ArticleThe Journal of physiology1995
Skeletal muscle DHP receptor mutations alter calcium currents in human hypokalaemic periodic paralysis myotubes.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 55 citations in OpenAlex.
- Calcium channel gating.Pflugers Archiv : European journal of physiology · 2018Review
- When muscle CaThe Journal of physiology · 2018Review
- Elevated resting HThe Journal of physiology · 2017Article
- How voltage-gated calcium channels gate forms of homeostatic synaptic plasticity.Frontiers in cellular neuroscience · 2014Review
- Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels.Pflugers Archiv : European journal of physiology · 2010Review
- Calcium channelopathies.Neuromolecular medicine · 2006Review
- Calcium currents and transients in co-cultured contracting normal and Duchenne muscular dystrophy human myotubes.The Journal of physiology · 2001Article
- Functional roles of gamma2, gamma3 and gamma4, three new Ca2+ channel subunits, in P/Q-type Ca2+ channel expressed in Xenopus oocytes.The Journal of physiology · 2001Article
- The human skeletal muscle Na channel mutation R669H associated with hypokalemic periodic paralysis enhances slow inactivation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Skeletal muscle sodium current is reduced in hypokalemic periodic paralysis.Proceedings of the National Academy of Sciences of the United States of America · 2000Review
- Reduced voltage sensitivity of activation of P/Q-type Ca2+ channels is associated with the ataxic mouse mutation rolling Nagoya (tg(rol)).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Effects of mutations causing hypokalaemic periodic paralysis on the skeletal muscle L-type Ca2+ channel expressed in Xenopus laevis oocytes.The Journal of physiology · 1999Article
- Kinetics of inactivation and restoration from inactivation of the L-type calcium current in human myotubes.The Journal of physiology · 1999Article
- Gating of the L-type Ca channel in human skeletal myotubes: an activation defect caused by the hypokalemic periodic paralysis mutation R528H.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Genetic analysis of voltage-dependent calcium channels.Journal of bioenergetics and biomembranes · 1998Review
- L-type calcium current activation in cultured human myotubes.Journal of muscle research and cell motility · 1997Article
- Expression and functional characterization of the cardiac L-type calcium channel carrying a skeletal muscle DHP-receptor mutation causing hypokalaemic periodic paralysis.Pflugers Archiv : European journal of physiology · 1996Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Mutations in the gene encoding the alpha 1-subunit of the skeletal muscle dihydropyridine (DHP) receptor are responsible for familial hypokalaemic periodic paralysis (HypoPP), an autosomal dominant muscle disease. We investigated myotubes cultured from muscle of patients with arginine-to-histidine substitutions in putative voltage sensors, IIS4 (R528H) and IVS4 (R1239H), of the DHP receptor alpha 1-subunit. 2. Analysis of the messenger ribonucleic acid (mRNA) in the myotubes from such patients indicated transcription from both the normal and mutant genes. 3. In control myotubes, the existence of the slow L-type current and of two rapidly activating and inactivating calcium current components (T-type with a maximum at about -20 mV and 'third type' with a maximum at +10 to +20 mV) was confirmed. In the myotubes from patients with either mutation, the third-type current component was seen more frequently and, on average, with larger amplitude. 4. In myotubes with the IVS4 mutation (R1239H) the maximum L-type current density was smaller than control (-0.53 +/- 0.31 vs. -1.41 +/- 0.71 pA pF-1). The voltage dependence of activation was normal, and hyperpolarizing prepulses to -120 mV for 20 s did not increase the reduced current amplitude during test pulses. 5. In myotubes with the IIS4 mutation (R528H) the L-type current-voltage relation, determined at a holding potential of -90 mV, was normal. However, the voltage dependence of inactivation was shifted by about 40 mV to more negative potentials (voltage at half-maximum inactivation, V1/2 = -41.5 +/- 8.2 vs. -4.9 +/- 4.3 mV in normal controls).(ABSTRACT TRUNCATED AT 250 WORDS)
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