Slc35e1, an orphan transporter, is likely involved in diverse biological processes. While its exact function is still being explored, it may participate in transport-related pathways, which are crucial for maintaining cellular homeostasis and normal physiological functions [2,3].

In psoriasis, Slc35e1 -/- mice displayed a less severe imiquimod (IMQ)-induced psoriasis-like phenotype compared to wild-type siblings. SLC35E1 deficiency inhibited keratinocyte proliferation in both mice and cultured cells. It was found to regulate zinc ion concentrations and subcellular localization, and zinc ion chelation reversed the IMQ-induced psoriatic phenotype in Slc35e1 -/- mice [1]. In herpes simplex virus 1 (HSV-1) infection, knockout of SLC35E1 reduced HSV-1 replication, induced membranous invaginations and mislocalization of the nuclear egress complex, suggesting its role in HSV-1 nuclear egress [2].

In conclusion, Slc35e1 plays important roles in psoriasis by regulating keratinocyte proliferation through zinc ion homeostasis and in HSV-1 nuclear egress. The gene knockout mouse models of Slc35e1 have provided valuable insights into its functions in these disease-related processes, highlighting its potential as a therapeutic target for psoriasis and in understanding HSV-1 infection mechanisms.