Abstract
Significance G protein–coupled receptors (GPCRs) are important regulators of cellular and biological functions and are primary targets of therapeutic drugs. About 100 mammalian GPCRs are still considered orphan receptors because they lack a known endogenous ligand. We report the deorphanization of GPR182, which is expressed in endothelial cells of the microvasculature. We show that GPR182 is an atypical chemokine receptor, which binds CXCL10, 12, and 13. However, binding does not induce downstream signaling. Consistent with a scavenging function of GPR182, mice lacking GPR182 have increased plasma levels of chemokines. In line with the crucial role of CXCL12 in hematopoietic stem cell homeostasis, we found that loss of GPR182 results in increased egress of hematopoietic stem cells from the bone marrow.
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