mProX™ Human MRGPRF Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Patrick Liam (Creative Biolabs Scientific Support)
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Patrick Liam (Creative Biolabs Scientific Support)
Published Data
Fig.1 Suppressing MrgprF in A375 cells enhanced colony growth.
MrgprF knockdown enhanced A375 cell colony formation capacity, as depicted in the quantified results. The bars represent the mean ± SD. Statistical significance is indicated as *P < 0.05, **P < 0.01, and ***P < 0.001. Colony numbers are abbreviated as "Colony no.," with control represented by "Ctrl," scramble control shRNA by "Scramble," shRNA#1 by "sh#1," and shRNA#2 by "sh#2."
Ref: Shen, Qiushuo, et al. "MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling." Signal transduction and targeted therapy 7.1 (2022): 147.
Pubmed: 35504869
DOI: 10.1038/s41392-022-00945-9
Research Highlights
Kaczmarek I, et al. "Identifying G protein-coupled receptors involved in adipose tissue function using ." iScience, 2023.
In this study, the authors established FATTLAS, an interactive public database, to better understand the role of G protein-coupled receptors (GPCRs) in adipose tissue (AT) function. They extracted the GPCRome of non-obese and obese individuals and identified highly expressed and differentially regulated GPCRs. Using a (pre)adipocyte cell model, they investigated the functions of four specific GPCRs (GPR146, MRGPRF, FZD5, PTGER2) and found that they play a role in adipogenesis, adipocyte viability, cAMP levels, and adipocyte lipolysis. This study has identified four previously unrecognized GPCRs that are associated with AT function and adipogenesis.
Pubmed:
37766984
DOI:
10.1016/j.isci.2023.107841
You Z, et al. "lnc-MRGPRF-6:1 Promotes ox-LDL-Induced Macrophage Ferroptosis via Suppressing ." Mediators of inflammation, 2023.
Ferroptosis, a recent discovery in cell death, has been identified as a potential target for atherosclerosis (AS). Long noncoding RNAs (lncRNAs) have shown involvement in regulating ferroptosis. In a previous study, high expression of lnc-MRGPRF-6:1 was observed in patients with coronary atherosclerotic disease (CAD) and was associated with macrophage-mediated inflammation in AS. The current study aims to investigate the role of lnc-MRGPRF-6:1 in oxidized-low-density lipoprotein (ox-LDL)-induced macrophage ferroptosis in AS. Macrophages treated with ox-LDL were examined for ferroptosis-related markers and mitochondrial morphology. Knockdown and overexpression of lnc-MRGPRF-6:1 in THP-1-derived and human monocyte-derived macrophages were carried out to explore its role in ox-LDL-induced ferroptosis. Transcriptome sequencing, literature searching, quantitative real-time polymerase chain reaction and western blot techniques were utilized to investigate the specific signaling pathway involved. It was found that lnc-MRGPRF-6:1 may regulate ferroptosis via the suppression of glutathione peroxidase 4 (GPX4). Further analysis showed a correlation between lnc-MRGPRF-6:1 and GPX4 expression levels in CAD patients and controls. These results indicate that lnc-MRGPRF-6:1 promotes macrophage ferroptosis by inhibiting GPX4.
Pubmed:
37621767
DOI:
10.1155/2023/5513245
