Abstract
In primary cultures of neonatal rat heart cells we found a linear correlation between the number of L-type calcium channel-specific dihydropyridine (DHP) binding sites and spontaneous beating frequency (v).
Formation of glycoproteins in tissue culture was suppressed by different inhibitors of N-glycosylation. This inhibition alters to a different extent the binding of the DHP ligand (+)-[methyl-3H]PN 200-110 and v. The most severe but reversible effect occurs at 6 µ/ml tunicamycin (Bmax ≈ 45% and v ≈ 6%, resp., of control), a slight increase in Bmax at 0.1–0.5 mM castanospermine and 0.05–2.5 mM deoxymannojirimycin. The other inhibitors gave no significant alterations of Bmax. (Mol Cell Biochem 160/161:45–52, 1996)
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Henning, U., Wallukat, G., Holtzhauer, M. (1996). Influence of glycosylation inhibitors on dihydropyridine binding to cardiac cells. In: Krause, E.G., Vetter, R. (eds) Biochemical Mechanisms in Heart Function. Developments in Molecular and Cellular Biochemistry, vol 18. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1279-6_6
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