Slc39a9, also known as ZIP9, is a zinc transporter that has been identified as a membrane androgen receptor in various teleost and mammalian cell models [2]. It plays crucial roles in regulating zinc homeostasis, particularly in the secretory pathway [4]. It is involved in multiple biological processes, including egg activation, cell migration, and viral entry, and is associated with diseases like cancer [2,3,5]. Genetic models such as gene-knockout models have been instrumental in studying its functions.

In zebrafish, zip9-/- females showed reduced fecundity, embryo viability, and abnormal egg activation with depressed zinc release, indicating ZIP9's essential role in proper zinc modulation during egg activation [2]. In breast cancer cells, ZIP9 overexpression increased zinc levels and cell migration/invasion, while knockdown decreased these processes, suggesting its role in tumorigenic responses [3]. A genome-wide Nuclease technology screen identified SLC39A9 as a crucial entry factor for Ebola virus infection, with its genetic depletion reducing viral entry [1]. In periodontal ligament cells, knockdown of genes regulating SLC39A9 RNA m6A modification affected IL-6 expression, suggesting its involvement in the inflammatory response [6].

In conclusion, Slc39a9 is essential for zinc-related biological processes such as egg activation, cell migration, and immune-related responses. Gene-knockout models have revealed its significance in diseases like cancer and viral infections, providing valuable insights into potential therapeutic targets for these conditions.