mProX™ Human GPR34 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 After NPS stimulation, the expression of core clock components NPAS2, PER1, and CRY1 was clearly elevated.
BV-2 cells were transfected with Gpr34 shRNA or NC shRNA. The cells were then subjected to western blot to analyze the protein level of GPR34. The results are presented as mean ± SD. *p < 0.05.
Ref: Lin, Lu-Lu, et al. "GPR34 Knockdown Relieves Cognitive Deficits and Suppresses Neuroinflammation in Alzheimer's Disease via the ERK/NF-κB Signal." Neuroscience 528 (2023): 129-139.
Pubmed: 37557947
DOI: 10.1016/j.neuroscience.2023.08.001
Research Highlights
Xia A, et al. "Cryo-EM structures of human GPR34 enable the identification of selective ." Proceedings of the National Academy of Sciences of the United States of America, 2023.
The authors investigated the interaction between G(i) protein and LysoPS, a unique ligand, and found that the compound binds to a polar cavity formed by TM3, 6, and 7, as well as a hydrophobic groove formed by TM3-5. Through virtual screening and structural optimization, they identified a potent and selective antagonist, YL-365. By designing fusion proteins, they were able to determine the cryo-EM structure of the inactive GPR34 complexed with YL-365, revealing its binding mechanism and potential use in treating neuropathic pain. This study provides important insights into GPR34 and offers a new approach for treating diseases by targeting this receptor.
Pubmed:
37733739
DOI:
10.1073/pnas.2308435120
Lin LL, et al. "GPR34 Knockdown Relieves Cognitive Deficits and Suppresses Neuroinflammation in ." Neuroscience, 2023.
Alzheimer's disease (AD) is a neurodegenerative disease characterized by the aggregation of amyloid-beta (Abeta) and neuroinflammation. The role of G-protein-coupled receptor 34 (Gpr34) in AD is uncertain, despite its high expression in the hippocampus of APP/PS1 mouse model. This study aimed to elucidate the role of Gpr34 and its molecular mechanism. Data from GSE85162 were analyzed for differentially expressed genes in the hippocampus tissues of APP/PS1 mice. Gpr34 levels in hippocampus and BV-2 cells were determined, and the activation of ERK/NF-kappaB signal was assessed. Results showed that Gpr34 knockdown reduced the levels of TNF-alpha, IL-1beta, IL-6, and iNOS in BV-2 cells exposed to Abeta(1-42) and attenuated ERK/NF-kappaB signal activation. In vivo, Gpr34 knockdown improved cognitive deficits, reduced levels of TNF-alpha, IL-1beta, and IL-6, and suppressed microglial activation and ERK/NF-kappaB signal in APP/PS1 mice. These findings suggest that Gpr34 contributes to the pathogenesis of AD by promoting neuroinflammation and microglial activation through the ERK/NF-kappaB signal.
Pubmed:
37557947
DOI:
10.1016/j.neuroscience.2023.08.001
