Figure 2.
Figure 2. Selinexor does not affect MK apoptosis, proplatelet formation, or platelet activation. (A-B) Mature, round mouse MKs derived from murine fetal livers were treated with increasing doses of selinexor. Six hours later, viability of the MKs and the number of proplatelet-producing MKs were quantified. Bars represent 20 μm; n = 3. Mature donor human platelets were treated with increased concentrations of selinexor in the absence (C) or the presence (D) of thrombin, and platelet surface P-selectin was analyzed by fluorescence-activated cell sorter (FACS). Representative images of resting (C) and activated (D) platelets stained with actin (phalloidin, red) and anti-β1-tubulin antibody (green). Bars represent 2 μm; n = 3. DMSO, dimethyl sulfoxide.

Selinexor does not affect MK apoptosis, proplatelet formation, or platelet activation. (A-B) Mature, round mouse MKs derived from murine fetal livers were treated with increasing doses of selinexor. Six hours later, viability of the MKs and the number of proplatelet-producing MKs were quantified. Bars represent 20 μm; n = 3. Mature donor human platelets were treated with increased concentrations of selinexor in the absence (C) or the presence (D) of thrombin, and platelet surface P-selectin was analyzed by fluorescence-activated cell sorter (FACS). Representative images of resting (C) and activated (D) platelets stained with actin (phalloidin, red) and anti-β1-tubulin antibody (green). Bars represent 2 μm; n = 3. DMSO, dimethyl sulfoxide.

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