EC Number   |
General Information |
Reference |
|---|
    2.7.4.6 | drug target |
as an essential enzyme in Aspergillus fumigatus, nucleoside-diphosphate kinase is an attractive target for antifungals |
-, 761072 |
| 2.7.4.6 | drug target |
the enzyme may have potential target as a new therapeutic strategy against white spot syndrome virus infection in shrimp |
762220 |
| 2.7.4.6 | evolution |
enzymes from Halomonas sp strain 593 and Chromohalobacter salexigens strain DSM3043 show very high sequence homology to each other, in both enzymes, residue C139 is conserved |
-, 738396 |
| 2.7.4.6 | malfunction |
deletion in the ndk gene results in significantly reduced adhesion and invasion of Epithelioma papulosum cyprini (EPC) cells and biofilm formation |
-, 761842 |
| 2.7.4.6 | malfunction |
depletion of NME3 causes renal developmental defects |
761483 |
| 2.7.4.6 | malfunction |
loss of Nm23-H1 in diploid cells leads to cytokinetic furrow regression, followed by cytokinesis failure and generationof tetraploid cells. The loss of Nm23-H1, an event suspected to promote metastasis, additionally functions at an earlier stage of tumor development to drive the acquisition of chromosomal instability |
723631 |
| 2.7.4.6 | malfunction |
mutations in the NME3 gene may aggravate the ciliopathy phenotypes observed in humans |
761483 |
| 2.7.4.6 | malfunction |
nucleoside diphosphate kinase B depletion alone impairs caveolae formation, vascular endothelial growth factor (VEGF)-induced phosphorylation of c-Src/Cav-1 but not of ERK1/2/AKT/eNOS. Primary mouse brain endothelial cells from nucleoside diphosphate kinase Bx02-/-x02 mice show no change in caveolae content and transendothelial-electrical resistance upon VEGF stimulation. Nucleoside diphosphate kinase Bx02-/-x02 primary mouse brain endothelial cells display an accumulation of intracellular vesicles and increased caveolin-1 levels. Dextran tracer analysis shows increased vascular permeability in the brain of nucleoside diphosphate kinase Bx02-/-x02 mice compared to wild type |
761594 |
| 2.7.4.6 | malfunction |
the stable knockout mutant Mtb Ndk-AS displays attenuated intracellular survival along with reduced persistence in the lungs of infected mice. Mutant Mtb Ndk-AS, which lost the capacity to disrupt Rac1-p67phox interaction, induces a strong ROS production. Given the established link between NOX2 activation and apoptosis, the proportion of Annexin V positive cells and levels of intracellular active caspase 3 are significantly higher in cells infected with Mtb Ndk-AS compared to wild-type Mtb. Knockdown of Ndk converts Mtb into a pro-apoptotic mutant strain that has a phenotype of increased susceptibility to intracellular killing and reduced virulence in vivo, phenotype, overview. Disruption of Ndk expression converts Mtb into a mutant strain that induces strong ROS and apoptosis responses. This phenotype is associated with reduced survival of Ndk mutant in vitro and in vivo |
739521 |
| 2.7.4.6 | metabolism |
nucleoside diphosphate kinase and flagellin from Pseudomonas aeruginosa induce interleukin 1 expression via the Akt/NF-kappaB signaling pathways |
738370 |
