Studies of protein kinase C in the rat basophilic leukemia (RBL-2H3) cell reveal that antigen-induced signals are not mimicked by the actions of phorbol myristate acetate and Ca2+ ionophore.

摘要: Exogenous activators of protein kinase C such as PMA in combination with a Ca2+ ionophore (A23187), cause secretion rat basophilic (RBL-2H3) cells,but they do so through stimulatory signals that are not the same those generated by Ag or oligomers IgE. On one hand, synergy between and A23187 suppression Ag-mediated (hydrolysis inositol phospholipids rise concentration cytosolic Ca2+) were totally dependent on C. The loss synergistic inhibitory actions PMA, for example, correlated (as determined immunoblotting techniques) when cells continuously exposed to PMA. Furthermore, permeabilization RBL-2H3 resulted both action but retained if before Ag-induced secretion, other was presence potent inhibitor this enzyme, staurosporine, which blocked completely secretory response A23187, did inhibit except at concentrations (greater than 10 nM) inhibited Ag-stimulated hydrolysis well. Also still showed some secretory-response (approximately 25% normal) depleted 98%) prolonged treatment Previous studies have indicated is much lower elicited stimulants matched give increase Ca2+.