ArticlePflugers Archiv : European journal of physiology1996
Expression and functional characterization of the cardiac L-type calcium channel carrying a skeletal muscle DHP-receptor mutation causing hypokalaemic periodic paralysis.
Article in Pflugers Archiv : European journal of physiology, 1996. 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, 45 citations in OpenAlex.
- Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.Biochimica et biophysica acta · 2013Review
- Cardiac L-type calcium channel (Cav1.2) associates with gamma subunits.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- 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
- Gating of the HypoPP-1 mutations: II. Effects of a calcium-channel agonist BayK 8644.Pflugers Archiv : European journal of physiology · 2007Article
- 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: I. Mutant-specific effects and cooperativity.Pflugers Archiv : European journal of physiology · 2007Article
- Functional roles of the gamma subunit of the skeletal muscle DHP-receptor.Journal of muscle research and cell motility · 2006Review
- Muscle channelopathies and critical points in functional and genetic studies.The Journal of clinical investigation · 2005Review
- Altered inactivation of Ca2+ current and Ca2+ release in mouse muscle fibers deficient in the DHP receptor gamma1 subunit.The Journal of general physiology · 2004Article
- The CACNA1F gene encodes an L-type calcium channel with unique biophysical properties and tissue distribution.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Periodic paralysis: understanding channelopathies.Current neurology and neuroscience reports · 2002Review
- Excitation-contraction coupling in skeletal muscle of a mouse lacking the dihydropyridine receptor subunit gamma1.The Journal of physiology · 2001Article
- Modulation of L-type Ca2+ current but not activation of Ca2+ release by the gamma1 subunit of the dihydropyridine receptor of skeletal muscle.BMC physiology · 2001Article
- 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
- 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
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A histidine substitution for the outermost arginine in II/S4 of the alpha1 subunit of the human skeletal muscle dihydropyridine (DHP) receptor has been reported to cause hypokalaemic periodic paralysis (HypoPP). This mutation shifts the voltage dependence of L-type Ca curent inactivation in myotubes from HypoPP patients by -40 mV without affecting activation. Based on the strong homology of II/S4 in cardiac and skeletal muscle alpha1, we introduced the corresponding mutation into the rabbit cardiac alpha1 subunit (R650H). Wild type (WT) and mutant constructs were transiently transfected in HEK cells together with beta and alpha2delta subunits and Ca and Ba currents were studied using the whole-cell patch-clamp technique. In contrast to the results obtained from human myotubes, R650H produced a small (-5 mV) but significant shift of both the steady-state activation and inactivation curves. When external pH was increased from 7.4 to 8.4 in order to favour deprotonization of H650, the only difference between WT and mutant channels was a slightly reduced steepness of the inactivation curve. Additional cotransfection of the gamma subunit which is only found in skeletal but not in heart muscle, shifted the inactivation curves of both WT and R650H by -20 mV. We conclude that R650 plays a different role in voltage-dependent gating of the cardiac L-type Ca channel than the corresponding residue in the human skeletal muscle L-type channel, since a distinct and selective effect on the midpoint voltage of steady-state inactivation could not be found for R650H.
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