KCNQ4 is expressed in inner and outer hair cells of the inner ear where it determines electrical excitability. Accordingly, loss of function mutations of the KCNQ4 gene cause hearing loss. The present study utilized the Xenopus oocyte system to explore effects of SGK isoforms on KCNQ4 mediated K+-currents: KCNQ4 channels activated in a voltage dependent manner with half maximal activation at -10 mV. The peak channel activity was significantly increased by prepulsing. Coexpression of wild type SGK1 but not coexpression of the inactive mutant SGK1 significantly increased current amplitudes by 67 % and significantly increased the resting potential of KCNQ4 expressing oocytes. We describe for the first time a prepulse dependence of KCNQ4 channels with increased currents after hyperpolarizing prepulses and show that coexpression of SGK1 significantly attenuated the effect of prepulsing on peak currents. Mutation of Ser to Asp or Ala in the putative phosphorylation consensus sequence in KCNQ4 significantly decreased the sensitivity to SGK1-coexpression. In conclusion, SGK1 regulates amplitude currents and kinetic properties of KCNQ4 channel activity, an effect sensitive to mutations in the SGK1 consensus sequence of the channel.