ArticleBiophysical journal2001
A single residue differentiates between human cardiac and skeletal muscle Na+ channel slow inactivation.
Article in Biophysical journal, 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, 57 citations in OpenAlex.
- Structural mechanism of voltage-gated sodium channel slow inactivation.Nature communications · 2024Article
- In Silico Analysis of Tetrodotoxin Binding in Voltage-Gated Sodium Ion Channels from Toxin-Resistant Animal Lineages.Marine drugs · 2022Article
- Differential effects of modified batrachotoxins on voltage-gated sodium channel fast and slow inactivation.Cell chemical biology · 2022Article
- An open state of a voltage-gated sodium channel involving a π-helix and conserved pore-facing asparagine.Biophysical journal · 2022Article
- Molecular dissection of multiphase inactivation of the bacterial sodium channel NaThe Journal of general physiology · 2019Article
- The voltage-gated sodium channel pore exhibits conformational flexibility during slow inactivation.The Journal of general physiology · 2018Article
- Ion conduction and conformational flexibility of a bacterial voltage-gated sodium channel.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Structure and function of voltage-gated sodium channels at atomic resolution.Experimental physiology · 2014Review
- A gating charge interaction required for late slow inactivation of the bacterial sodium channel NavAb.The Journal of general physiology · 2013Article
- Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels II: a periodic paralysis mutation in Na(V)1.4 (L689I).The Journal of general physiology · 2013Article
- Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.The Journal of biological chemistry · 2013Article
- Crystal structure of a voltage-gated sodium channel in two potentially inactivated states.Nature · 2012Article
- Gating transitions in the selectivity filter region of a sodium channel are coupled to the domain IV voltage sensor.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Biophysical costs associated with tetrodotoxin resistance in the sodium channel pore of the garter snake, Thamnophis sirtalis.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2011Article
- A molecular switch between the outer and the inner vestibules of the voltage-gated Na+ channel.The Journal of biological chemistry · 2010Article
- The outer vestibule of the Na+ channel-toxin receptor and modulator of permeation as well as gating.Marine drugs · 2010Review
- Slow inactivation of the NaV1.4 sodium channel in mammalian cells is impeded by co-expression of the beta1 subunit.Pflugers Archiv : European journal of physiology · 2009Article
- Speeding the recovery from ultraslow inactivation of voltage-gated Na+ channels by metal ion binding to the selectivity filter: a foot-on-the-door?Biophysical journal · 2007Article
- Time-dependent molecular memory in single voltage-gated sodium channel.The Journal of membrane biology · 2007Article
- Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.The Journal of physiology · 2007Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Slow inactivation determines the availability of voltage-gated sodium channels during prolonged depolarization. Slow inactivation in hNa(V)1.4 channels occurs with a higher probability than hNa(V)1.5 sodium channels; however, the precise molecular mechanism for this difference remains unclear. Using the macropatch technique we show that the DII S5-S6 p-region uniquely confers the probability of slow inactivation from parental hNa(V)1.5 and hNa(V)1.4 channels into chimerical constructs expressed in Xenopus oocytes. Site-directed mutagenesis was used to test whether a specific region within DII S5-S6 controls the probability of slow inactivation. We found that substituting V754 in hNa(V)1.4 with isoleucine from the corresponding position (891) in hNa(V)1.5 produced steady-state slow inactivation statistically indistinguishable from that in wild-type hNa(V)1.5 channels, whereas other mutations have little or no effect on slow inactivation. This result indicates that residues V754 in hNa(V)1.4 and I891in hNa(V)1.5 are unique in determining the probability of slow inactivation characteristic of these isoforms. Exchanging S5-S6 linkers between hNa(V)1.4 and hNa(V)1.5 channels had no consistent effect on the voltage-dependent slow time inactivation constants [tau(V)]. This suggests that the molecular structures regulating rates of entry into and exit from the slow inactivated state are different from those controlling the steady-state probability and reside outside the p-regions.
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Registered trials
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.