Study identifies MD-1 as endogenous agonist for orphan receptor GPRC5B, linking macrophages to adipocyte signaling
By
Heng Zhu
Summary
This article describes research identifying MD-1 as an endogenous agonist for the orphan G protein-coupled receptor GPRC5B. Using a virion-based GPCR expression system combined with human protein microarrays, Johansen et al. discovered that the macrophage glycoprotein MD-1 stimulates Gαs-dependent signaling through GPRC5B. GPRC5B is found on adipocytes, and GPRC5B-deficient mice show resistance to high-fat diet-induced obesity and reduced adipose inflammation. Cell-cell contact experiments between macrophage and adipocyte cell lines demonstrated MD-1 stimulation through GPRC5B, potentially revealing a new mechanism in metabolic regulation and inflammation.
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Twitter / XStudy identifies MD-1 as endogenous agonist for orphan receptor GPRC5B, linking macrophages to adipocyte signalingscim.agKey quotes
· 5 pulledOne-third of all nonodorant G protein–coupled receptors (GPCRs) in humans are orphans with no known ligands.
Deorphanization of these GPCRs is hampered by the difficulty of producing purified recep...
GPRC5B-deficient mice are resistant to high-fat diet–induced obesity and have reduced adipose inflammation.
Using a virion-based GPCR expression system combined with human protein microarrays, Johansen et al. identified the macrophage glycoprotein MD-1 as a potential endogenous GPRC5B agonist.
Biochemical and functional assays showed that MD-1 stimulated Gαs-dependent signaling through GPRC5B.
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