mProX™ Human CYSLTR2 Stable Cell Line

Product Information

Target Protein

CYSLTR2

Target Family

Leukotriene Family

Target Protein Species

Mouse

Host Cell Type

Melan-a;CHO-K1;HEK293

Target Classification

GPCR Cell Lines

Target Research Area

CNS Research

Related Diseases

Asthma;Melanoma, Uveal

Gene ID

Mouse: 70086

UniProt ID

Mouse: Q920A1

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

CYSLTR2, a G-protein-coupled receptor, has been identified as a significant player in the pathogenesis of Uveal Melanoma (UM). A comprehensive bioinformatics analysis revealed the role of eight genes, including CYSLTR2, associated with the most common genetic anomalies in UM. Furthermore, CYSLTR2 has been implicated in both the early and late development of uveal melanoma, making mutant CysLT2R a promising therapeutic target. Another study concluded that the GPCR CysLTR2 mutant displays profound signaling bias for Gq/11 signaling pathways, suggesting its potential as a therapeutic target in uveal melanoma. Additionally, CYSLTR2-mutant melanocytic blue neoplasms frequently exhibit a heavily pigmented exophytic tumor, suggesting its involvement in melanocytic neoplasms4.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Laura (Verified Customer)

What is the significance of CYSLTR2 mutations in uveal melanoma? Aug 18 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

Mutations in CYSLTR2, particularly the p.Leu129Gln substitution, have been identified in uveal melanoma samples that lacked mutations in other common genes such as GNAQ, GNA11, and PLCB4. These mutations are recurrent and activating, suggesting a potential role in the tumorigenesis of uveal melanoma. Aug 18 2023

chat Patricia (Verified Customer)

How does the CYSLTR2 mutation affect the signaling pathways in uveal melanoma? Mar 19 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

The CYSLTR2 mutation, specifically the L129Q variant, displays profound signaling bias for Gq/11 signaling pathways. This mutation also escapes β-arrestin-mediated downregulation, which might contribute to the progression of uveal melanoma. Mar 19 2022

Published Data

Fig.1 The indispensable role of CYSLTR2 is evident in sustaining the unique melanocyte lineage characteristics within melan-a cells, which have been engineered to express the Leu129Gln CysLT₂R mutation, ensuring their growth and longevity.

Melan-a cells, expressing either wild-type or Leu129Gln CysLT₂R, were subjected to growth curve analysis with transfection of scrambled siRNA (siSCR) or CYSLTR2-targeting siRNA (siCYSLTR2), assessed using cell viability assay. While wild-type CysLT₂R cells were cultivated in the presence of 200 nM TPA, Leu129Gln CysLT₂R cells were grown with or without 200 nM TPA, all for a duration of 3 days. The fold growth increase, compared to day 1, represents the mean ± s.e.m. derived from six technical replicates, with statistical significance denoted as *P < 0.05.

Ref: Moore, Amanda R., et al. "Recurrent activating mutations of G-protein-coupled receptor CYSLTR2 in uveal melanoma." Nature genetics 48.6 (2016): 675-680.

Pubmed: 27089179

DOI: 10.1038/ng.3549

Research Highlights

Dai M, et al. "Immunomodulatory effects of one novel microRNA miR-63 in pearl oyster Pinctada ." Fish & shellfish immunology, 2023.
The novel microRNA miR-63, also known as novel-miR-63, was recently discovered in the pearl oyster Pinctada fucata martensii (Pm-novel-miR-63) and is known to be species-specific. Previous research by the authors has indicated that the expression of Pm-novel-miR-63 is significantly reduced 24 hours after nucleus transplantation. In this study, the authors aimed to analyze the function and regulatory role of Pm-novel-miR-63 in the immune response of pearl oysters. Their findings show that Pm-novel-miR-63 expression is increased after exposure to pathogen associated molecular patterns for 6-12 hours, and overexpression of Pm-novel-miR-63 leads to a decrease in the activity of immune and antioxidant enzymes in the serum. Further transcriptome analysis revealed that Pm-novel-miR-63 plays a role in regulating transplantation immunity through the Notch and mRNA surveillance signaling pathways. Target prediction and dual luciferase analysis indicated that Pm-GDP-FucTP, Pm-CysLTR2, and Pm-RLR are all targets of Pm-novel-miR-63. These findings highlight the potential of Pm-novel-miR-63 as a new interference target for controlling excessive immune rejection in pearl oyster culture.
Pubmed: 37586600 DOI: 10.1016/j.fsi.2023.109002

Kervarrec T, et al. "GRM1 Gene Fusions as an Alternative Molecular Driver in Blue Nevi and Related ." Modern pathology : an official journal of the United States and Canadian Academy , 2023.
In the study, two cases of GRM1 fusions and one case of ZEB2::GRM1 fusion were identified in patients (n=2) with blue nevi. One case had a GRM1 rearrangement identified through fluorescence in situ hybridization. SF3B1 comutations were observed in both melanomas, with a MYO10::GRM1 fusion. Array comparative genomic hybridization was used for three cases, revealing multiple copy number alterations in the two melanomas and limited alterations in the atypical BN, consistent with classical blue lesions. In all cases, GRM1 was highly expressed compared to a control group of blue lesions with typical mutations. Both melanomas rapidly progressed to visceral metastases, leading to a fatal outcome in one case and tumor progression under palliative care in the other. These findings suggest that GRM1 gene fusions could be a rare oncogenic driver in BN, and may not coexist with classical mutations, especially in plaque-type or Ota subtypes.
Pubmed: 37391170 DOI: 10.1016/j.modpat.2023.100264