Solute carrier family 7 member 1 (SLC7A1), commonly known as cationic amino acid transporter 1 (CAT-1), is a high-affinity, sodium-independent transporter located in the plasma membrane of many cell types[1][2][3]. It is responsible for the uptake and regulation of cationic amino acids, particularly L-arginine, L-lysine, and L-histidine, which are crucial for a variety of cellular processes including protein synthesis, nitric oxide production, and metabolic signaling pathways such as mTORC1[1][2]. SLC7A1 is essential for vascular endothelial function, cellular proliferation, immune response, and red blood cell development[1][2]. Dysregulation or genetic variants of SLC7A1 are associated with numerous diseases, including hypertension, cancer, muscular dystrophy, and metabolic and inflammatory conditions[1]. SLC7A1’s pivotal transport role also makes it critical in the maintenance of normal endothelial activity, cardiovascular health, and tumor cell metabolism[1][2]. It is part of the SLC7 transporter family (CAT subfamily) and operates mainly as a monomer, mediating sodium-independent transport[2][3].
Transport inhibitors may competitively block cationic amino acid binding and uptake[2].
Competitive inhibition or substrate competition (L-arginine, ADMA, L-homoarginine, etc.)[1][2].
Allosteric modulation affecting transporter localization or kinetic regulation[1].
03
Biological functions
Amino acid transport (notably L-arginine, L-lysine, L-histidine)[1][2][3]Regulation of nitric oxide (NO) synthesis[1][2]Modulation of cell metabolism[2]Cellular signaling (e.g., mTORC1 pathway via arginine availability)[2]Support of cell proliferation, endothelial function, and erythropoiesis[1]
04
Disease associations
Cancer (breast, colorectal, ovarian, KRAS-mutant non-small cell lung cancer)[1]Cardiovascular disease (hypertension, endothelial dysfunction)[1]Inflammatory skin diseases (e.g., psoriasis)[1]Neurodegenerative and neurological disorders (by its role in the brain and blood-brain barrier)[1]Muscle disease (Duchenne muscular dystrophy)[1]Diabetic kidney disease, heart failure, gestational dyslipidemia[1]Other
05
Safety considerations
Disrupting SLC7A1 function may impair systemic amino acid homeostasis and nitric oxide production, risking cardiovascular dysfunction, impaired immunity, anemia (impaired erythropoiesis), and exacerbation of metabolic or neurological issues[1].
06
Interacting drugs
No specific marketed drugs directly targeting SLC7A1 are highlighted in current clinical use or the reviewed sources as of September 2025. However, the SLC7 family transports a wide range of substrates and drug molecules, including some recognized by related members (such as l-DOPA and gabapentin, but these interact more with other SLC7 transporters and not specifically SLC7A1)[2]. Experimental or proposed inhibitors/modulators exist in research.
07
Biomarkers
SLC7A1 expression levels in tumors and endothelial tissue (potential biomarker of cancer progression or endothelial dysfunction, though not in routine clinical use)[1].L-arginine uptake, plasma arginine/ADMA ratios (as indirect readouts)[1].
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