Functional redundancy between RAP1 isoforms in murine platelet production and function

Author:

Stefanini Lucia1ORCID,Lee Robert H.2ORCID,Paul David S.2,O'Shaughnessy Ellen C.3,Ghalloussi Dorsaf2,Jones Christopher I.4,Boulaftali Yacine5,Poe Kathryn O.2,Piatt Raymond2,Kechele Dan O.6,Caron Kathleen M.6,Hahn Klaus M.3ORCID,Gibbins Jonathan M.4,Bergmeier Wolfgang27ORCID

Affiliation:

1. Department of Internal Medicine and Medical Specialties, Sapienza University of Rome, Rome, Italy;

2. McAllister Heart Institute and

3. Department of Pharmacology and Lineberger Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC;

4. Institute for Cardiovascular and Metabolic Research, University of Reading, Reading, United Kingdom;

5. Laboratory of Vascular Translational Science, Université Paris Diderot, Sorbonne Paris Cité, U1148 INSERM, Paris, France; and

6. Department of Cell Biology and Physiology and

7. Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC

Abstract

Key Points Deletion of both Rap1a and Rap1b impairs platelet production and abolishes platelet adhesion at sites of mechanical trauma. Platelet RAP1 signaling is dispensable for vascular integrity during development and at sites of inflammation.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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