EC Number   |
General Information |
Reference |
|---|
   7.2.2.9 | malfunction |
deletion mutant analysis demonstrates that CopA is an effective copper pump at low and high copper concentrations. The DELTAcopA mutant shows highly reduced growth at 2 mM. High toxicity of copper to the DELTAcopA |
720396 |
| 7.2.2.9 | malfunction |
deletion mutant analysis demonstrates that CopB is low-affinity copper export ATPase. For the DELTAcopB mutant strain 1.4 mM CuSO4 is needed to slow the onset and beginning of stationary phase at lower levels |
720396 |
| 7.2.2.9 | malfunction |
inactivation of ATP7A results in the neurodegenerative disorder Menkes disease |
719946 |
| 7.2.2.9 | malfunction |
mutations in the gene encoding ATP7B cause copper toxicity (Wilson disease) by altering enzyme trafficking and stability |
718542 |
| 7.2.2.9 | malfunction |
ran1 mutants display ethylene-like responses to the ethylene antagonist trans-cyclooctene and have altered copper homeostasis |
719895 |
| 7.2.2.9 | malfunction |
Wilson disease is caused by mutations in the Cu-transporting ATPase ATP7B |
719924 |
| 7.2.2.9 | metabolism |
copper delivery to the secretory pathway in yeast, and enzymatic cycle of Ccc2, modelling, overview |
-, 711976 |
| 7.2.2.9 | metabolism |
gene regulation of ATP7A by iron deprivation |
710815 |
| 7.2.2.9 | metabolism |
the catalytic cycle of ATP7A/7B is coupled to their intracellular trafficking, and these activities endow them with the biosynthetic and homeostatic functions that underlie the diverse range of physiological processes that depend upon their activities |
712175 |
| 7.2.2.9 | more |
ATP7B overexpression transfers a stable, positive selection advantage to MSCs in a high copper environment |
711097 |
