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1）Otsuka M, Matsumoto T, Morimoto R, et al. A human transporter protein that mediates the final excretion step for toxic organic cations. Proc Nat Acad Sci USA. 2005; 102: 17923-8
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2）寺田智祐, 乾 賢一. H＋/有機カチオンアンチポータ（MATE/SLC47A）. In: 御手洗哲也, 東原英二, 秋澤忠男, 他, 編. Annual Review 腎臓 2008. 東京: 中外医学社; 2008. p. 36-42
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3）Yonezawa A, Inui K. Importance of the multidrug and toxin extrusion MATE/SLC47A family to pharmacokinetics, pharmacodynamics/toxicodynamics and pharmacogenomics. Br J Pharmacol. 2011; 164: 1817-25
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4）Zhang X, Wright SH. MATE1 has an external COOH terminus, consistent with a 13-helix topology. Am J Physiol. Renal physiol. 2009; 297: F263-71
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5）Asaka J, Terada T, Tsuda M, et al. Identification of essential histidine and cysteine residues of the H+/organic cation antiporter multidrug and toxin extrusion （MATE）. Mol Pharmacol. 2007; 71: 1487-93
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6）Matsumoto T, Kanamoto T, Otsuka M, et al. Role of glutamate residues in substrate recognition by human MATE1 polyspecific H+/organic cation exporter. Am J Physiol Cell Physiol. 2008; 294: C1074-8
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7）Tanihara Y, Masuda S, Sato T, et al. Substrate specificity of MATE1 and MATE2-K, human multidrug and toxin extrusions/H+-organic cation antiporters. Biochem Pharmacol. 2007; 74: 359-71
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8）Sato T, Masuda S, Yonezawa A, et al. Transcellular transport of organic cations in double-transfected MDCK cells expressing human organic cation transporters hOCT1/hMATE1 and hOCT2/hMATE1. Biochem Pharmacol. 2008; 76: 894-903
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9）Kimura N, Masuda S, Tanihara Y, et al. Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. Drug Metabo Pharmacokinet. 2005; 20: 379-86
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10）Choi JH, Yee SW, Ramirez AH, et al. A common 5'-UTR variant in MATE2-K is associated with poor response to metformin. Clinical Pharmacol Ther. 2011; 90: 674-84
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11）Tsuda M, Terada T, Mizuno T, et al. Targeted disruption of the multidrug and toxin extrusion 1 （mate1） gene in mice reduces renal secretion of metformin. Mol Pharmacol. 2009; 75: 1280-6
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12）Toyama K, Yonezawa A, Masuda S, et al. Loss of multidrug and toxin extrusion 1 （MATE1） is associated with metformin-induced lactic acidosis. Br J Pharmacol. 2012; 166: 1183-91
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13）Toyama K, Yonezawa A, Tsuda M, et al. Heterozygous variants of multidrug and toxin extrusions （MATE1 and MATE2-K） have little influence on the disposition of metformin in diabetic patients. Pharmacogenet Genomics. 2010; 20: 135-8
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14）Yonezawa A, Inui K. Organic cation transporter OCT/SLC22A and H+/organic cation antiporter MATE/SLC47A are key molecules for nephrotoxicity of platinum agents. Biochem Pharmacol. 2011; 81: 563-8
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15）Nakamura T, Yonezawa A, Hashimoto S, et al. Disruption of multidrug and toxin extrusion MATE1 potentiates cisplatin-induced nephrotoxicity. Biochem Pharmacol. 2010; 80: 1762-7
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16）Tanihara Y, Masuda S, Katsura T, et al. Protective effect of concomitant administration of imatinib on cisplatin-induced nephrotoxicity focusing on renal organic cation transporter OCT2. Biochem Pharmacol. 2009; 78: 1263-71
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17）Iwata K, Aizawa K, Kamitsu S, et al. Effects of genetic variants in SLC22A2 organic cation transporter 2 and SLC47A1 multidrug and toxin extrusion 1 transporter on cisplatin-induced adverse events. Clin Exp Nephrol. (in press)
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18）Filipski KK, Mathijssen RH, Mikkelsen TS, et al. Contribution of organic cation transporter 2 （OCT2） to cisplatin-induced nephrotoxicity. Clin Pharmacol Ther. 2009; 86: 396-402
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19）Urakami Y, Kimura N, Okuda M, et al. Creatinine transport by basolateral organic cation transporter hOCT2 in the human kidney. Pharm Res. 2004; 21: 976-81
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20）Okuda M, Kimura N, Inui K. Interactions of fluoroquinolone antibacterials, DX-619 and levofloxacin, with creatinine transport by renal organic cation transporter hOCT2. Drug Metabo Pharmacokinet. 2006; 21: 432-6
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21）Sarapa N, Wickremasingha P, Ge N, et al. Lack of effect of DX-619, a novel des-fluoro（6）-quinolone, on glomerular filtration rate measured by serum clearance of cold iohexol. Antimicrob Agents Chemother. 2007; 51: 1912-7
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22）Imamura Y, Murayama N, Okudaira N, et al. Prediction of fluoroquinolone-induced elevation in serum creatinine levels: a case of drug-endogenous substance interaction involving the inhibition of renal secretion. Clin Pharmacol Ther. 2011; 89: 81-8
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