SLC6A14 Recombinant Rabbit mAb (S-5961)

SLC6A14 (solute carrier family 6 member 14), also known as ATB⁰⁺, is a sodium- and chloride-dependent amino acid transporter encoded by the SLC6A14 gene located on chromosome Xq24, and is notable for its broad substrate selectivity—it can transport all of the 18 proteinogenic amino acids except aspartate and glutamate, covering all essential amino acids as well as cationic and neutral amino acids such as arginine and glutamine. A distinctive feature of this transporter is its high concentrative capacity, typically driving substrates into cells against a concentration gradient with a stoichiometry of 3 Na⁺:1 amino acid, though recent studies have shown that substrate charge can modulate the sodium coupling mode: cationic amino acids require only two sodium ions for transport, and their turnover rate is 1.4- to 4-fold slower than that of neutral substrates. In terms of physiological distribution, SLC6A14 is expressed at very low levels in normal adult tissues, being mainly restricted to the luminal membrane of epithelial cells in the lung and intestine (ileum, colon). However, this expression pattern changes dramatically under pathological conditions: SLC6A14 is significantly upregulated in colon cancer, cervical cancer, pancreatic cancer, and estrogen receptor-positive breast cancer, a mechanism partly involving direct transcriptional activation of SLC6A14 by the Wnt/β-catenin signaling pathway, with β-catenin shown by chromatin immunoprecipitation to bind the SLC6A14 regulatory region. In tumor cells, SLC6A14 plays a central role in supplying key metabolic substrates such as glutamine, arginine, and leucine, and loss of its function leads to inhibition of mTOR signaling, upregulation of asparagine synthetase and CHOP, induction of autophagy, and suppression of cell proliferation. Notably, Slc6a14 knockout mice appear normal, fertile, and without compensatory upregulation of other transporters, yet exhibit halved tumor incidence and significantly delayed tumor growth—a "tumor-selective dependency" feature that makes SLC6A14 a highly attractive anticancer target. In the field of metabolic disease, the 3' untranslated region single nucleotide polymorphism rs2011162 of SLC6A14 is associated with human obesity; this variant reduces transporter expression by approximately 60%, and Slc6a14-deficient mice display obesity, fatty liver, and metabolic syndrome phenotypes only under high-fat diet conditions, suggesting that SLC6A14 plays a protective role in lipid metabolic regulation under conditions of nutrient excess.