ArticlePflugers Archiv : European journal of physiology2009
Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- Differential effects of modified batrachotoxins on voltage-gated sodium channel fast and slow inactivation.Cell chemical biology · 2022Article
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- Myotonia in a patient with a mutation in an S4 arginine residue associated with hypokalaemic periodic paralysis and a concomitant synonymous CLCN1 mutation.Scientific reports · 2019Article
- Alternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Skeletal muscle · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Interactions among DIV voltage-sensor movement, fast inactivation, and resurgent Na current induced by the NaVβ4 open-channel blocking peptide.The Journal of general physiology · 2013Article
- A thermosensitive mutation alters the effects of lacosamide on slow inactivation in neuronal voltage-gated sodium channels, NaV1.2.Frontiers in pharmacology · 2013Article
- Article
- Left-shifted nav channels in injured bilayer: primary targets for neuroprotective nav antagonists?Frontiers in pharmacology · 2012Article
- Gating behaviour of sodium currents in adult mouse muscle recorded with an improved two-electrode voltage clamp.The Journal of physiology · 2011Article
- In silico docking and electrophysiological characterization of lacosamide binding sites on collapsin response mediator protein-2 identifies a pocket important in modulating sodium channel slow inactivation.The Journal of biological chemistry · 2010Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In response to sustained depolarization or prolonged bursts of activity in spiking cells, sodium channels enter long-lived non-conducting states from which recovery at hyperpolarized potentials occurs over hundreds of milliseconds to seconds. The molecular basis for this slow inactivation remains unknown, although many functional domains of the channel have been implicated. Expression studies in Xenopus oocytes and mammalian cell lines have suggested a role for the accessory beta1 subunit in slow inactivation, but the effects have been variable. We examined the effects of the beta1 subunit on slow inactivation of skeletal muscle (NaV1.4) sodium channels expressed in HEK cells. Co-expression of the beta1 subunit impeded slow inactivation elicited by a 30-s depolarization, such that the voltage dependence was right shifted (depolarized) and recovery was hastened. Mutational studies showed this effect was dependent upon the extracellular Ig-like domain, but was independent of the intracellular C-terminal tail. Furthermore, the beta1 effect on slow inactivation was shown to be independent of the negative coupling between fast and slow inactivation.
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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.