mProX™ Human GPR137B Stable Cell Line
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- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 Defects in autophagy flux contribute to the LC3 phenotype in GPR137B-knockdown cells.
GPR137B siRNA knockdown results in autophagy flux deficiencies as determined by p62 staining and the fold change in p62 puncta number. The scale bar is 20 meters long. The error bars represent the standard deviation of the mean (P value was computed using a ratio paired, two-tailed Student's t-test; n = 3 separate experiments).
Ref: Gan, Lin, et al. "The lysosomal GPCR-like protein GPR137B regulates Rag and mTORC1 localization and activity." Nature cell biology 21.5 (2019): 614-626.
Pubmed: 31036939
DOI: 10.1038/s41556-019-0321-6
Research Highlights
Wenbo Qu et al. "Long Noncoding RNA Gpr137b-ps Promotes Advanced Atherosclerosis via the Regulation of Autophagy in Macrophages." Arteriosclerosis, thrombosis, and vascular biology, 2023
The current therapies for advanced atherosclerosis are limited in their ability to fully reverse the condition. High levels of amino acids, commonly found in Western diets, can lead to dysfunction in the mTORC1-autophagy signaling pathway in macrophages, which contributes to the progression of atherosclerotic plaques. With this in mind, researchers investigated the potential of Gpr137b-ps, a protein found to be upregulated in advanced plaques, to regulate autophagy in macrophages and control the progression of atherosclerosis. Their experiments on ApoE(-/-) mice and cell cultures demonstrated that Gpr137b-ps deficiency promoted autophagy and reduced plaque formation, and that this was achieved through the protein interfering with the binding of HSC70 to G3BP, which is involved in suppressing mTORC1 signaling. Further analysis using computational modeling revealed that this interaction is mediated by the W90-F92 motif in HSC70. These findings suggest that Gpr137b-ps may be a potential therapeutic target for the treatment of advanced atherosclerosis.
Wenbo Qu et al. "Long Noncoding RNA Gpr137b-ps Promotes Advanced Atherosclerosis via the Regulation of Autophagy in Macrophages." Arteriosclerosis, thrombosis, and vascular biology, 2023
Pubmed:
37767704
DOI:
10.1161/ATVBAHA.123.319037
Zohirul Islam et al. "Gpr137b is an orphan G-protein-coupled receptor associated with M2 macrophage polarization." Biochemical and biophysical research communications, 12 Feb. 2019
Two distinct macrophage subtypes, M1 and M2, characterized by unique phenotypes in their microenvironment, have garnered recent attention for their association with G-protein-coupled receptors (GPCRs) in polarization. However, limited information exists on GPCR-mediated macrophage polarization. This study focuses on Gpr137b, an orphan GPCR highly expressed in the mouse macrophage cell line RAW264, and its role in M2 macrophage polarization. Through CRISPR/Cas9 genome editing, Gpr137b-knockout (Gpr137b-KO) clones were created, showing frameshifting deletions in the Gpr137b ATG start codon region. Subsequent analyses revealed reduced M2 macrophage marker gene expression in Gpr137b-KO cells, establishing Gpr137b as a potential M2 macrophage polarization regulator.
Zohirul Islam et al. "Gpr137b is an orphan G-protein-coupled receptor associated with M2 macrophage polarization." Biochemical and biophysical research communications, 12 Feb. 2019
Pubmed:
30595385
DOI:
10.1016/j.bbrc.2018.12.140
