Ask about this productRelated genes to: OPN1SW antibody
- Gene:
- OPN1SW NIH gene
- Name:
- opsin 1, short wave sensitive
- Previous symbol:
- BCP
- Synonyms:
- BOP, CBT
- Chromosome:
- 7q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-01-17
Related products to: OPN1SW antibody
Related articles to: OPN1SW antibody
- Chromatic cues have long been implicated in refractive development, and OPN1MW variants are strongly associated with high myopia in humans. This study aimed to elucidate how cone opsin dysfunction translates into molecular and functional susceptibility to myopia. - Source: PubMed
Ye LinLi XianglianMao XiuyuMa JiayiYuan JiayueShi ZehuiFeng QianhongDai JinhuiJi Shunmei - Photopic vision, including fast motion and color perception in daylight, is mediated by cone opsins, specialized G protein-coupled receptors (GPCRs). Despite sharing the same chromophore, the three receptor subtypes absorb light at different wavelengths of the visible spectrum. The molecular mechanisms governing their spectral properties and exceptionally rapid responses remain largely unknown. We report cryo-electron microscopy structures of the human blue-sensitive (OPN1SW) and green-sensitive (OPN1MW) cone opsins in their dark-adapted states, combined with femtosecond-resolution spectroscopy, functional assays, and advanced simulations. The data reveal distinct chromophore stabilization mechanisms across human visual opsins and specific sequence adaptations in the GPCR microswitch motifs, underlining their structural plasticity and distinct activation mechanisms. These findings delineate the molecular basis of the evolutionary refinements fulfilling the needs of vision in daylight. - Source: PubMed
Publication date: 2026/06/25
Schmidt Sarah LDostal JakubSen SaumikHovan AndrejWalter DeborahAppleby Martin VKojima AsatoKato Hideaki EBeale John HKloz MiroslavSchertler Gebhard F XIsaikina Polina - Blue cone monochromacy (BCM) is an X-linked cone dystrophy characterized by loss of long- (L) and medium-wavelength (M) cone function. A common cause is the C203R missense mutation, which occurs in both OPN1LW and OPN1MW, or in hybrid OPN1LW/OPN1MW opsin genes. Because BCM primarily affects foveal cones, we generated Opn1mwC198R/Opn1sw-/-/Nrl-/- (C198RAC) mice carrying the murine equivalent of the human C203R mutation on an all-cone retinal background. C198RAC mice exhibited absent photopic ERG responses and significantly shortened cone outer segments, recapitulating foveal cone deficits in BCM. Metabolomic profiling further revealed altered retinal metabolism, including reduced cGMP and elevated oxidative stress-related metabolites. To evaluate therapy, we delivered AAV8-Y733F expressing human L-opsin (OPN1LW) cDNA under the cone-specific PR2.1 promoter at 1 and 5 months of age. Treatment restored cone function, regenerated outer segment structures, and provided rescue for at least 5 months post-injection in both early- and late-treatment groups. These results demonstrate that densely packed cones expressing only the C198R mutant opsin remain viable targets for gene therapy. Together, this study establishes the C198RAC mouse as a cone-rich model mimicking foveal cone conditions in BCM and provides compelling preclinical evidence that AAV-mediated gene augmentation can rescue cone outer segment structure and function, supporting the feasibility of gene therapy for BCM. - Source: PubMed
Publication date: 2026/06/11
Cahill Marion EChmelik KathrynBrothers Brooke AAshcraft Madyson EGuan TongjuPuja ArtjolaXiang YinxiaoShaw Lee MDu JianhaiDeng Wen-Tao - Ultraviolet B (UVB) irradiation initiates cutaneous vitamin D-related photochemistry from 7-dehydrocholesterol (7-DHC), which is also the immediate precursor of cholesterol via 7-dehydrocholesterol reductase (DHCR7). Thus, DHCR7 occupies a branch-point position linking cholesterol biosynthesis and UVB-associated vitamin D-related metabolism. How keratinocytes regulate this metabolic relationship under UVB remains unclear. We examined whether OPN1SW is associated with DHCR7 protein abundance, conditioned medium 25-hydroxyvitamin D3 [25(OH)D3] (a vitamin D-related readout) and sterol-pool responses in UVB-exposed keratinocytes. A UVB dose that preserved > 80% cell viability, 10 mJ/cm, increased OPN1SW protein abundance and reduced DHCR7 protein abundance in human epidermal keratinocytes and HaCaT cells. These changes were accompanied by increased conditioned medium 25(OH)D3 and a reduced cellular sterol-pool readout. OPN1SW overexpression increased DHCR7 protein abundance under basal conditions. Under UVB exposure, OPN1SW overexpression attenuated UVB-associated DHCR7 reduction, attenuated the UVB-associated increase in conditioned medium 25(OH)D3 and partially preserved the sterol-pool readout. Conversely, OPN1SW knockdown exacerbated DHCR7 reduction under UVB and was accompanied by higher conditioned medium 25(OH)D3 and a lower sterol-pool readout. DHCR7 knockdown produced concordant shifts in these readouts, supporting a contributory role for DHCR7. Together, these findings support the presence of a UVB-responsive OPN1SW-DHCR7 module that may contribute to keratinocyte adaptation to UVB exposure. - Source: PubMed
Yang YatingZeng WenChen GuangsuZhang WeiSu YushenLu Hongguang - In mammals, melanopsin (OPN4) is a retinal photopigment found on a subset of intrinsically photosensitive ganglion cells, which synchronize the central circadian clock with the light-dark cycle. Peripheral tissues have also been found to express melanopsin, but its function remains to be explored. In this study, we investigated whether cold temperature pulses (34°C) could modulate clock gene expression in murine 3T3-L1 preadipocytes and the role of melanopsin in regulating this response. We detected the presence of the cone opsin (OPN1SW), rhodopsin (OPN2), and melanopsin (OPN4) using immunocytochemistry. We demonstrated the role of OPN4 in the upregulation of the clock gene in 3T3-L1 cells in response to cold-temperature pulses (34°C), through a pharmacological assay employing a well-established OPN4 antagonist. Then, we determined the profile of the clock gene , using luciferase as the bioluminescence reporter. 3T3-L1 cells subjected to constant temperature (37°C) or repeated cold-temperature pulses (34°C) exhibited an oscillatory bioluminescence profile. The cold-temperature pulses induced an increase in the amplitude of bioluminescence and a phase delay in comparison to control cells. These findings suggest that temperature detection through melanopsin could be an important pathway for peripheral clock modulation, with direct implications for metabolism control. - Source: PubMed
Publication date: 2026/05/29
Zanetti Giovannade Assis Leonardo Vinícius MonteiroMoraes Maria Natháliade Lauro Castrucci Ana Maria