A selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-bromocinnamyl(amino)ethyl]-5-isoquinolinesulfonamide (H-89), inhibits phosphatidylcholine biosynthesis in HeLa cells.
In this study, we report that the potent and selective inhibitor of cyclic AMP-dependent protein kinase, N-[2-bromocinnamyl(amino)ethyl]-5-isoquinolinesulfonamide (H-89) interferes with the incorporation of choline into phosphatidylcholine in HeLa cells. Treatment of cells with 10 microM H-89 for 1 h decreases the phosphatidylcholine biosynthesis by 50%. This inhibition is prevented by simultaneous addition of 10 microM forskolin, while the choline uptake itself is not affected by H-89.
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Institut fur Molekularbiologie und Biochemie, Freien Universität Berlin, Germany.
Wieprecht
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Wieder
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Reutter
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D005576:Colforsin / Q000494:pharmacology; D006367:HeLa Cells; D006801:Humans; D007546:Isoquinolines / Q000494:pharmacology*; D007700:Kinetics; D010713:Phosphatidylcholines / Q000096:biosynthesis*; D047428:Protein Kinase Inhibitors; D013449:Sulfonamides; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D007546:Isoquinolines; D010713:Phosphatidylcholines; D047428:Protein Kinase Inhibitors; D013449:Sulfonamides; D005576:Colforsin; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; D013755:Tetradecanoylphorbol Acetate