Slc39a10, also known as ZIP10, is a zinc transporter belonging to the SLC39A subfamily. It plays a crucial role in maintaining zinc homeostasis, which is essential for various biological processes. Zinc homeostasis is involved in numerous cellular functions, and Slc39a10 is associated with pathways like MAPK/ERK, PI3K/AKT, and JAK-STAT, influencing processes such as hematopoiesis, immune response, and cell proliferation [1,2,5]. Genetic models, especially knockout (KO) and conditional knockout (CKO) mouse models, have been instrumental in studying its functions.

In zebrafish and mouse models, Slc39a10-deficient animals exhibit more severe impaired hematopoiesis compared to those lacking transferrin receptor 1, highlighting zinc's significant role in hematopoiesis, especially in early hematopoietic stem cells (HSCs). Loss of Slc39a10 in fetal HSCs causes zinc deficiency, leading to DNA damage, apoptosis, and G1 cell cycle arrest, which can be largely restored by zinc supplementation [1]. In macrophage-specific Slc39a10-knockout mice, reduced intracellular zinc concentration leads to p53 stabilization and increased apoptosis upon LPS stimulation, demonstrating its role in macrophage survival during inflammation [3]. T cell-specific deletion of Slc39a10 in transgenic mice protects against disease progression in inflammatory bowel disease (IBD) and experimental autoimmune encephalomyelitis (EAE), and induces massive apoptosis, suggesting its role in T cell-mediated autoimmune diseases [4].

In conclusion, Slc39a10 is essential for processes like hematopoiesis, macrophage and lymphocyte survival, and immune responses. The use of KO and CKO mouse models has provided insights into its role in diseases such as anemia, zinc deficiency-related disorders, autoimmune diseases, and certain cancers. Understanding Slc39a10's functions offers potential therapeutic targets for these disease areas.