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Regulators of G protein signaling (RGS) proteins are known to interact with and negatively regulate/turn-off G protein activation. RGS18 is identified as an R4 subfamily member of this family with specific expression in hematopoietic progenitors, myeloerythroid cells, megakaryocytes and platelets. Studies focused on understanding its function in platelet biology have been limited, in part, due to lack of pharmacological inhibitors. Thus, the present study investigated the function of RGS18 in platelets, using the RGS18 knockout mouse model (RGS18(-/-)). We identified phenotypic differences between RGS18(-/-) and wild-type (WT) mice, and show that RGS18 plays a significant role in hemostasis and thrombosis. Hence, RGS18 deficiency markedly shortened bleeding as well as occlusion times (in vivo). Furthermore, RGS18(-/-) platelets displayed hyper-responsiveness with regards to agonist induced aggregation (in vitro). This gain of function phenotype may serve as the mechanism or explain, at least in part, the enhanced hemostasis and thrombosis phenotype observed in the RGS18 deletion mice. Collectively, our findings provide valuable insight and highlight a critical and direct role for RGS18 in modulating platelet function.
Pubmed ID: 25969426
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UK’s national facility for mouse genetics and use of mouse models for preclinical study of human disease.Offers services to researchers around the world. Services include free archiving of mouse lines to protect them for future use, distribution of mouse lines from the Archive, breeding and phenotyping of genetically altered mice, and genome engineering services to generate new mouse models.Offers archiving and distribution of mouse lines to safeguard germplasm collected from unique strains and make it readily available to the scientific community.
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