ArticleiScience2026
A Rac-PI3Kβ feedback loop drives GPVI-dependent platelet activation.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
6 authors.
Funding
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Abstract
Class I PI3Kβ is critical in controlling platelet activation and preserving thrombus stability under high shear. PI3Kβ is unique among class I phosphoinositide 3-kinases (PI3Ks) in being activated by Rho-family GTPases Rac and Cdc42, positioning it as a potential key link between Rho-family GTPases and platelet signaling. Here, we combined pharmacological inhibition with genetic approaches to define a direct Rho-PI3Kβ signaling axis in mouse platelets. Platelets from knockin mice carrying two point mutations within the Rho-binding domain (RBD) of the PI3Kβ catalytic subunit p110β exhibited impaired GPVI-mediated platelet signaling, functional responses, and spreading on fibrinogen. Pharmacological inhibition with the PI3Kβ-selective inhibitor AZD6482 demonstrated that these responses largely depend on the p110β RBD. Inhibition of Rac/Cdc42 in wild-type platelets phenocopied the knockin defects, supporting a direct role for Rho GTPases in PI3Kβ activation. Conversely, Rac activation was impaired in RBD-mutant and AZD6482-treated platelets, revealing a Rac-PI3Kβ feedback loop that amplifies GPVI-dependent platelet activation.
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