American Society of Hematology

Figure 6

$Figure 6. Phosphorylated MARCKS and Arp2 are downregulated in proplatelet-producing MKs. Murine fetal liver MKs were cultured as described in Methods and lysed at indicated times. Cell fractions were separated by BSA gradient as described in Methods. (A) Representative western blot. (B) Western blots were quantified relative to the loading control, and then normalized to the total amount of protein at day 5 (n = 4; *P < .05, **P < .01, ***P < .005, compared with D5:total). (C) Proposed model of the role of MARCKS vs P-MARCKS in proplatelet formation. (D) MKs on day 4 were treated with PMA (500 pg/mL, PKC activator), CK636 (1 μM, Arp2 inhibitor), or both simultaneously, and percent proplatelet formation over time was quantified using the Incucyte imaging system (n = 3; *P < .05, compared with control).$

Phosphorylated MARCKS and Arp2 are downregulated in proplatelet-producing MKs. Murine fetal liver MKs were cultured as described in Methods and lysed at indicated times. Cell fractions were separated by BSA gradient as described in Methods. (A) Representative western blot. (B) Western blots were quantified relative to the loading control, and then normalized to the total amount of protein at day 5 (n = 4; *P < .05, **P < .01, ***P < .005, compared with D5:total). (C) Proposed model of the role of MARCKS vs P-MARCKS in proplatelet formation. (D) MKs on day 4 were treated with PMA (500 pg/mL, PKC activator), CK636 (1 μM, Arp2 inhibitor), or both simultaneously, and percent proplatelet formation over time was quantified using the Incucyte imaging system (n = 3; *P < .05, compared with control).

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