PKC-mediated exocytosis is impaired in platelets lacking pleckstrin. PMA-induced exocytosis was analyzed biochemically (A,C), as well as by flow cytometry (B,D). The effect of the pleckstrin loss on function mutation on the δ (dense) granule secretion was analyzed in a Lumi-Aggregometer (Chrono-Log). (A) A representative tracing is shown, and pooled results showing the mean and SD derived from 5 experiments for PMA and 4 experiments with thrombin are plotted (C). Platelets lacking pleckstrin had a consistent deficit in dense granule section (P < .01 for all time points). The flow histogram (B) shows the relative surface exposure of P-selectin as a marker of α granule fusion with the cell membrane. The pooled analysis derived from 4 experiments is shown (D). For all doses and time points, paired analysis showed a P < .05.