Fig. 6.
Fig. 6. 14-3-3ζ dissociates from GpIb during platelet aggregation in response to pathologic shear stress, and disassociation is inhibited by prostacyclin. / Intact washed human platelets were sheared in a cone-plate viscometer at a force of 90 dynes/cm2. (A) Shear stress caused the dissociation of 14-3-3ζ from platelet GpIbα immunoprecipitated with mAb AN51, and that platelet treatment with 100 ng/mL prostacyclin, which stimulated PKA, inhibited the decrease of immunodetectable 14-3-3ζ from the immunoprecipitated GpIbα. (B) Platelet aggregation in response to 90 dynes/cm2 shear stress and its inhibition by prostacyclin. Aggregation is reported as a decrease in the number of single particles in the sheared platelet suspension (n = 3).

14-3-3ζ dissociates from GpIb during platelet aggregation in response to pathologic shear stress, and disassociation is inhibited by prostacyclin.

Intact washed human platelets were sheared in a cone-plate viscometer at a force of 90 dynes/cm2. (A) Shear stress caused the dissociation of 14-3-3ζ from platelet GpIbα immunoprecipitated with mAb AN51, and that platelet treatment with 100 ng/mL prostacyclin, which stimulated PKA, inhibited the decrease of immunodetectable 14-3-3ζ from the immunoprecipitated GpIbα. (B) Platelet aggregation in response to 90 dynes/cm2 shear stress and its inhibition by prostacyclin. Aggregation is reported as a decrease in the number of single particles in the sheared platelet suspension (n = 3).

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