ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Gating of the L-type Ca channel in human skeletal myotubes: an activation defect caused by the hypokalemic periodic paralysis mutation R528H.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Targeted Therapies for Skeletal Muscle Ion Channelopathies: Systematic Review and Steps Towards Precision Medicine.Journal of neuromuscular diseases · 2021Pooled it
- A Review of Genetic and Physiological Disease Mechanisms Associated With Cav1 Channels: Implications for Incomplete Congenital Stationary Night Blindness Treatment.Frontiers in genetics · 2021Article
- Skeletal muscle CaPflugers Archiv : European journal of physiology · 2020Review
- When muscle CaThe Journal of physiology · 2018Review
- Stac3 enhances expression of human CaThe Journal of general physiology · 2018Article
- Na leak with gating pore properties in hypokalemic periodic paralysis V876E mutant muscle Ca channel.The Journal of general physiology · 2017Article
- Elevated resting HThe Journal of physiology · 2017Article
- Channelopathies of skeletal muscle excitability.Comprehensive Physiology · 2015Review
- Physiological and ultrastructural features of human induced pluripotent and embryonic stem cell-derived skeletal myocytes in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Biophysics, pathophysiology, and pharmacology of ion channel gating pores.Frontiers in pharmacology · 2014Review
- Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.Biochimica et biophysica acta · 2013Review
- A calcium channel mutant mouse model of hypokalemic periodic paralysis.The Journal of clinical investigation · 2012Article
- Pathophysiological role of omega pore current in channelopathies.Frontiers in pharmacology · 2012Article
- A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis.The Journal of clinical investigation · 2011Article
- A malignant hyperthermia-inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channels.The Journal of general physiology · 2010Article
- Rapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.The Journal of physiology · 2009Article
- Gating pore currents in DIIS4 mutations of NaV1.4 associated with periodic paralysis: saturation of ion flux and implications for disease pathogenesis.The Journal of general physiology · 2008Article
- A Na+ channel mutation linked to hypokalemic periodic paralysis exposes a proton-selective gating pore.The Journal of general physiology · 2007Article
- Gating of the HypoPP-1 mutations: II. Effects of a calcium-channel agonist BayK 8644.Pflugers Archiv : European journal of physiology · 2007Article
- Gating of the HypoPP-1 mutations: I. Mutant-specific effects and cooperativity.Pflugers Archiv : European journal of physiology · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The skeletal muscle L-type Ca channel serves a dual role as a calcium-conducting pore and as the voltage sensor coupling t-tubule depolarization to calcium release from the sarcoplasmic reticulum. Mutations in this channel cause hypokalemic periodic paralysis (HypoPP), a human autosomal dominant disorder characterized by episodic failure of muscle excitability that occurs in association with a decrease in serum potassium. The voltage-dependent gating of L-type Ca channels was characterized by recording whole-cell Ca currents in myotubes cultured from three normal individuals and from a patient carrying the HypoPP mutation R528H. We found two effects of the R528H mutation on the L-type Ca current in HypoPP myotubes: (1) a mild reduction in current density and (2) a significant slowing of the rate of activation. We also measured the voltage dependence of steady-state L-type Ca current inactivation and characterized, for the first time in a mammalian preparation, the kinetics of both entry into and recovery from inactivation over a wide range of voltages. The R528H mutation had no effect on the kinetics or voltage dependence of inactivation.
Indexed as
Identifiers
9852570PMC6793372W1915689849What OpenQuestion holds
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.