Associated Papers
Population-specific putative causal variants shape quantitative traits.
Koyama S et al.
Nature Genetics, 2024
39363016 (PubMed )
Supplement: 41588_2024_1913_MOESM3_ESM.xlsx › ST8_Missense_PPI___0.1
The pathogenesis of gout: molecular insights from genetic, epigenomic and transcriptomic studies.
Leask MP et al.
Nature Reviews. Rheumatology, 2024
Examining the Association of Rare Allelic Variants in Urate Transporters SLC22A11, SLC22A13, and SLC17A1 with Hyperuricemia and Gout.
Vávra J et al.
Disease Markers, 2024
OAT10/SLC22A13 Acts as a Renal Urate Re-Absorber: Clinico-Genetic and Functional Analyses With Pharmacological Impacts.
Toyoda Y et al.
Frontiers in Pharmacology, 2022
Dysfunctional missense variant of OAT10/SLC22A13 decreases gout risk and serum uric acid levels.
Higashino T et al.
Annals of the Rheumatic Diseases, 2020
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