mProX™ Human GPR149 Stable Cell Line

Product Information

Target Family

Orphan Family

Target Protein Species

Mouse

Host Cell Type

Oligodendrocyte precursor cells;CHO-K1;HEK293

Target Classification

Other Targets Drug Discovery Assays and Products

Gene ID

Human:344758

UniProt ID

Human:Q86SP6

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

GPR149 is another orphan G protein-coupled receptor that has garnered attention in the scientific community. Recent studies have highlighted its potential role in myelination processes. Specifically, GPR149 has been shown to act as a negative regulator of myelination and remyelination, suggesting its involvement in demyelinating diseases. Additionally, GPR149 has been linked to diabetic nephropathy, a complication of diabetes that affects the kidneys. Moreover, methylation patterns of GPR149 have been proposed as potential prognostic markers for clear cell renal cell carcinoma. These findings underscore the importance of GPR149 in various physiological and pathological contexts.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Donna (Verified Customer)

How does GPR149 influence myelination processes? Jan 15 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

GPR149 acts as a negative regulator of myelination and remyelination. Its expression is downregulated during the differentiation of oligodendrocyte precursor cells (OPCs) into oligodendrocytes (OLs). GPR149 deficiency promotes OPC to OL differentiation, leading to earlier myelin development. Jan 15 2022

chat Ashley (Verified Customer)

What role does GPR149 play in fertility? May 01 2020

chat Patrick Liam (Creative Biolabs Scientific Support)

GPR149 is an oocyte-enriched gene. Deletion of GPR149 in mice has been shown to lead to increased fertility. Specifically, high levels of GPR149 expression were observed in germinal vesicle and meiosis II stage oocytes. May 01 2020

Published Data

Fig.1 GPR149 regulates MAPK/ERK pathway

HA-GPR149 was transfected into WT OPCs (oligodendrocyte precursor cells), resulting in GPR149 overexpression. Following this, Western blot analysis was conducted to assess ERK phosphorylation (p-ERK) in OPCs infected with either CTL or GPR149-expressing lentivirus. The results, presented as means ± SEM, were analyzed statistically using an unpaired student's t-test, revealing significant differences (*p < 0.05). The Western blot data clearly demonstrated that the overexpression of GPR149 in OPCs led to a notable increase in ERK1/2 phosphorylation levels.

Ref: Suo, Na, et al. "The orphan G protein-coupled receptor GPR149 is a negative regulator of myelination and remyelination." Glia 70.10 (2022): 1992-2008.

Pubmed: 35758525

DOI: 10.1002/glia.24233

Research Highlights

Vincent E Provasek et al. "lncRNA Sequencing Reveals Neurodegeneration-associated FUS Mutations Alter Transcriptional Landscape of iPS Cells That Persists In Motor Neurons." Research square, 27 Jun. 2023
The study conducted by the authors aimed to investigate the effect of Fused-in Sarcoma (FUS) gene mutations, specifically R521H and P525L, on the transcriptome of induced pluripotent stem cells (iPSCs) and iPSC-derived motor neurons (iMNs). Through RNA sequencing (RNA Seq), differentially expressed mRNAs and lncRNAs were characterized, and potential lncRNA-mRNA target pairs (TAR pairs) were predicted. Results showed that FUS mutations significantly altered the expression profiles of mRNAs and lncRNAs in iPSCs, with key regulated TAR pairs identified. Reverse transcription PCR (RT-PCR) validation confirmed these findings in both iPSCs and iMNs, indicating persistent transcriptional alterations from iPSCs into differentiated iMNs. Functional enrichment analyses suggested FUS mutations can potentially impact pathways related to neuronal development and carcinogenesis. Additionally, Ingenuity Pathway Analysis (IPA) and GO network analysis revealed associations related to RNA metabolism, lncRNA regulation, and DNA damage repair. These findings offer valuable insight into the underlying molecular mechanisms of ALS-associated FUS mutations and highlight potential therapeutic targets for the treatment of ALS.
Vincent E Provasek et al. "lncRNA Sequencing Reveals Neurodegeneration-associated FUS Mutations Alter Transcriptional Landscape of iPS Cells That Persists In Motor Neurons." Research square, 27 Jun. 2023
Pubmed: 37461717 DOI: 10.21203/rs.3.rs-3112246/v1

Na Suo et al. "The orphan G protein-coupled receptor GPR149 is a negative regulator of myelination and remyelination." Glia, 2022
The myelin sheath, necessary for proper neuronal function, is produced by oligodendrocytes (OLs) in the central nervous system (CNS) and Schwann cells in the peripheral nervous system. OLs differentiate from oligodendrocyte precursor cells (OPCs) and are crucial for myelination during development and repair after CNS demyelination. Understanding the mechanisms of myelin development and repair is clinically important. This study reveals that GPR149, a G protein-coupled receptor found in OPCs, inhibits OL differentiation, myelination, and remyelination. GPR149 is downregulated during OL differentiation and its absence leads to early myelin development and enhanced myelin regeneration in a model of demyelination. This effect may be mediated through the MAPK/ERK pathway. These findings suggest that targeting GPR149 may be a promising approach to promote myelin repair in demyelinating diseases.
Na Suo et al. "The orphan G protein-coupled receptor GPR149 is a negative regulator of myelination and remyelination." Glia, 2022
Pubmed: 35758525 DOI: 10.1002/glia.24233