ArticleChannels (Austin, Tex.)
Shab K (+) channel slow inactivation: a test for U-type inactivation and a hypothesis regarding K (+) -facilitated inactivation mechanisms.
Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Mutations within the selectivity filter reveal that Kv1 channels have distinct propensities to slow inactivate.The Journal of general physiology · 2022Article
- Activity-dependent modulation of neuronal KThe Journal of biological chemistry · 2022Article
- Conductance stability and Na+ interaction with Shab K+ channels under low K+ conditions.Channels (Austin, Tex.) · 2021Article
- Kv2 channel-AMIGO β-subunit assembly modulates both channel function and cell adhesion molecule surface trafficking.Journal of cell science · 2021Article
- KV1.2 channels inactivate through a mechanism similar to C-type inactivation.The Journal of general physiology · 2020Article
- Shaker IR T449 mutants separate C- from U-type inactivation.The Journal of membrane biology · 2014Article
- Recovery from slow inactivation of Shab K(+) channels.Channels (Austin, Tex.)Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herein, we report the first characterization of Shab slow inactivation. Open Shab channels inactivate within seconds, with two voltage-independent time constants. Additionally, Shab presents significant closed-state inactivation. We found that with short depolarizing pulses, shorter than the slowest inactivation time constant, the resulting inactivation curve has a marked U-shape, but as pulse duration increases, approaching steady-state conditions, the U-shape vanishes, and the resulting inactivation curves converge to the classical Boltzmann h∞ curve. Regarding the mechanism of inactivation, we found that external K (+) and TEA facilitate both open- and closed-state inactivation, while the cavity blocker quinidine hinders inactivation. These results together with our previous observations regarding the K (+) -dependent stability of the K (+) conductance, suggest the novel hypothesis that inactivation of Shab channels, and possibly that of other Kv channels whose inactivation is facilitated by K (+) , does not involve a significant narrowing of the extracellular entry of the pore. Instead, we hypothesize that there is only a rearrangement of a more internal segment of the pore that affects the central cavity and halts K (+) conduction.
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