ApoE-Dependent Modulation of HDL and Atherosclerosis by G2A in LDL Receptor–Deficient Mice Independent of Bone Marrow–Derived Cells
Author:
Affiliation:
1. From the Department of Microbiology, University of Alabama at Birmingham.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine
Reference27 articles.
1. Loss of G2A promotes macrophage accumulation in atherosclerotic lesions of low density lipoprotein receptor-deficient mice
2. Absence of the G Protein–Coupled Receptor G2A in Mice Promotes Monocyte/Endothelial Interactions in Aorta
3. Gi-independent macrophage chemotaxis to lysophosphatidylcholine via the immunoregulatory GPCR G2A
4. Lysophospholipids of Different Classes Mobilize Neutrophil Secretory Vesicles and Induce Redundant Signaling through G2A
5. Prostaglandins Other Lipid Mediat 2008
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