Fig. 5: OPN3 mediates melanin cap formation via the calcium signaling pathway.

a, b HEK and HaCaT calcium fluxes were quantified by flow cytometry. n = 3 independent experiments. Statistical significance was determined by t-test analysis. **P < 0.01, ***P < 0.001. c, d Phosphorylated Ca²⁺/calmodulin-dependent protein kinase (CaMK)II and cyclic adenosine monophosphate response element-binding (CREB) protein were analyzed by WB 1 h after irradiation of HEK and HaCaT with 3 J cm⁻² UVA. 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 t-test analysis. *P < 0.05, **P < 0.01, ***P < 0.001. e After siRNA inhibited OPN3 irradiated without or with UVA, calcium fluxes were quantified by flow cytometry. n = 3 independent experiments. Statistical significance was determined by one-ANOVA with post-test. *P < 0.05, **P < 0.01. f After siRNA inhibited OPN3 irradiated without or with UVA, WB was used to analyze changes of OPN3, p-CaMKII, and p-CREB protein expression levels in HEK (n = 3 independent experiments). 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 < 0.001, ****P < 0.0001.