AI Article Synopsis

  • WNT-3a regulates platelet function by influencing the activity of four GTPase proteins: Rap1, Cdc42, Rac1, and RhoA.
  • It inhibits integrin-α(IIb)β(3) adhesion through the inactive form of Rap1b, while enhancing Cdc42 and Rac1-GTP levels, which disrupts normal platelet spreading.
  • Additionally, WNT-3a affects the interaction between Daam-1 and Dishevelled upon platelet activation, leading to changes in RhoA-GTP levels, suggesting WNT-3a's role as an upstream regulator of GTPase activity in platelets.

Article Abstract

Here we provide evidence that WNT-3a modulates platelet function by regulating the activity of four key GTPase proteins: Rap1, Cdc42, Rac1 and RhoA. We observe WNT-3a to differentially regulate small GTPase activity in platelets, promoting the GDP-bound form of Rap1b to inhibit integrin-α(IIb)β(3) adhesion, while concomitantly increasing Cdc42 and Rac1-GTP levels thereby disrupting normal platelet spreading. We demonstrate that Daam-1 interacts with Dishevelled upon platelet activation, which correlates with increased RhoA-GTP levels. Upon pre-treatment with WNT-3a, this complex disassociates, concurrent with a reduction in RhoA-GTP. Together these data implicate WNT-3a as a novel upstream regulator of small GTPase activity in platelets.

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http://dx.doi.org/10.1016/j.febslet.2012.05.060DOI Listing

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