Tappei Takada

TL;DR: It is shown that decreased extra-renal urate excretion caused by ABCG2 dysfunction is a common mechanism of hyperuricemia, and the 'overproduction type' in the current concept of hyperURicemia should be renamed 'renal overload type', which consists of two subtypes—'extra-renals urate underexcretion' and genuine 'urate overproduction'.

TL;DR: In a Japanese population, another risk variant in ABCG2, namely the Q126X nonfunctional mutation, confers an even higher risk associated with an increase in uric acid deposition in the blood and may cause gout in Asians, lending weight to previously reported GWAS.

TL;DR: This Article failed to indicate that the term ENBT1 was previously used as the name of a putative transporter involved in the dipyridamole-insensitive, purine-selective nucleobase transport system in primary human cardiac microvascular endothelial cells.

TL;DR: It is demonstrated that the SNPs of ABCG2 and SLC2A9 were differentially associated with types of gout and clinical parameters underlying specific subtypes (renal underexcretion type and renal overload type) and the effect of the risk allele of each SNP on clinical parameters showed significant linear relationships.

TL;DR: Results show that ABCG2 plays physiologically important roles in both renal and extra-renal urate excretion mechanisms, and indicate the importance ofABCG2 as a promising therapeutic and screening target of hyperuricemia and gout.