β-Adrenergic Stimulation of L-type Ca 2+ Channels in Cardiac Myocytes Requires the Distal Carboxyl Terminus of α 1C but Not Serine 1928
Why the study?
Does truncating the distal carboxyl terminus or mutating serine 1928 of the alpha1C subunit alter the beta-adrenergic upregulation of cardiac L-type Ca2+ channels in adult guinea pig myocytes?
Population
Adult guinea pig myocytes
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Challenges S1928-centric models of β-adrenergic ICaL regulation; extends α1C carboxyl-terminus mechanisms but leaves open human disease relevance.
Structured PICO
Does truncating the distal carboxyl terminus or mutating serine 1928 of the alpha1C subunit alter the beta-adrenergic upregulation of cardiac L-type Ca2+ channels in adult guinea pig myocytes?
P
Population
Adult guinea pig myocytes
I
Intervention
Truncation of the distal carboxyl terminus of the alpha1C subunit at amino acid residue 1905 or mutation of the putative protein kinase A site at serine 1928 to alanine using novel dihydropyridine-insensitive alpha1C adenoviruses, coexpressed with beta2 subunits
O
Outcome
Increase of peak L-type Ca2+ current (ICaL) induced by isoproterenolsurrogate
The distal carboxyl-terminus of alpha1C is essential for beta-adrenergic upregulation of cardiac L-type Ca2+ channels, but phosphorylation of serine 1928 is not required.
Cite This Study
Ganesan et al. (2006) studied this question.