mProX™ Human GPR84 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 LPS-induced inflammation is regulated by GPR84.
Before subjecting cells to LPS stimulation, Gpr84 was effectively silenced using siRNA, leading to a notable decrease in the mRNA expression of cytokines induced by LPS. The data presented represent the means ± SEM of four biological replicates, each with three technical repetitions, with the asterisk (*) indicating significant differences compared to NC cells when exposed to LPS stress.
Ref: Yin, Chengcong, et al. "Regulatory role of Gpr84 in the switch of alveolar macrophages from CD11blo to CD11bhi status during lung injury process." Mucosal Immunology 13.6 (2020): 892-907.
Pubmed: 32719411
DOI: 10.1038/s41385-020-0321-7
Research Highlights
Zhang X, et al. "Pro-phagocytic function and structural basis of GPR84 signaling.." Nature communications, 2023.
In this study, the authors focus on GPR84, a G protein-coupled receptor (GPCR) that is activated by endogenous medium-chain fatty acids (MCFAs), and investigate its pro-inflammatory signaling and pro-phagocytic activities in inducing phagocytosis of cancer cells by macrophages. They demonstrate that the synthetic agonist 6-OAU, when combined with blockade of the CD47 protein on cancer cells, can activate GPR84 and enhance phagocytosis. Additionally, the authors determine the high-resolution structure of the GPR84-G(i) signaling complex with 6-OAU, providing insights into the receptor's activation, selectivity for MCFAs, and potential ligand binding and dissociation mechanisms. These findings contribute to a better understanding of GPR84 signaling and offer potential for novel drug development.
Pubmed:
37709767
DOI:
10.1038/s41467-023-41201-0
Luscombe VB, et al. "Kinetic insights into agonist-dependent signalling bias at the pro-inflammatory ." European journal of pharmacology, 2023.
GPR84, a G-protein coupled receptor (GPCR) associated with inflammation, poses challenges for targeting strategies aimed at reducing excessive inflammation in disease due to limited knowledge of its functional role. To address this, the authors created heterologous cell lines with low GPR84 expression levels that mimicked primary cell responses. These cell lines were then used to investigate the signalling profile and localization of GPR84 upon treatment with two known agonists, 6-OAU and DL-175. DL-175 displayed a delayed impedance response, suppressed activation of Akt and impaired GPR84 internalization from the plasma membrane compared to 6-OAU. These differences were transient and only observed at early time points, underscoring the importance of receptor number and kinetic readouts in understanding signalling bias. This study provides new insights into GPR84 signalling and demonstrates the potential of these cell lines in evaluating new agonists.
Pubmed:
37543157
DOI:
10.1016/j.ejphar.2023.175960
