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A single case report (PMID:36246649) provides evidence for an association between OPN4 and delayed sleep phase disorder. In this study, a male carrier was identified with a heterozygous missense variant, c.502C>T (p.Arg168Cys), which was functionally shown to disrupt melanopsin activity. The functional assay demonstrated that this variant renders the protein non‑functional, suggesting a loss‑of‑function pathogenic mechanism that disrupts normal circadian photoentrainment.
Overall, the available data support a limited gene‑disease relationship. Although the genetic evidence is restricted to a single proband, the experimental data provide supportive functional validation. This evidence, while preliminary, offers valuable insights for differential diagnosis and therapeutic decision‑making in patients with delayed sleep phase disorder.
Gene–Disease AssociationLimitedEvidence is based on a single proband (PMID:36246649) with functional data supporting a pathogenic role. Genetic EvidenceLimitedOnly one missense variant, c.502C>T (p.Arg168Cys), has been reported in the context of DSWPD without additional familial segregation data (PMID:36246649). Functional EvidenceModerateIn vitro studies demonstrated that the p.Arg168Cys variant abolishes melanopsin function, consistent with a loss‑of‑function mechanism (PMID:36246649). |