SNP CommunicationEthnic Differences in ATP-binding Cassette Transporter, Sub-family G, Member 2 (ABCG2/BCRP): Genotype Combinations and Estimated Functions
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Cited by (26)
Intestinal Hyperuricemia as a Driving Mechanism for CKD
2023, American Journal of Kidney DiseasesDevelopment of precision medicine approaches based on inter-individual variability of BCRP/ABCG2
2019, Acta Pharmaceutica Sinica BCitation Excerpt :Other SNPs have minor allele frequencies of less than 1%. The frequencies of the two prevalent ABCG2 variants (Table 236–41) differ among various ethnic groups with minor allele frequencies higher (20%–40%) in East Asians (Chinese36,37, Japanese37–39, and Korean40) and lower (2%–10%) in Caucasians36–38,41 and Africans36–38. The minor allele frequencies of these two ABCG2 variants in the 1000 Genomes Project (http://www.internationalgenome.org/) populations show a similar global distribution.
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 :In human kidney, the urate transportsome is located at the apical membrane of proximal tubular cells and contains several urate transporters [15–17], such as ATP-binding cassette transporter, subfamily G, member 2 (ABCG2/BCRP), organic anion transporter 4 (OAT4/SLC22A11), urate transporter 1 (URAT1/SLC22A12), type 1 sodium-dependent phosphate transporter (NPT1/SLC17A1), and multidrug resistance protein 4 (MRP4/ABCC4). 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.
Determinants of Achieving Serum Urate Goal with Treat-to-Target Urate-Lowering Therapy in Gout
2023, Arthritis and RheumatologyClinical Features of Gout
2023, A Clinician's Pearls and Myths in Rheumatology: Second Edition
This study was supported by grants from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan, including the MEXT KAKENHI (grant numbers 221S0002, 25293145, 22689021, 25670307), the Ministry of Health, Labour and Welfare of Japan, the Ministry of Defense of Japan, the Japan Society for the Promotion of Science, the Takeda Science Foundation, the AstraZeneca VRI Research Grant, the Kawano Masanori Memorial Foundation for Promotion of Pediatrics, and the Gout Research Foundation of Japan.
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Masayuki Sakiyama and Hirotaka Matsuo contributed equally to this work.