ArticleBiophysical journal2003
Cardiac-type EC-coupling in dysgenic myotubes restored with Ca2+ channel subunit isoforms alpha1C and alpha1D does not correlate with current density.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- STAC3 incorporation into skeletal muscle triads occurs independent of the dihydropyridine receptor.Journal of cellular physiology · 2018Article
- Role of putative voltage-sensor countercharge D4 in regulating gating properties of CaChannels (Austin, Tex.) · 2018Article
- How and why are calcium currents curtailed in the skeletal muscle voltage-gated calcium channels?The Journal of physiology · 2017Review
- Physiological and pharmacological modulation of the embryonic skeletal muscle calcium channel splice variant CaV1.1e.Biophysical journal · 2015Article
- The juvenile myoclonic epilepsy mutant of the calcium channel β(4) subunit displays normal nuclear targeting in nerve and muscle cells.Channels (Austin, Tex.) · 2014Article
- Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.Biochimica et biophysica acta · 2013Review
- Stable incorporation versus dynamic exchange of β subunits in a native Ca2+ channel complex.Journal of cell science · 2013Article
- Surface traffic of dendritic CaV1.2 calcium channels in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- A CaV1.1 Ca2+ channel splice variant with high conductance and voltage-sensitivity alters EC coupling in developing skeletal muscle.Biophysical journal · 2009Article
- Computer modeling of siRNA knockdown effects indicates an essential role of the Ca2+ channel alpha2delta-1 subunit in cardiac excitation-contraction coupling.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Bridging the myoplasmic gap: recent developments in skeletal muscle excitation-contraction coupling.Journal of muscle research and cell motility · 2007Review
- Multiple loops of the dihydropyridine receptor pore subunit are required for full-scale excitation-contraction coupling in skeletal muscle.Biophysical journal · 2005Article
- Differential contribution of skeletal and cardiac II-III loop sequences to the assembly of dihydropyridine-receptor arrays in skeletal muscle.Molecular biology of the cell · 2004Article
- Slow calcium signals after tetanic electrical stimulation in skeletal myotubes.Biophysical journal · 2004Article
- The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes.Channels (Austin, Tex.)Article
- Activity and calcium regulate nuclear targeting of the calcium channel beta4b subunit in nerve and muscle cells.Channels (Austin, Tex.)Article
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5 authors.
Funding
Abstract
Ca(2+)-induced Ca(2+)-release (CICR)-the mechanism of cardiac excitation-contraction (EC) coupling-also contributes to skeletal muscle contraction; however, its properties are still poorly understood. CICR in skeletal muscle can be induced independently of direct, calcium-independent activation of sarcoplasmic reticulum Ca(2+) release, by reconstituting dysgenic myotubes with the cardiac Ca(2+) channel alpha(1C) (Ca(V)1.2) subunit. Ca(2+) influx through alpha(1C) provides the trigger for opening the sarcoplasmic reticulum Ca(2+) release channels. Here we show that also the Ca(2+) channel alpha(1D) isoform (Ca(V)1.3) can restore cardiac-type EC-coupling. GFP-alpha(1D) expressed in dysgenic myotubes is correctly targeted into the triad junctions and generates action potential-induced Ca(2+) transients with the same efficiency as GFP-alpha(1C) despite threefold smaller Ca(2+) currents. In contrast, GFP-alpha(1A), which generates large currents but is not targeted into triads, rarely restores action potential-induced Ca(2+) transients. Thus, cardiac-type EC-coupling in skeletal myotubes depends primarily on the correct targeting of the voltage-gated Ca(2+) channels and less on their current size. Combined patch-clamp/fluo-4 Ca(2+) recordings revealed that the induction of Ca(2+) transients and their maximal amplitudes are independent of the different current densities of GFP-alpha(1C) and GFP-alpha(1D). These properties of cardiac-type EC-coupling in dysgenic myotubes are consistent with a CICR mechanism under the control of local Ca(2+) gradients in the triad junctions.
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