Disease relevance of Opn1sw

• By contrast, temporal and spatial expression of Pou4f2 and Pax6 in developing ganglion and amacrine cells and PNA and blue opsin in developing cone cells was relatively normal in the mutant [1].
• Pancreatic cancer was induced by treatment with 40 mg/kg body wt N-nitrosobis-(2-oxopropyl)amine (BOP) [2].
• Furthermore, the incidence of BOP-induced gall bladder adenocarcinoma was elevated in cabbage-fed hamsters irrespective of dietary fat intake [2].
• Feeding cabbage in the high fat diet elevated the yield of BOP-induced pancreatic ductular carcinoma (1.6 carcinomas/effective animal) in comparison with that observed in hamsters fed cabbage in a low fat diet or in those given a high fat diet without cabbage, 0.6-0.8 carcinomas/effective animal (P less than 0.05) [2].

High impact information on Opn1sw

• Here, we show that S opsin transcription is higher than that of M opsin, which supports ultraviolet (UV) sensitivity greater than midwavelength sensitivity [3].
• In Nrl-/- retinas, the GFP+ photoreceptors express S-opsin, consistent with the transformation of rod precursors into cones [4].
• The first transgenic model expressed a murine cone pigment, S-opsin, together with the endogenous rhodopsin in the rod cell [5].
• Western blot analysis with a hamster anti-BOP mAb have detected the BOP protein in muscle cells and in COS 7 cells transfected with Bop cDNA constructs [6].
• The BOP proteins expressed in CTLs and muscle contain zinc finger-like motifs with homology to those of the ETO/MTG8 proto-oncogene and several other proteins of interest [6].

Chemical compound and disease context of Opn1sw

• In vivo administration of analog RC-160 inhibits the growth of Dunning R-3327 prostate cancers in rats, MXT mammary tumors in mice and BOP-induced ductal pancreatic cancers in hamsters [7].

Biological context of Opn1sw

• Comparison of wild-type and mutant lacZ reporter transgenes showed that the RORbeta-binding sites in Opn1sw are required for expression in mouse retina [8].
• We showed that selective stimulation of rhodopsin also led to phosphorylation of S-opsin [5].
• We report that the orphan nuclear receptor RORbeta (retinoid-related orphan receptor beta) activates the S opsin gene (Opn1sw) through binding sites upstream of the gene [8].
• The introns of the blue opsin gene have evolved at the average rate of introns in primate genes [9].
• Our results imply that in the Syrian hamster low levels of S opsin colocalize with M opsin in a common cone phenotype [10].

Anatomical context of Opn1sw

• Retinoid X receptor (gamma) is necessary to establish the S-opsin gradient in cone photoreceptors of the developing mouse retina [11].
• Photoreceptor development was analyzed by using peanut agglutinin (PNA)-rhodamine and blue cone opsin antibody to label cones and rhodopsin antibody to label rods [1].
• Blue-cone bipolar cells comprise only 1-2% of the bipolar cell population, and their dendrites selectively contact S-opsin-expressing cones [12].

Associations of Opn1sw with chemical compounds

• [D-Pro10]Dyn A-(2-11) was prepared by solid phase synthesis using Fmoc-protected amino acids, and the tyrosine derivatives were coupled to the peptide with BOP ((benzotriazol-1-yloxy)tris(dimethylamino)phosphonium hexafluorophosphate) [13].
• Alternatively, certain target compounds 3 were synthesized by reaction of 7 with appropriately functionalized glycine precursors under Schotten-Bauman or BOP chloride condensation conditions to provide C-5 acylamino intermediates, followed by Red-Al reduction and deprotection steps [14].
• BOPP also chelates paramagnetic ions such as Mn(2+), and therefore its tissue accumulation and selectivity can be detected noninvasively by using magnetic resonance imaging [15].
• One week after birth, Crj:CD-1 mice of both sexes were subcutaneously administered N-nitrosobis(2-oxopropyl)amine (BOP) at a dose of 50 mg/kg as an initiation treatment and starting 2 weeks thereafter they were fed diets supplemented with MeIQx at concentrations of 300, 30, 3 or 0 ppm or PhIP at 200, 50, 10 or 0 ppm for 23 weeks [16].

Regulatory relationships of Opn1sw

• The results identify Opn1sw as a target gene for RORbeta and suggest a key role for RORbeta in regulating opsin expression in the color visual system [8].
• Binding of endogenous TH to TRbeta2 is required to inhibit S-opsin and to activate M-opsin [17].

Other interactions of Opn1sw

• Here we show that exogenous TH inhibits S-opsin expression, but activates M-opsin expression [17].
• Using opsin antibodies and a sensitive detection protocol, we here show that S opsin immunoreactivity colocalizes with M opsin immunoreactivity in a common type of cone photoreceptor [10].
• Thus, Grk1 is essential to normal inactivation of both S- and M-mouse cone opsins, but S-opsin has access to a relatively effective, Grk1-independent inactivation pathway [18].
• These results suggested that even though the number of cones expressing S-opsin is increased, the physiological function of the S-cone system is not enhanced in rd7 mice [19].

Analytical, diagnostic and therapeutic context of Opn1sw

• Cabbage was fed from before carcinogen treatment in low fat diet and, beginning 1 week after BOP treatment, cabbage was given in low fat and high fat diets in comparison with the respective non-cabbage-containing diets [2].
• PKC-positive cones are found primarily in the ventral retina, and double-label immunocytochemistry using a short wavelength-sensitive opsin antibody confirms that they specifically correspond to the UVWS cone subtype [20].
• Employing microarray and in situ hybridization analysis we have found that the rd7 retina contains a modestly increased number of S-opsin-expressing cells that ultrastructurally appear to be normal cones [21].

References