mProX™ Human GPR148 Stable Cell Line

Product Information

Target Family

Orphan Family

Target Protein Species

Human

Host Cell Type

CHO-K1;HEK293

Target Classification

Other Targets Drug Discovery Assays and Products

Target Research Area

Cardiovascular Research;CNS Research

Related Diseases

Hypotrichosis-Lymphedema-Telangiectasia-Renal Defect Syndrome;Autism Spectrum Disorder

Gene ID

Human:344561

UniProt ID

Human:Q8TDV2

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

GPR148, an orphan G protein-coupled receptor, has been the subject of scientific exploration in recent years. Although the specific function and ligands of GPR148 remain to be fully elucidated, emerging research has started to shed light on its potential roles. For instance, GPR148 has been implicated in the regulation of myelination and remyelination processes. Specifically, GPR148 is enriched in oligodendrocyte precursor cells (OPCs) and has been shown to negatively regulate the differentiation of OPCs to oligodendrocytes, as well as myelination and remyelination. This suggests that targeting GPR148 might offer therapeutic avenues for promoting myelin repair in demyelinating diseases. Furthermore, GPR148 has been associated with diabetic nephropathy, indicating its potential involvement in kidney-related pathologies. As research continues, the understanding of GPR148's role in various physiological and pathological processes is expected to expand.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Sarah (Verified Customer)

How is GPR148 related to the GPCR Class A Rhodopsin receptors? Jul 24 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

GPR148 is a member of the GPCR Class A Rhodopsin receptors. Phylogenetic studies based on sequence-structure have been conducted to understand the evolutionary relationships and potential ligand associations for these receptors. Jul 24 2020

chat Kevin (Verified Customer)

Are there any genetic variations involving GPR148 that may have clinical implications? Oct 10 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

Yes, small rare recurrent deletions and reciprocal duplications in the 2q21.1 region, which includes GPR148 and the brain-specific ARHGEF4, have been identified. These genetic variations may have potential implications in neurological disorders. Oct 10 2022

Published Data

Fig.1 The CHO-β-arrestin system overexpressing LGR6 or GPR148 was used to assess ligand-receptor interaction (MaR1).

In the investigation, CHO-K1 cells with heightened expression of LGR6 or GPR148 were subjected to MaR1 treatment, revealing noteworthy statistical differences (*P < 0.05, ***P < 0.001) for MaR1 versus vehicle in LGR6 cells. Additionally, a comparison between LGR6 and GPR148 cells was performed. Interestingly, MaR1, administered in concentrations ranging from 10^-13 M to 10^-8 M, did not induce a substantial rise in RLU in GPR148 cells. These findings, derived from three independent experiments, are presented as mean ± SEM, with significance levels denoted as #P < 0.05 and ##P < 0.01.

Ref: Chiang, Nan, et al. "Maresin 1 activates LGR6 receptor promoting phagocyte immunoresolvent functions." The Journal of clinical investigation 129.12 (2019): 5294-5311.

Pubmed: 31657786

DOI: 10.1172/JCI129448

Research Highlights

Jyoti Rani et al. "Identification of perturbed pathways rendering susceptibility to tuberculosis in type 2 diabetes mellitus patients using BioNSi simulation of integrated networks of implicated human genes." Journal of biosciences, 2022
In patients with type 2 diabetes mellitus (T2DM), chronic hyperglycemia and inflammation contribute to an increased vulnerability to tuberculosis (TB), resulting in poor control of the disease. To investigate which pathways in T2DM patients lead to susceptibility to TB, an integrative approach was utilized. A total of 36 genes associated with type 2 diabetes-related TB (T2DMTB) were collected from literature and analyzed for differential expression in T2DM patient data (GSE26168). Notably, the gene DEFA1 showed significant differential expression at P(adj) <0.05. In addition, several other genes and microRNAs were differentially expressed at P(adj) <0.05, including TNFRSF10A, MSRA, GPR148, SLC37A3, PXK, PROK2, REV3L, PGM1, HIST3H2A, PLAC4, LETM2, EMP2, and hsa-miR-146a. These genes and microRNAs, along with 28 others from the T2DMTB set and any other differentially expressed genes at P(adj) <0.05, were analyzed in STRING, resulting in a highly connected network with a confidence score of 0.7 or higher. KEGG pathway analysis was performed, and pathways related to both diabetes and TB were retained. Simulation of the network with BioNSi using gene expression data revealed that NF-kappa B and Toll-like receptor pathways were significantly perturbed, ranking highly in multiple gene expression datasets comparing T2DM patients to healthy controls. Other pathways, including necroptosis and FoxO signaling, also showed high ranking in various gene expression datasets. The perturbation of these pathways may contribute to the susceptibility to TB in T2DM patients.
Jyoti Rani et al. "Identification of perturbed pathways rendering susceptibility to tuberculosis in type 2 diabetes mellitus patients using BioNSi simulation of integrated networks of implicated human genes." Journal of biosciences, 2022
Pubmed: 36476775

Stefania Gimelli et al. "Recurrent microdeletion 2q21.1: report on a new patient with neurological disorders." American journal of medical genetics. Part A, 2014
In this study, the genes GPR148, FAM123C (AMER3), ARHGEF4, FAM168B, and PLEKHB2 were evaluated in comparison with previously reported cases in the literature to establish a more precise genotype-phenotype correlation of 2q21.1 microdeletions. The analysis of our patient's clinical characteristics provides valuable insight for understanding the implications of these genetic deletions. This study highlights the importance of further research in this area to better understand the impact of these genetic alterations on human health.
Stefania Gimelli et al. "Recurrent microdeletion 2q21.1: report on a new patient with neurological disorders." American journal of medical genetics. Part A, 2014
Pubmed: 24591035 DOI: 10.1002/ajmg.a.36357