Phorbol ester inhibits myoblast fusion and activates beta-adrenergic receptor coupled adenylate cyclase

FEBS Lett. 1985 Jul 8;186(2):281-5. doi: 10.1016/0014-5793(85)80725-0.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclases / metabolism*
  • Animals
  • Cell Fusion / drug effects
  • Cells, Cultured
  • Chick Embryo
  • Creatine Kinase / metabolism
  • Isoenzymes
  • Kinetics
  • Muscles / drug effects
  • Muscles / metabolism
  • Muscles / physiology*
  • Phorbols / pharmacology*
  • Receptors, Adrenergic, beta / physiology*
  • Tetradecanoylphorbol Acetate / pharmacology*

Substances

  • Isoenzymes
  • Phorbols
  • Receptors, Adrenergic, beta
  • Creatine Kinase
  • Adenylyl Cyclases
  • Tetradecanoylphorbol Acetate