ヒグチ　ケイ   Higuchi Kei   樋口　慧    所属   東邦大学  薬学部 薬学科    職種   准教授
論文種別	原著
言語種別	日本語
査読の有無	査読なし
招待の有無	招待あり
表題	[Analysis of Endogenous Metabolite Transporters for the Development of Novel Pharmaceutical Therapies and Drug Targets].
掲載誌名	正式名：Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
掲載区分	国内
巻・号・頁	144(12),1051-1054頁
著者・共著者	Kei Higuchi
担当区分	筆頭著者,責任著者
発行年月	2024/12/01
概要	Transporters are critical for maintaining the homeostasis of metabolites within cells, organelles, and extracellular fluids. Various transporters have been targeted for development as pharmaceutical therapies, including glucose transporter (SLC5A2/SGLT2) and urate transporter (SLC22A12/URAT1). The solute carrier transporter family includes many orphan transporters with unknown physiological functions and substrates, largely because of the difficulties in optimizing the transporter probes and constructing convenient evaluation systems for functional analysis. However, the analysis of these transporters is important as they may be potential candidates for pharmaceutical therapies or drug targets. This review focuses on the analysis of the SLC16A family, which encodes monocarboxylate transporters (MCTs), as it contains orphan transporters known to be associated with several disease pathologies. We successfully identified taurine, cephradine, and 5-carboxyfluorescein as new substrates for rat Slc16a6/MCT7, SLC16A13/MCT13, and SLC16A5/MCT6, respectively. These substrates enabled the functional analysis of the transporters in mammalian cells. We found that the co-expression of ancillary proteins, such as ancillary protein basigin/CD147 and embigin/GP70, enhanced the transport functions of these transporters. Interestingly, the functions of MCT6 and MCT13 were affected by extracellular chloride and potassium ions, respectively, but MCT7 was unaffected. These findings are helpful for elucidating the pathophysiological roles and substrates of orphan and uncharacterized MCTs.
DOI	10.1248/yakushi.24-00130
PMID	39617467