mProX™ Human GPR132 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 GPR132 inhibited AML cell growth.
The images display colony formation involving Tet-On AML cells. These cells were grown in a semi-solid medium and subjected to a 1 μg/mL doxycycline treatment, resulting in the induction of GPR132 overexpression. On the seventh day of culture, colonies were observed and photographed using a microscope. Scale bars, measuring 100 μm, provide a reference for the observed structures.
Ref: Yi, Chunyang, et al. "Activation of orphan receptor GPR132 induces cell differentiation in acute myeloid leukemia." Cell Death & Disease 13.11 (2022): 1004.
Pubmed: 36437247
DOI: 10.1038/s41419-022-05434-z
Research Highlights
Wang JL, et al. "Functional screening and rational design of compounds targeting GPR132 to treat ." Nature metabolism, 2023.
Chronic inflammation is a key factor in the development of type 2 diabetes mellitus, particularly due to the presence of macrophages in the islets. By conducting a comprehensive analysis of lipid-transmembrane receptor signaling in these macrophages, researchers identified the importance of endogenous 9(S)-hydroxy-10,12-octadecadienoic acid-G-protein-coupled receptor 132 (GPR132)-Gi signaling in islet macrophage reprogramming. Macrophages lacking GPR132 were found to reverse metabolic disorders in mice with high-fat diets. With the help of cryo-electron microscopy, the team was able to design potent and selective GPR132 agonists and antagonists, culminating in the identification of NOX-6-18, a selective GPR132 antagonist that modulates macrophage reprogramming in the pancreatic islets and improves glucose metabolism and weight gain in high-fat diet-fed mice. This study not only sheds light on the role of intra-islet lipid signaling in islet macrophage reprogramming, but also presents a promising strategy for identifying important G-protein-coupled receptor targets and designing potential treatments for challenging conditions such as diabetes.
Pubmed:
37770763
DOI:
10.1038/s42255-023-00899-4
