GPR183 Membrane Protein Introduction

Introduction of GPR183

GPR183 is encoded by the GPR183 gene. It belongs to a member of G protein-coupled receptors family which has been extensively studied during the past few decades because it mediates cellular responses to diverse environmental signals and offers numerous possibilities for therapeutic applications. GPR183 is an orphan seven-transmembrane receptor originally identified as the most up-regulated gene (>200-fold) in EBV-infected cells, it is also known as Epstein-Barr virus-induced G-protein coupled receptor 2 (EBI2).

Function of GPR183 Membrane Protein

GPR183 plays a role in germinal B cell development, especially after activation by B cell receptor and CD40 stimulation. The protein levels of GPR183 are significantly higher in B-lymphocyte cell lines and lymphoid tissues but not in T-lymphocyte cell lines or peripheral blood T lymphocytes. The expression of GPR183 turns off when B cell moves to the germinal center from the periphery and turns on when B cells exit the germinal center and re-enter the periphery. GPR183 is also a receptor for oxysterols, the most potent activator for 7α,25-dihydroxycholesterol (7a,25-OHC). In addition, GPR183 was reported to guide immune cell migration and plays a role in embryonic HSPC development. Blocking GPR183 signaling attenuates HSPC generation significantly while activating GPR183 signaling leads to more functional HSPCs. GPR183 is functionally expressed in multiple sclerosis patients and is important for the development of human inflammatory bowel disease (IBD). Therefore, GPR183 is a possible therapeutic target for the treatment of human sclerosis and IBD.

Fig.1 The signaling pathway of GPR183 (EIB2) in inflammation. (Guillemot, 2016)

Application of GPR183 Membrane Protein in Literature

1. Emgård J., et al. Oxysterol Sensing through the Receptor GPR183 Promotes the Lymphoid-Tissue-Inducing Function of Innate Lymphoid Cells and Colonic Inflammation. Immunity. 2018, 48, 120-132. PubMed ID: 29343433
   
   

   This article not only indicates that oxysterol-GPR183-dependent positioning within tissues controls ILC3 migration, lymphoid tissue organogenesis, and colitis but also points toward GPR183 is a therapeutic target for the treatment of human IBD.

2. Guillemot O., et al. Oxysterols in Metabolic Syndrome: From Bystander Molecules to Bioactive Lipids. Trends Mol. Med. 2016, 22(7):594-614. PubMed ID: 27286741
   
   

   This article reports two G-protein coupled receptors (GPCRs), CXCR2 and GPR183 (EBI2), which are involved in immune processes have been recently found to bind oxysterols.

3. Hannedouche S., et al. Oxysterols direct immune cell migration via EBI2. Nature. 2011, 475, 524-527. PubMed ID: 21796212
   
   

   This article demonstrates that CH₂₅H activates EBI2 biological activity in mice model and EBI2-oxysterol signaling pathway plays a vital role in the humoral immune responses and adaptive immune responses.

4. Kristine N., et al. EBI2, GPR18, and GPR17 - Three Structurally Related but Biologically Distinct 7TM Receptors. Curr Top Med Chem. 2011, 11, 618-628. PubMed ID: 21673108
   
   

   Authors in this group identify and characterize the first ligand targeting EBI2, GSK682753A, which provides a useful tool for further characterization of EBI2 as well as potential lead compounds.

5. Benned-Jensen T., et al. Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation. FEBS Open Bio. 2013, 3, 156-160. PubMed ID: 23772388
   
   

   This article demonstrates that the ligand of EBI2 inhibits the activation triggers pertussis toxin-sensitive MAP kinase phosphorylation and provides additional therapeutic options for inhibiting EBI2 activity.

GPR183 Preparation Options

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Reference

1. Guillemot O., et al. (2016). Oxysterols in Metabolic Syndrome: From Bystander Molecules to Bioactive Lipids. Trends Mol. Med. 22(7):594-614.

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