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Heterologous regulation of the cardiac calcium channel alpha 1 subunit by skeletal muscle beta and gamma subunits implications for the structure of cardiac l type calcium channels



Heterologous regulation of the cardiac calcium channel alpha 1 subunit by skeletal muscle beta and gamma subunits implications for the structure of cardiac l type calcium channels



Journal of Biological Chemistry 266(32): 21943-21947



High threshold L-type Ca2+ channels of skeletal muscle are thought to consist of a complex of .alpha.1, .alpha.2.delta., .beta., and .lambda. subuits. Expression of the cloned .alpha.1 subunit from skeletal and cardiac muscle has established that this protein is the dihydropyridine-sensitive ion-conducting subunit. However, the kinetics of the skeletal muscle .alpha.1 alone expressed in mouse L-cells were abnormally slow and were accelerated to within the normal range by coexpression with the skeletal muscle .beta. subunit. The kinetics of cardiac muscle .alpha.1 were also slowed but to a lesser extent and were not altered by coexpression with skeletal muscle .alpha.2. We show here that coexpression of the skeletal muscle .beta. subunit with the cardiac .alpha.1 subunit in Xenopus laevis oocytes produced: 1) an increase in the peak voltage-sensitive current, 2) a shift of the peak current-voltage relationship to more hyperpolarized potentials, and 3) an increase in the rate of activation. Coexpression of the skeletal muscle .lambda. subunit did not have a significant effect on currents elicited by .alpha.1. However, when .gamma. was coexpressed with .beta. and .alpha.1, both peak currents and rates of activation at more negative potentials were increased. These results indicate that rather than simply amplifying expression of .alpha.1, heterologous skeletal muscle .beta. and .gamma. subunits can modulate the biophysical properties of cardiac .alpha.1.

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Accession: 007397128

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