Fig. 6: OPN3 mediates melanin cap formation via the PLC-β signaling pathway.

a HEK treated with PTX was stimulated with 3 J cm⁻² UVA, and calcium flux was quantified by flow cytometry. n = 3 independent experiments. Statistical significance was determined by one-ANOVA with post-test. **P < 0.01, ***P < 0.001. b HEK treated with PTX were stimulated with 3 J cm⁻² UVA, and p-CaMKII and p-CREB protein expression level was analyzed by WB. WB analyses were normalized using β-tubulin as a loading control, and the relative protein level was quantified using Quantity One software. Statistical significance was determined by one-ANOVA with post-test. **P < 0.01, ***P < 0.001. c HEK were irradiated without and with UVA, and PLC-β protein levels were determined by WB. d HEK treated with PTX were stimulated with 3 J cm⁻² UVA; protein level was analyzed by WB. e HEK were transfected with siRNA against OPN3 irradiated with UVA and lysed after 1 h. Lysates were analyzed by WB using the indicated antibodies (anti-OPN3 and anti-PLC-β). β-tubulin was used as a loading control. f HEK treated with U73122 were stimulated with 3 J cm⁻² UVA; calcium flux was quantified by flow cytometry. n = 3 independent experiments. Statistical significance was determined by one-ANOVA with post-test. ***P < 0.001, ****P < 0.0001. g HEK treated with U73122 were stimulated with 3 J cm⁻² UVA; p-CaMKII, p-CREB, DCTN1, and Dync1i1 protein expression level was analyzed by WB. WB analyses were normalized using β-tubulin as a loading control, and the relative protein level was quantified using Quantity One software. Statistical significance was determined by one-ANOVA with post-test. **P < 0.01, ***P < 0.001, ****P < 0.0001.