GRK6 regulates the hemostatic response to injury through its rate-limiting effects on GPCR signaling in platelets

Author:

Chen Xi1ORCID,Gupta Shuchi23ORCID,Cooper Matthew1ORCID,DeHelian Daniel23ORCID,Zhao Xuefei14,Naik Meghna U.1,Wurtzel Jeremy G. T.1,Stalker Timothy J.23,Goldfinger Lawrence E.1ORCID,Benovic Jeffrey5,Brass Lawrence F.23ORCID,McKenzie Steven E.1,Naik Ulhas P.1,Ma Peisong1ORCID

Affiliation:

1. Cardeza Foundation for Hematologic Research, Department of Medicine, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA;

2. Department of Medicine and

3. Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania School of Medicine, Philadelphia, PA;

4. Cyrus Tang Hematology Center, Soochow University, Suzhou, China; and

5. Department of Biochemistry and Molecular Biology, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA

Abstract

Key pointsGRK6 regulates the hemostatic response by limiting platelet activation via thrombin and adenosine 5′-diphosphate. GRK6 regulates the hemostatic response by reducing PAR1/4- and P2Y12-dependent signaling.

Publisher

American Society of Hematology

Subject

Hematology

Reference45 articles.

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2. Desensitization of G protein-coupled receptors;Freedman;Recent Prog Horm Res,1996

3. The role of receptor kinases and arrestins in G protein-coupled receptor regulation;Krupnick;Annu Rev Pharmacol Toxicol,1998

4. G protein-coupled receptor kinases: past, present and future;Komolov;Cell Signal,2018

5. Mechanisms of regulation of the expression and function of G protein-coupled receptor kinases;Penela;Cell Signal,2003

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