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dependent (Kv)4.2-encoded A-type K ϩ channels play an important role in controlling neuronal excitability and are subject to modulation by various protein kinases, including ERK. In studies of ERK modulation, the organic compound U0126 is often used to suppress the activity of MEK, which is a kinase immediately upstream from ERK. We have observed that the inactivation time constant of heterologously expressed Kv4.2 channels was accelerated by U0126 at 1-20 M. This effect, however, was not Kv4doi:10.1152/ajpcell.00206.2005 pmid:16135544 fatcat:ql6mx5zvj5cfze6s4gc6zm6eki