NDLI: ABCG2: the molecular mechanisms of urate secretion and gout.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Woodward, Owen M.
Description	Author Affiliation: Woodward OM ( Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland OWoodward@som.umaryland.edu.)
Abstract	The human propensity for high levels of serum uric acid (SUA) is a trait that has defied explanation. Is it beneficial? Is it pathogenic? Its role in the human diseases like gout and kidney stones was discovered over a century ago [Richette P, Bardin T. Lancet 375: 318-328, 2010; Rivard C, Thomas J, Lanaspa MA, Johnson RJ. Rheumatology (Oxford) 52: 421-426, 2013], but today emerging new genetic and epidemiological techniques have revived an age-old debate over whether high uric acid levels (hyperuricemia) independently increase risk for diseases like hypertension and chronic kidney disease [Feig DI. J Clin Hypertens (Greenwich) 14: 346-352, 2012; Feig DI, Madero M, Jalal DI, Sanchez-Lozada LG, Johnson RJ. J Pediatr 162: 896-902, 2013; Feig DI, Soletsky B, Johnson RJ. JAMA 300: 924-932, 2008; Wang J, Qin T, Chen J, Li Y, Wang L, Huang H, Li J. PLoS One 9: e114259, 2014; Zhu P, Liu Y, Han L, Xu G, Ran JM. PLoS One 9: e100801, 2014]. Part of the mystery of the role uric acid plays in human health stems from our lack of understanding of how humans regulate uric acid homeostasis, an understanding that could shed light on the historic role of uric acid in human adaptation and its present role in human pathogenesis. This review will highlight the recent work to identify the first important human uric acid secretory transporter, ABCG2, and the identification of a common causal ABCG2 variant, Q141K, for hyperuricemia and gout.
File Format	HTM / HTML
ISSN	1931857X
e-ISSN	15221466
DOI	10.1152/ajprenal.00242.2015
Journal	AJP: Renal Physiology
Issue Number	6
Volume Number	309
Language	English
Publisher	American Physiological Society
Publisher Date	2015-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Gout Models, Molecular Discipline Nephrology Metabolism Blood Atp-binding Cassette Transporters Discipline Physiology Hyperuricemia Neoplasm Proteins Uric Acid Genetics Protein Conformation
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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The genetics of hyperuricaemia and gout.

ABCG2 is a high-capacity urate transporter and its genetic impairment increases serum uric acid levels in humans.

The rs2231142 variant of the ABCG2 gene is associated with uric acid levels and gout among Japanese people.

ABCG2/BCRP dysfunction as a major cause of gout.

Recent advances in renal urate transport: characterization of candidate transporters indicated by genome-wide association studies.

ABCG2 dysfunction increases the risk of renal overload hyperuricemia.

ABCG transporters and disease.

Polymorphisms of uric transporter proteins in the pathogenesis of gout in a Chinese Han population.

Gout-causing Q141K mutation in ABCG2 leads to instability of the nucleotide-binding domain and can be corrected with small molecules.

ABCG2: the molecular mechanisms of urate secretion and gout.

Similar Documents

The genetics of hyperuricaemia and gout.

ABCG2 is a high-capacity urate transporter and its genetic impairment increases serum uric acid levels in humans.

The rs2231142 variant of the ABCG2 gene is associated with uric acid levels and gout among Japanese people.

ABCG2/BCRP dysfunction as a major cause of gout.

Recent advances in renal urate transport: characterization of candidate transporters indicated by genome-wide association studies.

ABCG2 dysfunction increases the risk of renal overload hyperuricemia.

ABCG transporters and disease.

Polymorphisms of uric transporter proteins in the pathogenesis of gout in a Chinese Han population.

Gout-causing Q141K mutation in ABCG2 leads to instability of the nucleotide-binding domain and can be corrected with small molecules.

ABCG2: the molecular mechanisms of urate secretion and gout.