title: Quasi-specific access of the potassium channel inactivation gate.
abstract: Many voltage-gated potassium channels open in response to membrane depolarization and then inactivate within milliseconds. Neurons use these channels to tune their excitability. In Shaker K(+) channels, inactivation is caused by the cytoplasmic amino terminus, termed the inactivation gate. Despite having four such gates, inactivation is caused by the movement of a single gate into a position that occludes ion permeation. The pathway that this single inactivation gate takes into its inactivating position remains unknown. Here we show that a single gate threads through the intracellular entryway of its own subunit, but the tip of the gate has sufficient freedom to interact with all four subunits deep in the pore, and does so with equal probability. This pathway demonstrates that flexibility afforded by the inactivation peptide segment at the tip of the N-terminus is used to mediate function.
authors.affiliation: 1] Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA [2].
authors.forename: Gaurav
authors.initials: G
authors.lastname: Venkataraman
authors.affiliation: Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Deepa
authors.initials: D
authors.lastname: Srikumar
authors.affiliation: Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Miguel
authors.initials: M
authors.lastname: Holmgren
mesh_terms: D015640:Ion Channel Gating; D015221:Potassium Channels / Q000737:chemistry* / Q000502:physiology
chemical_list: D015221:Potassium Channels