Scientists have used quantitative analysis methods to identify the role Rac1 plays in blood platelets.
In a study undertaken by a team at the Department of Biomedical Engineering at Oregon Health & Science University and published by the Journal of Molecular Signaling, scientists hoped to look into the carefully regulated change in shape blood platelets undergo to serve as the primary mediators of hemostasis and thrombosis.
This change is dependent on the Rho GTPase family member Rac1, but prior to the study, little was known as to how.
Using quantitative analysis processes, such as Western blotting experiments, the scientists confirmed that P-Rex1 is expressed in platelets and associated with Rac1.
They found that platelets from P-Rex1-/--deficient mice treated with platelet agonists or exposed to platelet activating surfaces of fibrinogen, collagen and thrombin responded to platelet agonists and activating surfaces similarly to wild type platelets.
"Our study demonstrates that Rac1 interacts with P-Rex1 from platelets, however, the GEF activity of P-Rex1 is not likely essential to PAR and P2Y GPCR- and Rac1-mediated platelet lamellipodia formation and spreading," the study claimed.
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