Effect of PKC activation or inhibition on thrombin- or ADP-induced intracellular Ca²⁺-transients in human erythroid progenitors. (A) The PKC inhibitor BIM (30 μmol/L) markedly enhanced thrombin (2 U/mL)- or ADP (10 μmol/L)-evoked cellular Ca²⁺-release. (B) Stimulation of PKC with PMA (10 nmol/L) abolished the effect of thrombin and of ADP. (C) Addition of EGTA (4 mmol/L) to the experimental medium. Ca²⁺-release from internal stores by thrombin or ADP was similarly blocked by PKC activation. Results are representative for two to eight independent experiments.