Introduction of ADGRG3
ADGRG3, also known as G-protein coupled receptor 97 (GPR97) or G-protein coupled receptor PGR26, is a protein encoded by the human ADGRG3 gene. As a member of the adhesion GPCR family which is characterized by an extended extracellular region often possessing N-terminal protein modules, ADGRG3 possesses both an exceptionally long extracellular region, characteristic of cell adhesion proteins and an intracellular region reminiscent of other GPCRs.
|Basic Information of ADGRG3|
|Protein Name||Adhesion G-protein coupled receptor G3|
|Aliases||G-protein coupled receptor 97, G-protein coupled receptor PGR26|
|Organism||Homo sapiens (Human)|
Function of ADGRG3 Membrane Protein
The G protein-coupled receptor (GPCR) family is the largest membrane protein family which participates in a variety of physiologic functions and can be used as major targets of pharmaceutical drugs. Among them, ADGRG3 is a newly identified adhesion GPCR that was originally identified in mouse intestinal lymphatic endothelium. In addition, the expression of ADGRG3 can also be found in the hypothalamus, heart, kidney, and especially highly on thymus, spleen, and blood of mice. In immune cells, ADGRG3 is expressed on leukocytes, such as neutrophils, eosinophils, and mast cells. ADGRG3 is also expressed in murine pre-B cells and thymocytes. Studies have shown that ADGRG3 plays a critical role in the central nervous system, the immune system and tumor formation. It is able to regulate migration of human lymphatic endothelial cells. What’s more, ADGRG3 has been demonstrated to be over-expressed in some immunocytes, including lymphatic endothelial cells, mast cells, and eosinophils.
Fig.1 G-protein coupled receptor (GPCR) structure.
Application of ADGRG3 Membrane Protein in Literature
1. Wang J., et.al. Gpr97/Adgrg3 ameliorates experimental autoimmune encephalomyelitis by regulating cytokine expression. Acta Biochimica et Biophysica Sinica. 2018, 50(7): 666-675. PubMed ID: 29860267
This article suggests that Gpr97 plays an important role in the development of EAE and may have a therapeutic potential for the treatment of CNS autoimmunity.
2. Fang W., et.al. Gpr97 Exacerbates AKI by Mediating Sema3A Signaling. Journal of the American Society of Nephrology. 2018, 29(5): 1475-89. PubMed ID: 29531097
This article reveals that Gpr97 is an important mediator of AKI, and pharmacologic targeting of Gpr97-mediated Sema3A signaling at multiple levels may provide a novel approach for the treatment of AKI.
3. Shi J., et.al. Gpr97 is dispensable for metabolic syndrome but is involved in macrophage inflammation in high-fat diet-induced obesity in mice. Scientific reports. 2016, 6: 24649. PubMed ID: 27089991
This article indicates that Gpr97 might be required for local inflammation development in obesity-relative tissues, but does not play a role in metabolic disorder in HFD-induced obesity.
4. Shi JP., et.al. Gpr97 is dispensable for inflammation in OVA-induced asthmatic mice. PloS one. 2015, 10(7): e0131461. PubMed ID: 26132811
This article suggests that there is no obvious alteration in the inflammatory response or airway remodeling of the Gpr97-deficient mice with OVA-induced asthma. It indicates that the Gpr97-deficient mice with OVA-induced asthma.
5. Valtcheva N., et.al. The orphan adhesion G protein-coupled receptor GPR97 regulates migration of lymphatic endothelial cells via the small GTPases RhoA and Cdc42. Journal of Biological Chemistry. 2013, 288(50): 35736-48. PubMed ID: 24178298
This article finds that GPR97-deficient primary human LECs displays increased adhesion and collective cell migration, whereas single cell migration is decreased as compared with nontargeting siRNA-transfected control LECs. It indicates that GPR97 plays a possible role in lymphatic remodeling.
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