ArticleBiophysical journal1997
Defective fast inactivation recovery and deactivation account for sodium channel myotonia in the I1160V mutant.
Article in Biophysical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- Characterization of a new sodium channel mutation at arginine 1448 associated with moderate Paramyotonia congenita in humans.The Journal of physiology · 1999Trial
- Translational approach to address therapy in myotonia permanens due to a new SCN4A mutation.Neurology · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Biophysical characterization of M1476I, a sodium channel founder mutation associated with cold-induced myotonia in French Canadians.The Journal of physiology · 2012Article
- Mechanisms underlying a life-threatening skeletal muscle Na+ channel disorder.The Journal of physiology · 2011Article
- 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
- Paroxysmal extreme pain disorder mutations within the D3/S4-S5 linker of Nav1.7 cause moderate destabilization of fast inactivation.The Journal of physiology · 2008Article
- K-aggravated myotonia mutations at residue G1306 differentially alter deactivation gating of human skeletal muscle sodium channels.Cellular and molecular neurobiology · 2005Article
- A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4-S5 linker in fast inactivation.The Journal of physiology · 2005Article
- Cooperative effect of S4-S5 loops in domains D3 and D4 on fast inactivation of the Na+ channel.The Journal of physiology · 2004Article
- A double mutation in families with periodic paralysis defines new aspects of sodium channel slow inactivation.The Journal of clinical investigation · 2000Article
- The delay in recovery from fast inactivation in skeletal muscle sodium channels is deactivation.Cellular and molecular neurobiology · 2000Article
- Activation and inactivation of the voltage-gated sodium channel: role of segment S5 revealed by a novel hyperkalaemic periodic paralysis mutation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Differential effects of homologous S4 mutations in human skeletal muscle sodium channels on deactivation gating from open and inactivated states.The Journal of physiology · 1999Article
- Enhanced slow inactivation by V445M: a sodium channel mutation associated with myotonia.Biophysical journal · 1999Article
- Fast- and slow-gating modes of the sodium channel are altered by a paramyotonia congenita-linked mutation.Journal of bioenergetics and biomembranes · 1998Article
- Functional expression of the Ile693Thr Na+ channel mutation associated with paramyotonia congenita in a human cell line.The Journal of physiology · 1998Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The skeletal muscle sodium channel mutant I1160V cosegregates with a disease phenotype producing myotonic discharges (observed as muscle stiffness) that are worsened by elevated K+ levels but unaffected by cooling. The I1160V alpha-subunit was co-expressed with the beta1-subunit in Xenopus oocytes. An electrophysiological characterization was undertaken to examine the underlying biophysical characteristics imposed by this mutation. Two abnormalities were found. 1) The voltage dependence of steady-state fast inactivation was reduced in I1160V, which resulted in faster rates of closed-state fast inactivation onset and recovery in I1160V compared with wild-type channels. 2) The rates of deactivation were slower in I1160V than in wild-type channels. Using a computer-simulated model, the combination of both defects elicited myotonic runs under conditions of elevated K+, consistent with the observed phenotype of the mutant.
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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.