Isoform-dependent activation of adenylyl cyclase by proteolysis

FEBS Lett. 1997 Jan 20;401(2-3):223-6. doi: 10.1016/s0014-5793(96)01475-5.

Abstract

Recent findings have suggested that the cellular proteolytic system plays a major role in the regulation of various intra- and extra-cellular signaling. It was previously shown that proteolytic treatment of adenylyl cyclase leads to the activation of this enzyme. We demonstrate that this activation occurs in an adenylyl cyclase isoform-dependent manner. The type II isoform was strongly activated (approximately 500%), the type III isoform was modestly activated (approximately 30%),and the type V isoform was inhibited by trypsin. Activation of type II adenylyl cyclase occurred in trypsin dose- and time-dependent manners and was blocked by a trypsin inhibitor in a dose-dependent manner. Other proteases, such as thrombin and plasminogen, similarly activated the type II isoform, but not the others. Our data suggest that proteolytic activation is an isoform- and thus cell type-dependent mechanism of altering adenylyl cyclase catalytic activity.

MeSH terms

  • Adenylyl Cyclases / genetics
  • Adenylyl Cyclases / metabolism*
  • Animals
  • Cells, Cultured
  • Endopeptidases / metabolism*
  • Enzyme Activation
  • Fibrinolysin / pharmacology
  • Insecta
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Ovomucin / pharmacology
  • Recombinant Proteins / genetics
  • Recombinant Proteins / metabolism
  • Thrombin / pharmacology
  • Trypsin / metabolism
  • Trypsin Inhibitors / pharmacology

Substances

  • Isoenzymes
  • Recombinant Proteins
  • Trypsin Inhibitors
  • Ovomucin
  • Endopeptidases
  • Trypsin
  • Thrombin
  • Fibrinolysin
  • Adenylyl Cyclases