Product Information
Catalog Number:
MC1129
Lot Number:
MC1129-021325
Quantity:
Available 1mg, 5mg, or 10mg per vial
Protein concentration: 16.78 mg/mL
Packaging Buffer: 20mM Gly-Gly, 1mM MgCl2, 25mM Sucrose (pH 7.2)
Host cell:
HEK293T
Transfection:
Expression vector containing full-length human GPR75 cDNA (GenBank accession number AF072693.1) with FLAG tag sequence at N-terminus
Recommended Storage:
Liquid nitrogen upon receiving
Data Sheet
Background: GPR75 is a class A orphan G protein-coupled receptor expressed in most tissues, but highly expressed in the brain. Studies have suggested that GPR75 is involved in hypertension, metabolic syndrome, obesity, and cancer, and may be a viable therapeutic target for the treatment of these conditions. Binding studies have shown that the eicosanoid 20-hydroxyeicosatetraenoic acid (20-HETE) and the chemokine CCL5 (RANTES) bind to GPR75, but the outcomes of these binding interactions are disputed. GPR75 associates with Gαq, and therefore its activation should result in an increase in [cytoplasmic Ca2+] through the phospholipase C / inositol triphosphate pathway.
Application: Functional assays
Figure 1. Receptor expression on cell surface measured by flow cytometry (FACS) using an anti-FLAG antibody. Thin line: parental cells; thick line: receptor-expressing cells.
References:
Pascale et al. (2021) Uncovering the signalling, structure and function of the 20-HETE-GPR75 pairing: Identifying the chemokine CCL5 as a negative regulator of GPR75. Br J Pharmacol. 178:3813-3828.
Dashti et al. (2023) G Protein-Coupled Receptor 75 (GPR75) As a Novel Molecule for Targeted Therapy of Cancer and Metabolic Syndrome. Asian Pac J Cancer Prev. 24(5):1817-1825.
Ignatov et al. (2006) RANTES stimulates Ca2+ mobilization and inositol triphosphate (IP3) formation in cells transfected with G protein-coupled receptor 75. Br J Phamacol. 149:490-497.
Garcia et al. (2017) 20-HETE Signals Through G Protein-Coupled Receptor GPR75 (Gq) to Affect Vascular Function and Trigger Hypertension. Circ Res. 120(11):1776- 1788.