Slc16a10, also known as TAT1 (T-type amino acid transporter 1), is an aromatic amino acid transporter. It is involved in the facilitated diffusion of aromatic amino acids across membranes, such as basolateral membranes of kidney, small intestine and liver epithelial cells, and plasma membranes of non-epithelial cells like skeletal myocytes [2,5,6]. This function is crucial for maintaining extracellular aromatic amino acid homeostasis, and it may also play a role in the efflux of other neutral amino acids [5,6]. It is also associated with processes like melanogenesis and tryptophan homeostasis [1,3].

In Slc16a10-defective mice (tat1(-/-)), plasma, muscle and kidney aromatic amino acid (AAA) concentrations increase under normal and high-protein diets, indicating its role in equilibrating AAA concentrations across specific membranes [5]. In melanocytes, overexpression of Slc16a10 promotes melanogenesis by enhancing the uptake of phenylalanine, and knockdown reduces UVB-induced melanin production and phenylalanine uptake [1]. In A549 cells, knocking down Slc16a10 reduces the expression of inflammatory factors IL-1β and TNF-α after LPS treatment, suggesting its potential role in acute lung injury [4].

In conclusion, Slc16a10 is essential for maintaining aromatic amino acid homeostasis and has implications in processes like melanogenesis and the inflammatory response in acute lung injury. Studies using gene-knockout mouse models have been instrumental in revealing these functions, highlighting its significance in understanding physiological and pathological processes related to amino acid metabolism and associated diseases.