NADP-ME1 have reduced seed viability relative to the wild type. Seeds of the loss-of-function mutant display higher levels of protein carbonylation than those of the wild type |
762132 |
