Slc23a4, also known as sodium-dependent nucleobase transporter 1 (SNBT1), is a key gene involved in the intestinal absorption of nucleobases and their analogs in non-primate animals. It codes for a sodium-dependent carrier-mediated transport system at the brush border membrane of epithelial cells in the small intestine, which is crucial for the uptake of compounds like uracil, thymine, guanine, hypoxanthine, and xanthine [2,3].

In mice, studies on gene-targeted Slc23a4-deficient models have shown significant implications. For example, in Xdh-deficient mice, pseudogenization of Slc23a4 (Slc23a4 -/-) in combination with high Hprt activity (Hprt(high)Xdh(- / -)Slc23a4(- / -) mice) led to a longer lifespan and reaching adulthood, although they still exhibited renal impairment, high plasma creatinine levels, and anemia. Female Hprt(high)Xdh(- / -)Slc23a4(- / -) mice produced non-surviving offspring. This indicates that Slc23a4 plays a role in the survival and renal function of Xdh-deficient mice [1].

In conclusion, Slc23a4 is essential for the intestinal absorption of nucleobases in non-primate animals. The study of Slc23a4-deficient mouse models has provided insights into its role in the survival and renal function of Xdh-deficient mice, contributing to our understanding of related disease conditions such as type 1 xanthinuria-like phenotypes in mice [1].