Fig. 3.
Fig. 3. CP-CPK inhibits FcγRIIA-mediated PtdOH production. / 32P-labeled platelets were incubated or not with CP-CPK, A3P5PS, or CP-CPK and 1-μmol/L epinephrine (1 minute, 37°C) as described in “Materials and methods” and activated by FcγRIIA cross-linking during different periods of time (A) or during 2 minutes (B). Increasing concentrations of CP-CPK (C) or AR-C69931MX (D) were also tested. The inhibitory effects of these compounds were overcome in a dose-dependent manner by epinephrine (C,D). Lipids were immediately extracted, PtdOH was separated by TLC, and the radioactivity incorporated into PtdOH was quantified by PhosphorImager analysis. Data are representative of 2 independent experiments with very similar results (A), mean ± standard errors of 6 independent experiments (B), or representative of 3 independent experiments (C,D). **Significant difference (P < .01) according to Studentt test.

CP-CPK inhibits FcγRIIA-mediated PtdOH production.

32P-labeled platelets were incubated or not with CP-CPK, A3P5PS, or CP-CPK and 1-μmol/L epinephrine (1 minute, 37°C) as described in “Materials and methods” and activated by FcγRIIA cross-linking during different periods of time (A) or during 2 minutes (B). Increasing concentrations of CP-CPK (C) or AR-C69931MX (D) were also tested. The inhibitory effects of these compounds were overcome in a dose-dependent manner by epinephrine (C,D). Lipids were immediately extracted, PtdOH was separated by TLC, and the radioactivity incorporated into PtdOH was quantified by PhosphorImager analysis. Data are representative of 2 independent experiments with very similar results (A), mean ± standard errors of 6 independent experiments (B), or representative of 3 independent experiments (C,D). **Significant difference (P < .01) according to Studentt test.

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