Phorbol ester inhibits myoblast fusion and activates beta-adrenergic receptor coupled adenylate cyclase.
Primary cultures of myoblasts, derived from embryonic chick pectoral muscle, were treated with phorbol ester (TPA) for 8-96 h. TPA treatment blocked the fusion of myoblasts along with the expression of the MM form of creatine kinase. Interestingly, TPA treatment markedly increased the activity of beta-adrenergic receptor coupled adenylate cyclase (AC) activity. The study suggests that TPA treatment augments the functional interaction between a coupling Ns protein and catalytic unit of AC. The likely significance of these results is briefly presented.
Sulakhe
P V
PV
Johnson
D D
DD
Phan
N T
NT
Wilcox
R
R
D000262:Adenylyl Cyclases / Q000378:metabolism*; D000818:Animals; D002459:Cell Fusion / Q000187:drug effects; D002478:Cells, Cultured; D002642:Chick Embryo; D003402:Creatine Kinase / Q000378:metabolism; D007527:Isoenzymes; D007700:Kinetics; D009132:Muscles / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D010704:Phorbols / Q000494:pharmacology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D007527:Isoenzymes; D010704:Phorbols; D011943:Receptors, Adrenergic, beta; D003402:Creatine Kinase; D000262:Adenylyl Cyclases; D013755:Tetradecanoylphorbol Acetate