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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells.

Heteromeric KCNQ5/Q3 channels were stably expressed in Chinese Hamster ovary cells and characterized using the whole cell voltage-clamp technique. KCNQ5/Q3 channels were activated by the novel anticonvulsant, retigabine (EC(50) 1.4 microM) by a mechanism that involved drug-induced, leftward shifts in the voltage-dependence of channel activation (-31.8 mV by 30 microM retigabine). KCNQ5/Q3 channels were inhibited by linopirdine (IC(50) 7.7 microM) and barium (IC(50) 0.46 mM), at concentrations similar to those required to inhibit native M-currents. These findings identify KCNQ5/Q3 channels as a molecular target for retigabine and raise the possibility that activation of KCNQ5/Q3 channels may be responsible for some of the anti-convulsant activity of this agent. Furthermore, the sensitivity of KCNQ5/Q3 channels to linopirdine supports the possibility that potassium channels comprised of KCNQ5 and KCNQ3 may make a contribution to native M-currents.[1]

References

  1. Characterization of KCNQ5/Q3 potassium channels expressed in mammalian cells. Wickenden, A.D., Zou, A., Wagoner, P.K., Jegla, T. Br. J. Pharmacol. (2001) [Pubmed]
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