Publication | Open Access
Phorbol ester inhibits myoblast fusion and activates β‐adrenergic receptor coupled adenylate cyclase
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Citations
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References
1985
Year
Creatine KinaseCellular PhysiologyMolecular PharmacologyProtein ExpressionSkeletal MusclePhorbol Ester Inhibitsβ‐Adrenergic ReceptorProtein DegradationCell SignalingHealth SciencesTpa TreatmentH. Tpa TreatmentMolecular PhysiologyBiochemistryG Protein-coupled ReceptorAdenylate CyclaseReceptor (Biochemistry)Mechanism Of ActionPharmacologyProtein PhosphorylationSignal TransductionCellular EnzymologyPhysiologyCellular BiochemistryMedicine
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 β‐adrenergic receptor coupled adenylate cyclase (AC) activity. The study suggests that TPA treatment augments the functional interaction between a coupling N s protein and catalytic unit of AC. The likely significance of these results is briefly presented.
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