Equilibrative nucleoside transporter 3 (ENT3) is responsible for transporting nucleotide synthesis precursors, such as hydrophilic nucleosides and nucleobases within cells¹. ENT3 structure includes 11 transmembrane domains and a 51-residue hydrophilic N-terminal region containing two dileucine motifs that are characteristic of endosomal/lysosomal targeting sequences^1,2.

ENT3 is encoded by the SLC29A3 gene and is expressed in several mouse and human tissues such as placenta, heart, neurons, and astrocytes. In addition, human ENT3 is predominantly expressed in mitochondria in human hepatocytes. Human ENTs are high-capacity transporters, bidirectional, Na⁺-independent with a wide substrate selectivity^1,2. 

The human ENT family consists of four members: ENT1- ENT4. Nucleoside transport function of ENT3 is maximal at pH 5.5 suggesting that the protein is localized to acidic intracellular compartments; probably lysosomes^1,2.

Studies show that mutations in human ENT3 can cause various clinical disorders including H syndrome, pigmented hypertrichosis with insulin-dependent diabetes mellitus syndrome, lysosomal storage-like disorders and mitochondrial disorders^1,2.