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Quasi-specific access of the potassium channel inactivation gate

Author

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  • Gaurav Venkataraman

    (Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health
    Present address: CNC Building, Stanford University, Palo Alto, California 94304, USA)

  • Deepa Srikumar

    (Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health)

  • Miguel Holmgren

    (Molecular Neurophysiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health)

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.

Suggested Citation

  • Gaurav Venkataraman & Deepa Srikumar & Miguel Holmgren, 2014. "Quasi-specific access of the potassium channel inactivation gate," Nature Communications, Nature, vol. 5(1), pages 1-6, September.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5050
    DOI: 10.1038/ncomms5050
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