Any feedback?
Literature summary for 2.7.4.3 extracted from
- A mutation in CFTR modifies the effects of the adenylate kinase inhibitor Ap5A on channel gating (2008), Biophys. J., 95, 5178-85.
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| expression in HeLa cell | Homo sapiens |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| L1254A | mutant in cystic fibrosis transmembrane conductance regulator. Cystic fibrosis transmembrane conductance regulator shows adenylate kinase activity in the presence of ATP plus physiologic concentrations of AMP or ADP. P1,P5-di(adenosine-5') pentaphosphate increases the activity of the mutant. The mutation increases the EC50 for ATP by more than 10-fold and reduces channel activity by prolonging the closed state. P1,P5-di(adenosine-5') pentaphosphate changes the relationship between ATP concentration and current. At submaximal ATP concentrations, P1,P5-di(adenosine-5') pentaphosphate stimulates current by stabilizing the channel open state | Homo sapiens |
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| P1,P5-di(adenosine-5')pentaphosphate | - |
Homo sapiens |  |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.
Release 2023.1 (January 2023)
Legal
Curated at
Member of
