ArticleThe Journal of general physiology2001
Inactivation of BK channels mediated by the NH(2) terminus of the beta3b auxiliary subunit involves a two-step mechanism: possible separation of binding and blockade.
Article in The Journal of general physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Disruption of a side portal pathway permits closed-state inactivation by BK β subunit N termini.The Journal of general physiology · 2025Article
- Ball-and-chain inactivation of a human large conductance calcium-activated potassium channel.Nature communications · 2025Article
- Reverse-engineered models reveal differential membrane properties of autonomic and cutaneous unmyelinated fibers.PLoS computational biology · 2024Article
- Resurgent current in context: Insights from the structure and function of Na and K channels.Biophysical journal · 2024Review
- The Sulfated Steroids Pregnenolone Sulfate and Dehydroepiandrosterone Sulfate Inhibit theMolecular pharmacology · 2022Article
- LINGO1 is a regulatory subunit of large conductance, CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Regulation of BK Channels by Beta and Gamma Subunits.Annual review of physiology · 2019Review
- Article
- Presynaptic BK channels control transmitter release: physiological relevance and potential therapeutic implications.The Journal of physiology · 2016Review
- Reconstruction of Cell Surface Densities of Ion Pumps, Exchangers, and Channels from mRNA Expression, Conductance Kinetics, Whole-Cell Calcium, and Current-Clamp Voltage Recordings, with an Application to Human Uterine Smooth Muscle Cells.PLoS computational biology · 2016Article
- Modulation of BK Channel Function by Auxiliary Beta and Gamma Subunits.International review of neurobiology · 2016Review
- A fast BK-type KCa current acts as a postsynaptic modulator of temporal selectivity for communication signals.Frontiers in cellular neuroscience · 2014Article
- Inter-α/β subunits coupling mediating pre-inactivation and augmented activation of BKCa(β2).Scientific reports · 2013Article
- Stereospecific binding of a disordered peptide segment mediates BK channel inactivation.Nature · 2012Article
- BK channel activation: structural and functional insights.Trends in neurosciences · 2010Review
- Closed-channel block of BK potassium channels by bbTBA requires partial activation.The Journal of general physiology · 2009Article
- Differential regulation of action potentials by inactivating and noninactivating BK channels in rat adrenal chromaffin cells.Biophysical journal · 2009Article
- N-terminal inactivation domains of beta subunits are protected from trypsin digestion by binding within the antechamber of BK channels.The Journal of general physiology · 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
- BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
A family of auxiliary beta subunits coassemble with Slo alpha subunit to form Ca(2)+-regulated, voltage-activated BK-type K(+) channels. The beta subunits play an important role in regulating the functional properties of the resulting channel protein, including apparent Ca(2)+ dependence and inactivation. The beta3b auxiliary subunit, when coexpressed with the Slo alpha subunit, results in a particularly rapid ( approximately 1 ms), but incomplete inactivation, mediated by the cytosolic NH(2) terminus of the beta3b subunit (Xia et al. 2000). Here, we evaluate whether a simple block of the open channel by the NH(2)-terminal domain accounts for the inactivation mechanism. Analysis of the onset of block, recovery from block, time-dependent changes in the shape of instantaneous current-voltage curves, and properties of deactivation tails suggest that a simple, one step blocking reaction is insufficient to explain the observed currents. Rather, blockade can be largely accounted for by a two-step blocking mechanism (C(n) <---> O(n) <---> O(*)(n) <---> I(n)) in which preblocked open states (O*(n)) precede blocked states (I(n)). The transitions between O* and I are exceedingly rapid accounting for an almost instantaneous block or unblock of open channels observed with changes in potential. However, the macroscopic current relaxations are determined primarily by slower transitions between O and O*. We propose that the O to O* transition corresponds to binding of the NH(2)-terminal inactivation domain to a receptor site. Blockade of current subsequently reflects either additional movement of the NH(2)-terminal domain into a position that hinders ion permeation or a gating transition to a closed state induced by binding of the NH(2) terminus.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.