{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSLC47A1 encodes MATE1, a critical H⁺‐coupled antiporter predominantly expressed on the apical membranes of renal tubular cells and bile canaliculi in the liver. MATE1 functions to extrude an array of endogenous and exogenous organic cations—including drugs such as metformin, cimetidine, paraquat, and other toxins—directly into urine and bile, thereby contributing to detoxification and drug clearance. Studies using recombinant expression systems have demonstrated that MATE1 mediates electroneutral organic cation/H⁺ exchange driven by an inward proton gradient, establishing its role as a key exporter in renal and hepatic elimination processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical excretory role, MATE1 is characterized by a remarkable polyspecificity that enables the transport of a wide range of substrates—from therapeutic agents (including metformin and cisplatin) to endogenous metabolites such as asymmetric dimethylarginine, L‐arginine, and agmatine, as well as dietary components like flavonoids. Genetic and functional studies have revealed that both coding variants and promoter polymorphisms affecting SLC47A1 alter expression levels, substrate affinities, and transport kinetics, thereby influencing drug pharmacokinetics, efficacy, adverse effects, and even the risk for conditions such as lactic acidosis. Furthermore, current investigations using specialized assay conditions and site‐directed mutagenesis have refined our understanding of the structural determinants of ligand interaction and transporter regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMore recently, emerging evidence has expanded the functional repertoire of MATE1. Novel roles include mediating lipid remodeling and cellular resistance to ferroptosis, as well as modulating drug–drug interactions that influence the toxicity of chemotherapeutic agents and targeted therapies. For instance, inhibition of MATE1 by agents such as pazopanib may exacerbate cisplatin‐induced nephrotoxicity, while expression levels of MATE1 are implicated in the effectiveness of imatinib in chronic myeloid leukemia. Such insights, combined with refined assay methodologies, underscore the clinical impact of SLC47A1 genetic variability in personalized medicine and drug disposition."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Masato Otsuka, Takuya Matsumoto, Riyo Morimoto, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "The effect of novel promoter variants in MATE1 and MATE2 on the pharmacokinetics and pharmacodynamics of metformin."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Clin Pharmacol Ther (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/clpt.2012.210"}], "href": "https://doi.org/10.1038/clpt.2012.210"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23267855"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23267855"}]}, {"type": "r", "ref": 22, "children": [{"type": "t", "text": "Hideyuki Motohashi, Yumi Nakao, Satohiro Masuda, et al. 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