NoteA Common Variant of Organic Anion Transporter 4 (OAT4/SLC22A11) Gene Is Associated with Renal Underexcretion Type Gout
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Cited by (43)
Regulation of organic anion transporters: Role in physiology, pathophysiology, and drug elimination
2021, Pharmacology and TherapeuticsCitation Excerpt :As OAT3-Ile305Phe variant accounts for about 3.5% allele frequency in Asians, a clinical study showed that OAT3-Ile305Phe variant significantly suppressed the renal clearance of cefotaxime, in healthy volunteers (Yee et al., 2013). Besides, a SNP (Position at chromosome11: 64088038, A/G) of OAT4 was associated with renal underexcretion type gout by analysis of OAT4 gene in gout patients and healthy volunteers, suggesting that OAT4 expressed at apical membrane of renal proximal tubule cells contributed to urate transport in humans (Kolz et al., 2009; Sakiyama et al., 2014). Cho et al found that five new SNPs in the human URAT1 gene were significantly associated with uric acid concentration in blood by analyzing subjects with normal uric acid level and subjects with hyperuricemia (Cho, Kim, Chung, & Jee, 2015).
Pharmacological urate-lowering approaches in chronic kidney disease
2019, European Journal of Medicinal ChemistryCitation Excerpt :OAT1-3 proteins are on the basolateral membrane of proximal tubule for the uptake of urate from blood and operating as exchangers for mediating urate efflux [11,12]. On the contrary, OAT4 and OAT10 are on the luminal side, of whom elevated expression is associated with renal underexcretion type hyperuricemia [13,14]. The main transporter in the luminal epithelium of proximal tubule for urate reabsorption is URAT1 (Urate transporter 1).
Renal organic anion transporters in drug–drug interactions and diseases
2018, European Journal of Pharmaceutical SciencesCitation Excerpt :On the one hand, OATs can be affected by renal failure and disease in terms of mRNA and protein expression level, and transport activity, showing altered renal clearance of their substrates (Lowenstein and Grantham 2016; Schwenk and Pai 2016; Wang and Sweet 2013). On the other hand, OATs, as a functional protein mediating the accumulation of organic anions from the blood and urine into proximal tubule cells, has an impact on the progression of disease by elimination of toxicity products (Bulacio and Torres 2013; Sakiyama et al. 2014; Watanabe et al. 2014). It is difficult to answer whether the altered OATs is the consequence or the reason of the diseases.
Recent advance in the pharmacogenomics of human Solute Carrier Transporters (SLCs) in drug disposition
2017, Advanced Drug Delivery ReviewsCitation Excerpt :It showed that OAT4-L29P, − R48Y, − V155G and –T392I have reduced transport activity (Table 2), which are partially due to the impaired protein expression of these variant transporters. Literature also demonstrated that OAT4 genetic polymorphisms may be associated with the altered renal clearance of torsemide and renal underexcretion type gout [146,153,154]. However, the molecular findings on OAT4 genotypes cannot readily be used to interpret the in vivo observations.
Common variant of PDZ domain containing 1 (PDZK1) gene is associated with gout susceptibility: A replication study and meta-analysis in Japanese population
2016, Drug Metabolism and PharmacokineticsCitation Excerpt :Common variants of ABCG2 [18] significantly increase gout [19–21] and hyperuricemia risks [22,23]. Additionally, OAT4 [24], URAT1 [25–28], and NPT1 [27–30] genes are associated with gout susceptibility. PDZK1 and sodium protein exchanger regulatory factor 1 (NHERF 1) assemble the scaffolding network connecting these transporters in the transportsome [16,17].
Can uric acid affect the immune microenvironment in bladder cancer? A single-center multi-omics study
2024, Molecular Carcinogenesis
This study was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan (including the Grant-in-Aid for Scientific Research on Special Priority Areas of Cancer and Innovative Areas), the Ministry of Health, Labour and Welfare of Japan, the Ministry of Defense of Japan, the Japan Society for the Promotion of Science, the Kawano Masanori Memorial Foundation for Promotion of Pediatrics, the Gout Research Foundation of Japan and the AstraZeneca VRI Research Grant.