EC Number   |
Inhibitors |
Structure |
|---|
   7.2.2.13 | 8-methoxycoumestrol |
inhibits the isozyme alpha1beta1 Na,K-ATPase, mechanism, overview |
   |
| 7.2.2.13 | A-769662 |
inhibits the Na+-K+-ATPase transport activity and cell surface abundance in L6 cells, which is independent of AMP kinase activation, overview |
|
| 7.2.2.13 | Ouabain |
interaction is dependent on the conformation and phosphorylation state of the protein |
|
| 7.2.2.13 | isovaleric acid |
isovaleric acid injection significantly inhibits Na+,K+-ATPase activity by 25% in cerebral cortex of rats 2 or 24 h after administration, while pre-treatment of rats with creatine completely prevents the inhibitory effects of isovaleric acid on Na+,K+-ATPase |
|
| 7.2.2.13 | oubain |
K+ completely abolishes oubain binding to alpha1-beta1 isoenzymes. Residual oubain binding is still observed at high K+ concentrations for alpha2-beta1 and alpha3-beta1 complexes |
|
| 7.2.2.13 | oubain |
K+ protects against inhibition, probably due to phosphorylating effect |
|
| 7.2.2.13 | Lyn kinase |
Lyn kinase directly binds to the Na+,K+-ATPase alpha3 subunit for regulation of activity |
|
| 7.2.2.13 | palytoxin |
mild, non-toxic, exposures to the Na+/K+-ATPase inhibitor palytoxin synergistically sensitizes the vulnerability of neurons to normally non-toxic concentrations of domoic acid, leaving NMDA receptor-mediated excitotoxic response unaltered. Palytoxin causes a voltage-sensitive Na+ channel-independent increase in intracellular Na+. Enhancement of the excitotoxic response to domoic acid by palytoxin is time-dependent and is not affected by gene expression inhibitors |
|
| 7.2.2.13 | more |
molecular docking and modelling, and inhibitory potencies of steroid-like compounds from Chinese medicinal products, used for promoting the blood circulation, with Na+,K+-ATPase, overview |
|
| 7.2.2.13 | (3E,5beta,15beta,16beta)-16-(acetyloxy)-3-[(2-aminoethoxy)imino]-8-methyl-14,15-epoxybufa-20,22-dienolide |
most potent inhibitor |
|
