Slc16a10, also known as TAT1, is an aromatic amino acid transporter. It plays a crucial role in maintaining extracellular aromatic amino acid homeostasis, participating in pathways related to amino acid transport and metabolism. It is essential for physiological processes like melanogenesis, tryptophan homeostasis, and may be involved in the transepithelial (re)absorption of amino acids from the small intestine and kidney proximal tubule [1,2,4,5,6]. Gene-knockout mouse models have been valuable for studying its function.

In Slc16a10-defective mice (tat1(-/-)), there is an increase in plasma, muscle, and kidney aromatic amino acid (AAA) concentration under normal and high-protein diets, along with an aromatic aminoaciduria. This indicates that Slc16a10 is required to equilibrate AAA concentration across specific membranes [5]. In the context of disease, knockdown of Slc16a10 in A549 cells reduces the expression of inflammatory cytokines (IL-1β and TNF-α) after LPS treatment, suggesting it may be a potential target for acute lung injury treatment [3]. Also, Slc16a10 deficiency in mice, along with Slc16a2 deficiency, leads to hearing loss, retarded development of the sensory epithelium, and progressive degeneration of cochlear hair cells [7].

In conclusion, Slc16a10 is essential for maintaining aromatic amino acid homeostasis and is involved in biological processes such as melanogenesis, tryptophan regulation, and cochlear development. The study of Slc16a10 using gene-knockout mouse models has provided insights into its role in diseases like acute lung injury and hearing loss, highlighting its potential as a therapeutic target in these disease areas.