Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN)
Copyright policy )Granulocyte chemotaxis and disease expression are differentially regulated by GRK subtype in an acute inflammatory arthritis model (K/BxN)
Chemokine receptors are G-protein coupled receptors (GPCRs) phosphorylated by G-protein receptor kinases (GRKs) after ligand-mediated activation. We hypothesized that GRK subtypes differentially regulate granulocyte chemotaxis and clinical disease expression in the K/BxN model.
- Brigham and Women's Faulkner Hospital United States
- University of North Carolina at Chapel Hill United States
- Duke University United States
- Novartis (Switzerland) Switzerland
- Howard Hughes Medical Institute United States
Male, Mice, Knockout, G-Protein-Coupled Receptor Kinase 2, Interleukin-6, Arthritis, Complement C5a, G-Protein-Coupled Receptor Kinases, Arthritis, Experimental, Leukotriene B4, Mice, Inbred C57BL, Chemotaxis, Leukocyte, Mice, Acute Disease, Animals, Granulocytes
Male, Mice, Knockout, G-Protein-Coupled Receptor Kinase 2, Interleukin-6, Arthritis, Complement C5a, G-Protein-Coupled Receptor Kinases, Arthritis, Experimental, Leukotriene B4, Mice, Inbred C57BL, Chemotaxis, Leukocyte, Mice, Acute Disease, Animals, Granulocytes
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