title: [Recent progress and prospects for research on urate efflux transporter ABCG2].
abstract: ABCG2 is a high-capacity urate exporter. Two frequent variants, Q126X and Q141K are a nonfunctional and half-functional variant, respectively. The estimated ABCG2 dysfunction based on the combination of Q126X and Q141K haplotype raises gout/hyperuricemia risk. ABCG2 dysfunction accounts for about 80% of gouty patients. Severe ABCG2 dysfunction particularly increased the risk of early-onset gout. Hyperuricemia has been clinically classified into urate 'overproduction type' and/or 'underexcretion type' based solely on renal urate excretion, without considering an extra-renal pathway. A major cause of'overproduction' hyperuricemia is not true overproduction of urate but rather'extra-renal urate underexcretion' by common ABCG2 dysfunction. As ABCG2 dysfunction is a main cause of gout, ABCG2 research will provide a new approach for prevention and treatment of gout.
authors.forename: Kimiyoshi
authors.initials: K
authors.lastname: Ichida
mesh_terms: D000070997:ATP Binding Cassette Transporter, Subfamily G, Member 2; D018528:ATP-Binding Cassette Transporters / Q000502:physiology*; D006073:Gout / Q000378:metabolism; D006801:Humans; D033461:Hyperuricemia / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000502:physiology*; D027361:Organic Anion Transporters / Q000502:physiology*
chemical_list: C116614:ABCG2 protein, human; D000070997:ATP Binding Cassette Transporter, Subfamily G, Member 2; D018528:ATP-Binding Cassette Transporters; D009363:Neoplasm Proteins; D027361:Organic Anion Transporters; C103862:urate transporter