摘要

Voltage-dependent and calcium-activated K+ (MaxiK, BK) channels are widely expressed in many tissues and organs where they play various physiological roles. Here we report discovery of a functional trafficking signal in MaxiK channel accessory beta 4 subunit that could regulate activity of MaxiK alpha subunit (hSlo) on the plasma membrane. We demonstrate that beta 4 is mostly retained within the cell and removal or mutation of beta 4 trafficking signal significantly enhances its surface expression in HEK293T expression system. In hippocampal slices and cultured neurons we also observed significant beta 4 expressions within the neurons. Finally, we show that unlike SV1 and beta 1 subunits, beta 4 shows no dominant-negative effect on MaxiK channel alpha subunit. Taken together, we propose beta 4 subunit of MaxiK channel is mostly retained within the cells without interfering with other subunits. Removal of beta 4 retention signal increases its surface expression that may lead to reduction of the MaxiK channel activity and neuronal excitability.

  • 出版日期2014-3-17