Slc1a3, also known as a glutamate transporter gene, is crucial for regulating glutamate and other amino acid metabolisms. It is involved in multiple pathways, such as p53 and NF-κB pathways, and plays an important role in various biological processes and disease conditions. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its functions [1,2,3,4,5,6].

Knockdown of Slc1a3 in DF-1 or A549 cells inhibited Newcastle disease virus (NDV) infection, indicating that Slc1a3 propels glutaminolysis for glutamate utilization and NDV replication [1]. In gastric cancer, its overexpression was associated with poor prognosis, and it affected glucose metabolism and promoted cancer growth via the PI3K/AKT signalling pathway [4]. High expression of Slc1a3 in ovarian cancer cells was linked to poor prognosis, and its knockdown restrained cell proliferation, enhanced apoptosis, and inhibited migration [6].

In conclusion, Slc1a3 is a key regulator of amino acid metabolism and is involved in disease-related processes such as viral replication, cancer progression, and potentially hemiplegic migraine. Studies using loss-of-function models like Slc1a3 knockdown have revealed its role in promoting cancer cell proliferation, migration, and viral replication, highlighting its potential as a therapeutic target in cancer and for understanding virus-host interactions.