ArticleBiophysical journal1996
Impaired slow inactivation in mutant sodium channels.
Article in Biophysical journal, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
73 citing papers in PubMed, 180 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
- Article
- Genetic analysis of 37 cases with primary periodic paralysis in Chinese patients.Orphanet journal of rare diseases · 2024Article
- Periodic paralysis.Handbook of clinical neurology · 2024Review
- 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
- Changes in Resurgent Sodium Current Contribute to the Hyperexcitability of Muscles in Patients with Paramyotonia Congenita.Biomedicines · 2021Article
- Sodium Channelopathies of Skeletal Muscle.Handbook of experimental pharmacology · 2018Review
- Coexistence of CLCN1 and SCN4A mutations in one family suffering from myotonia.Neurogenetics · 2017Article
- State-dependent block of voltage-gated sodium channels by the casein-kinase 1 inhibitor IC261.Investigational new drugs · 2017Article
- A recessive Nav1.4 mutation underlies congenital myasthenic syndrome with periodic paralysis.Neurology · 2016Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Enhanced slow inactivation of the human skeletal muscle sodium channel causing normokalemic periodic paralysis.Cellular and molecular neurobiology · 2014Article
- Block of human cardiac sodium channels by lacosamide: evidence for slow drug binding along the activation pathway.Molecular pharmacology · 2014Article
- A naturally occurring amino acid substitution in the voltage-dependent sodium channel selectivity filter affects channel gating.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2013Article
- Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.The Journal of biological chemistry · 2013Article
- Kinetic model of Nav1.5 channel provides a subtle insight into slow inactivation associated excitability in cardiac cells.PloS one · 2013Article
- Use-dependent block of the voltage-gated Na(+) channel by tetrodotoxin and saxitoxin: effect of pore mutations that change ionic selectivity.The Journal of general physiology · 2012Article
- Biophysical characterization of M1476I, a sodium channel founder mutation associated with cold-induced myotonia in French Canadians.The Journal of physiology · 2012Article
- Keeping hyperactive voltage-gated sodium channels in silent mode.The Journal of physiology · 2012Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hyperkalemic periodic paralysis (HyperPP) is a disorder in which current through Na+ channels causes a prolonged depolarization of skeletal muscle fibers, resulting in membrane inexcitability and muscle paralysis. Although HyperPP mutations can enhance persistent sodium currents, unaltered slow inactivation would effectively eliminate any sustained currents through the mutant channels. We now report that rat skeletal muscle channels containing the mutation T698M, which corresponds to the human T704M HyperPP mutation, recover very quickly from prolonged depolarizations. Even after holding at -20 mV for 20 min, approximately 25% of the maximal sodium current is available subsequent to a 10-ms hyperpolarization (-100 mV). Under the same conditions, recovery is less than 3% in wild-type channels and in the F1304Q mutant, which has impaired fast inactivation. This effect of the T698M mutation on slow inactivation, in combination with its effects on activation, is expected to result in persistent currents such as that seen in HyperPP muscle.
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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.