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Your search keyword '"Obermair, Gerald J."' showing total 9 results
Start Over Author "Obermair, Gerald J." Journal biophysical journal
9 results on '"Obermair, Gerald J."'

1. A Complex of RIM2alpha and RIM-Binding Protein 2 Stabilizes Slow Voltage-Dependent Inactivation of Cochlear Inner Hair Cell Cav1.3 L-Type Ca2+ Channels

Author

Ortner, Nadine J., primary, Pinggera, Alexandra, additional, Siller, Anita, additional, Hofer, Nadja, additional, Brandt, Niels, additional, Raffeiner, Andrea, additional, Lang, Isabelle, additional, Stefan, Eduard, additional, Obermair, Gerald J., additional, Engel, Jutta, additional, and Striessnig, Jörg, additional

Published
2018
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4. Is There a Contribution of Both Cav1.4 and Cav1.3 L-Type Calcium Channels to Retinal Synaptic Transmission?

Author

Burtscher, Verena, primary, Knoflach, Dagmar, additional, Kugler, Christof, additional, Scharinger, Anja, additional, Glösmann, Martin, additional, Blatsios, Georgios, additional, Janecke, Andreas, additional, Striessnig, Jörg, additional, Obermair, Gerald J., additional, Schicker, Klaus W., additional, and Koschak, Alexandra, additional

Published
2014
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5. Expression of the Embryonic Cav1.1 Splice Variant in Adult Mice Alters Excitation-Contraction Coupling but Does not Cause Dystrophic Myotonia

Author

Sultana, Nasreen, primary, Benedetti, Ariane, additional, Sztretye, Monika, additional, Dienes, Beatrix, additional, Szentesi, Peter, additional, Tuluc, Petronel, additional, Quarta, Serena, additional, Obermair, Gerald J., additional, Schwarzer, Christoph, additional, Kress, Michaela, additional, Csernoch, Laszlo, additional, and Flucher, Bernhard E., additional

Published
2014
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8. Cardiac-type EC-Coupling in Dysgenic Myotubes Restored with Ca2+Channel Subunit Isoforms α1Cand α1DDoes not Correlate with Current Density

Author

Kasielke, Nicole, Obermair, Gerald J., Kugler, Gerlinde, Grabner, Manfred, and Flucher, Bernhard E.

Abstract

Ca2+-induced Ca2+-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 Ca2+release, by reconstituting dysgenic myotubes with the cardiac Ca2+channel α1C(CaV1.2) subunit. Ca2+influx through α1Cprovides the trigger for opening the sarcoplasmic reticulum Ca2+release channels. Here we show that also the Ca2+channel α1Disoform (CaV1.3) can restore cardiac-type EC-coupling. GFP-α1Dexpressed in dysgenic myotubes is correctly targeted into the triad junctions and generates action potential-induced Ca2+transients with the same efficiency as GFP-α1Cdespite threefold smaller Ca2+currents. In contrast, GFP-α1A, which generates large currents but is not targeted into triads, rarely restores action potential-induced Ca2+transients. Thus, cardiac-type EC-coupling in skeletal myotubes depends primarily on the correct targeting of the voltage-gated Ca2+channels and less on their current size. Combined patch-clamp/fluo-4 Ca2+recordings revealed that the induction of Ca2+transients and their maximal amplitudes are independent of the different current densities of GFP-α1Cand GFP-α1D. These properties of cardiac-type EC-coupling in dysgenic myotubes are consistent with a CICR mechanism under the control of local Ca2+gradients in the triad junctions.

Published
2003
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9. Cardiac-type EC-coupling in dysgenic myotubes restored with Ca2+ channel subunit isoforms alpha1C and alpha1D does not correlate with current density.

Author

Kasielke N, Obermair GJ, Kugler G, Grabner M, and Flucher BE

Subjects
Adaptation, Physiological physiology, Calcium physiology, Calcium Channels, Cell Line, Muscle Fibers, Skeletal, Mutagenesis, Site-Directed, Mutation, Myocardial Contraction physiology, Protein Isoforms, Protein Subunits, Recombinant Proteins metabolism, Sarcoplasmic Reticulum physiology, Statistics as Topic, Structure-Activity Relationship, Action Potentials physiology, Calcium Channels, L-Type physiology, Calcium Signaling physiology, Heart physiology, Membrane Potentials physiology, Muscle Contraction physiology, Muscle, Skeletal physiology
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.

Published
2003
Full Text
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