ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- β2 and β3a regulatory subunits can coassemble in the same BK channels.The Journal of general physiology · 2026Article
- Disruption of a side portal pathway permits closed-state inactivation by BK β subunit N termini.The Journal of general physiology · 2025Article
- Resurgent current in context: Insights from the structure and function of Na and K channels.Biophysical journal · 2024Review
- Dyshomeostatic modulation of CaeLife · 2021Article
- Regulation of BK Channels by Beta and Gamma Subunits.Annual review of physiology · 2019Review
- Regulatory γ1 subunits defy symmetry in functional modulation of BK channels.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Modulation of BK Channel Function by Auxiliary Beta and Gamma Subunits.International review of neurobiology · 2016Review
- BK channel opening involves side-chain reorientation of multiple deep-pore residues.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Stereospecific binding of a disordered peptide segment mediates BK channel inactivation.Nature · 2012Article
- Interactions between beta subunits of the KCNMB family and Slo3: beta4 selectively modulates Slo3 expression and function.PloS one · 2009Article
- Species-specific Differences among KCNMB3 BK beta3 auxiliary subunits: some beta3 N-terminal variants may be primate-specific subunits.The Journal of general physiology · 2008Article
- Modes of operation of the BKCa channel beta2 subunit.The Journal of general physiology · 2007Article
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Authors and funding
4 authors.
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Abstract
Large-conductance, Ca2+- and voltage-activated K+ (BK) channels are broadly expressed proteins that respond to both cellular depolarization and elevations in cytosolic Ca2+. The characteristic functional properties of BK channels among different cells are determined, in part, by tissue-specific expression of auxiliary beta subunits. One important functional property conferred on BK channels by beta subunits is inactivation. Yet, the physiological role of BK channel inactivation remains poorly understood. Here we report that as a consequence of a specific mechanism of inactivation, BK channels containing the beta3a auxiliary subunit exhibit an anomalous slowing of channel closing. This produces a net repolarizing current flux that markedly exceeds that expected if all open channels had simply closed. Because of the time dependence of inactivation, this behavior results in a Ca2+-independent but time-dependent increase in a slow tail current, providing an unexpected mechanism by which use-dependent changes in slow afterhyperpolarizations might regulate electrical firing. The physiological significance of inactivation in BK channels mediated by different beta subunits may therefore arise not from inactivation itself, but from the differences in the amplitude and duration of repolarizing currents arising from the beta-subunit-specific energetics of recovery from inactivation.
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