ArticleFrontiers in immunology2025
P-Rex1 controls phagocytosis and the killing of bacteria by murine neutrophils independently of its catalytic activity.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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Who cites it
1 citing paper in PubMed.
- P-Rex1 limits the agonist-induced internalization of GPCRs independently of its Rac-GEF activity.Cell reports · 2025Article
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Authors and funding
6 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Introduction: P-Rex1 is a guanine-nucleotide factor for the small GTPase Rac (Rac-GEF) that is known to mediate neutrophil migration and ROS production in response to the activation of GPCRs. These roles of P-Rex1 are assumed to require its activation of Rac. Methods: Here, we used mice which lack P-Rex1 ( Results: We show that P-Rex1 mediates migration, ROS, and NETs through its Rac-GEF activity, but is dispensable for the degranulation of azurophil, specific and gelatinase granules. Surprisingly, P-Rex1 mediates the clearance of bacteria Discussion: Together, our study identifies P-Rex1 as a regulator of NET formation and phagocytosis in neutrophils and reveals that P-Rex1 mediates bactericidal activity and phagocytosis independently of its catalytic Rac-GEF activity, through mechanisms not obviously linked to other recently identified adaptor functions.
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