mProX™ Human GPR39 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 GR39 promotes cardiomyocyte hypertrophy in vitro.
Suppression of Gpr39 leads to the inhibition of Ang II-triggered cardiomyocyte hypertrophy, as observed in this study. Cardiomyocytes underwent a 24-hour siRNA transfection, followed by exposure to Ang II (1 μM) for an additional 48 hours to induce hypertrophic changes. Subsequently, the cardiomyocytes were subjected to staining using α-actinin, and ImageJ software was employed to quantify cell size. The experiment was conducted with a sample size of five in each group, demonstrating statistically significant differences (**p < 0.01) in cell size alterations among the experimental conditions.
Ref: Liao, Hongjuan, et al. "GPR39 promotes cardiac hypertrophy by regulating the AMPK-mTOR pathway and protein synthesis." Cell Biology International 45.6 (2021): 1211-1219.
Pubmed: 33554444
DOI: 10.1002/cbin.11566
Research Highlights
Zhang L, et al. "Activation of G-protein-coupled receptor 39 reduces neuropathic pain in a rat ." Neural regeneration research, 2024.
The study focuses on researching the effects of the activated G-protein-coupled receptor 39 (GPR39) on neuropathic pain. Through interaction with sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), GPR39 has been found to attenuate inflammation. However, its role in attenuating neuropathic pain has not been established. Using a Sprague-Dawley rat model, the researchers discovered that GPR39 expression is decreased in the spinal dorsal horn in rats with spared nerve injury-induced neuropathic pain. By administering a specific agonist of GPR39, TC-G 1008, they were able to alleviate mechanical allodynia, improve spinal cord mitochondrial biogenesis, and reduce neuroinflammation. These effects were reversed by GPR39 small interfering RNA (siRNA), Ex-527 (SIRT1 inhibitor), and PGC-1alpha siRNA. In conclusion, the study shows that GPR39 activation can effectively ameliorate neuropathic pain through the SIRT1/PGC-1alpha pathway.
Pubmed:
37721302
DOI:
10.4103/1673-5374.380905
Rychlik M, et al. "Chronic memantine disrupts spatial memory and up-regulates Htr1a gene expression ." Brain research, 2023.
There was no significant impact of acute memantine treatment on the "where?" component of episodic-like memory (ELM). However, both wild-type (WT) and GPR39 knockout (KO) mice showed a slight improvement in the "where?" component after 12 days of memantine treatment. Additionally, GPR39KO mice exhibited disrupted spatial memory (SM) after 24 days of memantine treatment, which was linked to an increase in Htr1a hippocampal expression. Overall, these findings suggest that memantine may have a differential effect on ELM and SM depending on the duration of treatment and animal genotype.
Pubmed:
37716463
DOI:
10.1016/j.brainres.2023.148577
