A ROLE OF CALCYCLIN, A CA2-BINDING PROTEIN, ON THE CA2+-DEPENDENT INSULIN RELEASE FROM THE PANCREATIC BETA-CELL()

Exocytosis is an important example of cell activation. Ca2+ and calciu m-binding proteins are considered to modulate signal transduction in e xocytosis. We examined the role of calcyclin, calcium-binding protein, in the stimulus-secretion coupling in pancreatic beta cells. The pres ence of calcyclin in these cells was demonstrated immunologically. We permeabilized rat pancreatic islets with streptolysin-O and examined t he effects of calcyclin on insulin release. The Ca2+-stimulated insuli n release was enhanced by calcyclin, in a dose-dependent manner, where as this calcium-binding protein had no effect on insulin release from islets in low Ca2+ buffer or from the islets not subjected to the stre ptolysin-O treatment. Calgizzarin, another member of the S-100 protein family had no apparent effect on the Ca2+ stimulated secretion under parallel conditions. An anticalcyclin antibody suppressed the increase in insulin release induced by calcyclin. We propose that calcyclin ma y be involved in signal transduction of the Ca2+-induced release of in sulin.