mProX™ Human GRM6 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 GRM6, TRPM1, and LRIT3 localization at the dendritic terminals of ON-bipolar cells is independent of Gpr179 expression. Confocal pictures of Gpr179+/+ and Gpr179-/- mouse retinal slices.
Localization of GRM6, TRPM1, and LRIT3 at the distal ends of ON-bipolar cell dendrites remains unaffected by the presence or absence of Gpr179 expression. Representative confocal snapshots from retinal sections of Gpr179+/+ and Gpr179-/- mice are presented. The retinal sections from Gpr179+/+ (A) and Gpr179-/- (B) mice were immunostained for anti-GPR179 (in green), anti-GRM6 (in red), and DAPI (in white). Additionally, retinal sections from Gpr179+/+ (C) and Gpr179-/- (D) mice were immunostained for anti-LRIT3 (in green), anti-TRPM1 (in red), and DAPI (in white). The scale bar equals 10 µm, and the regions of interest include the outer nuclear layer (ONL), outer plexiform layer (OPL), and inner nuclear layer (INL).
Ref: Orhan, Elise, et al. "A new mouse model for complete congenital stationary night blindness due to Gpr179 deficiency." International Journal of Molecular Sciences 22.9 (2021): 4424.
Pubmed: 33922602
DOI: 10.3390/ijms22094424
Research Highlights
Esdaile E, et al. "Additional evidence supports GRM6 p.Thr178Met as a cause of congenital stationary ." Veterinary ophthalmology, 2023.
Congenital stationary night blindness (CSNB) is an ocular disorder characterized by nyctalopia. A previous study identified an autosomal recessive missense mutation in glutamate metabotropic receptor 6 (GRM6 c.533C>T, p.(Thr178Met)) in a Tennessee Walking Horse, referred to as CSNB2, which affects the retinal rod ON-bipolar cell signaling pathway by reducing the binding affinity of the neurotransmitter glutamate. The first aim of the present study was to determine the allele frequency of CSNB2 in breeds with known cases of CSNB and breeds closely related to the Tennessee Walking Horse. A total of 3518 horses from 14 breeds were evaluated, and the CSNB2 allele was identified in nine previously unreported breeds. The second aim was to confirm the link between genotype and CSNB phenotype by performing ocular examinations and electroretinograms (ERG) on 19 horses from three breeds, including one CSNB2 homozygote from each breed. All three homozygous horses showed an electronegative ERG waveform under scotopic light conditions, consistent with CSNB. The remaining 16 horses (seven CSNB2/N and nine N/N) had normal scotopic ERG results, and all horses showed normal photopic ERGs. These findings suggest that the GRM6 c.533C>T mutation likely causes CSNB in Tennessee Walking Horses, Standardbreds, and Missouri Fox Trotting Horses. To prevent the production of affected horses, genetic testing is recommended for breeds with the CSNB2 allele. This study is the largest to identify CSNB across breeds, indicating that the disorder may be underdiagnosed in horses.
Pubmed:
37815029
DOI:
10.1111/vop.13151
Takahashi K, et al. "Extended functional rescue following AAV gene therapy in a canine model of ." Vision research, 2023.
Congenital stationary night blindness (CSNB) is a group of inherited retinal diseases characterized by impaired vision in low light conditions. One subtype of CSNB is associated with faulty signaling of the mGluR6 protein at the tip of the ON-bipolar cells (ON-BCs). Previous studies have shown the short-term efficacy and safety of a gene therapy targeting ON-BCs using a specific adeno-associated virus (AAV) vector carrying the LRIT3 gene. In this study, it was demonstrated that this therapy also resulted in long-term functional and molecular recovery in all treated eyes for up to 32 months. However, further analysis revealed off-target expression of LRIT3 in other retinal cells, indicating the need for additional refinement of the therapy before its clinical use.
Pubmed:
37220680
DOI:
10.1016/j.visres.2023.108260
