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Bergmeier Lab has a new publication in Blood: Functional redundancy between RAP1 isoforms in murine platelet production and function.

This work demonstrates a crucial role for the small GTPase RAP1 in platelet production and function. Using mice deficient in one or both RAP1 isoforms, RAP1A and RAP1B, we were able to demonstrate that (1) megakaryocytes (MK) depend on RAP1 signaling during proplatelet formation,  the terminal step of MK development, (2) both isoforms play redundant roles in platelet integrin activation and adhesion, (3) lack of both RAP1 isoforms leads to marked bleeding and protection from thrombosis in mice, and (4) platelet RAP1 signaling is dispensable for vascular integrity during development and at sites of inflammation.

First authors of the study were Lucia Stefanini (Sapienza University of Rome, Italy) and Robert Lee (postdoc in Bergmeier lab). Significant contributions came from collaborators at UNC (Hahn and Caron labs) and the University of Reading, UK. Bergmeier Lab send additional thanks to Brian Cooley from the Animal Surgery Core and to Keith Burridge who shared important reagents.