Published online before print January 5, 2006, doi: 10.1161/01.RES.0000202692.23001.e2
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Submitted on November 8, 2005
Revised on December 15, 2005
Accepted on December 20, 2005
-Adrenergic Stimulation of L-type Ca2+ Channels in Cardiac Myocytes Requires the Distal Carboxyl Terminus of 
1C but Not Serine 1928
Anand N. Ganesan ;
* To whom correspondence should be addressed. E-mail: bor{at}jhmi.edu.
-Adrenoceptor stimulation robustly increases cardiac L-type Ca2+ current (ICaL); yet the molecular mechanism of this effect is still not well understood. Previous reports have shown in vitro phosphorylation of a consensus protein kinase A site at serine 1928 on the carboxyl terminus of the 
1C subunit; however, the functional role of this site has not been investigated in cardiac myocytes. Here, we examine the effects of truncating the distal carboxyl terminus of the 1C subunit at amino acid residue 1905 or mutating the putative protein kinase A at serine 1928 to alanine in adult guinea pig myocytes, using novel dihydropyridine-insensitive 1C adenoviruses, coexpressed with 2 subunits. Expression of 1C truncated at 1905 dramatically attenuated the increase of peak ICaL induced by isoproterenol. However, the point mutation S1928A did not significantly attenuate the -adrenergic response. The findings indicate that the distal carboxyl-terminus of 1C plays an important role in -adrenergic upregulation of cardiac L-type Ca2+ channels, but that phosphorylation of serine 1928 is not required for this effect.
Key words: protein kinase A • adenovirus • ion channel • calcium current • cAMP
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