Affinage

SLC2A9

Solute carrier family 2, facilitated glucose transporter member 9 · UniProt Q9NRM0

Length
540 aa
Mass
58.7 kDa
Annotated
2026-06-10
87 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC2A9 (GLUT9/URATv1) is a Na+-independent, voltage-driven, high-capacity facilitative urate transporter that mediates transcellular urate reabsorption in the kidney and regulates whole-body uric acid handling (PMID:18842065, PMID:18701466, PMID:30105595). Originally cloned as a facilitative glucose transporter family member with 12 predicted transmembrane domains and kidney/liver expression (PMID:10860667), it was reclassified when reconstitution in Xenopus oocytes showed urate is transported 45- to 60-fold faster than glucose, with transport that is saturable, electrogenic, enhanced by extracellular potassium, and dose-dependently inhibited by the uricosuric drug benzbromarone (PMID:18842065, PMID:18701466, PMID:18327257). Two isoforms partition the transport task across renal epithelia: the long isoform (SLC2A9-L) sorts to the basolateral membrane of proximal tubule cells via its unique N-terminus, while the short isoform (SLC2A9-S) localizes to the apical membrane of collecting duct cells (PMID:24409316). In vivo, inducible kidney-specific deletion sharply increases urinary urate excretion, establishing SLC2A9 as the principal mediator of renal urate reabsorption, while intestinal/enterocyte SLC2A9 governs whole-body urate clearance, with its loss producing hyperuricemia, hypertension, and dyslipidemia that are reversed by xanthine oxidase inhibition (PMID:30105595, PMID:25100214). Transcription is activated by the nuclear receptor HNF4α binding the isoform-1 promoter and is induced by p53 under oxidative stress, where urate import lowers intracellular ROS, linking SLC2A9 to antioxidant defense and chemoresistance (PMID:24858040, PMID:25209865). Cryo-EM structures in apo and urate-bound inward-open states define the urate selectivity pocket and an alternating-access mechanism, and map the loss-of-function disease mutations onto the transport pathway (PMID:39937868, PMID:29967582). Loss-of-function mutations in SLC2A9 cause renal hypouricemia type 2 in humans and analogous hyperuricosuria in dogs (PMID:19926891, PMID:36733941, PMID:18989453).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2000 Medium

    Establishing the molecular identity of SLC2A9 as a facilitative transporter family member set the structural and expression baseline before any transport function was known.

    Evidence cDNA cloning, Northern blot, hydropathy analysis, chromosomal mapping

    PMID:10860667

    Open questions at the time
    • No transport substrate identified in this study
    • Annotated as a glucose transporter, which proved misleading
  2. 2008 High

    The central question of what SLC2A9 transports was answered by reconstitution showing it is a high-capacity, Na+-independent, electrogenic urate transporter rather than a glucose transporter, redefining its physiological role.

    Evidence Xenopus oocyte expression, two-electrode voltage clamp, radiolabeled urate flux, siRNA knockdown, benzbromarone inhibition

    PMID:18327257 PMID:18701466 PMID:18842065

    Open questions at the time
    • Isoform-specific subcellular localization not resolved
    • Directionality (efflux vs reabsorption) in intact epithelium not directly shown
  3. 2008 Medium

    Linking SLC2A9 loss-of-function to human renal hypouricemia connected the transport activity to a defined disease, demonstrating its essential role in renal urate reabsorption.

    Evidence Patient sequencing plus mutant transporter functional assays in oocytes; positional cloning in Dalmatian dogs

    PMID:18989453 PMID:19026395

    Open questions at the time
    • Apical vs basolateral contribution to reabsorption not dissected
    • Dog study lacked direct in vitro transport assay
  4. 2009 High

    Homozygous null and missense mutations producing extreme fractional urate excretion confirmed GLUT9 as essential and non-redundant for renal urate reabsorption.

    Evidence Homozygosity mapping, sequencing, in vitro transport assay of L75R mutant

    PMID:19926891

    Open questions at the time
    • Mechanism of compensatory transport in heterozygotes unaddressed
  5. 2011 Medium

    In vivo kidney overexpression and additional patient mutations refined the model that renal SLC2A9 activity scales urate reabsorption and that disease mutations map to the urate-conducting channel.

    Evidence Kidney-specific transgenic mouse; oocyte transport assay with molecular modeling of R171C/T125M

    PMID:21810765 PMID:22132990

    Open questions at the time
    • Plasma urate unchanged in transgenic mice implies unquantified compensation
    • Channel model based on homology modeling, not experimental structure
  6. 2014 High

    Resolving the two isoforms' distinct polarized localizations explained how a single gene executes transcellular urate movement across different nephron segments.

    Evidence Isoform-specific antibody staining of human kidney, GFP-fusion in MDCK cells, N-terminal mutagenesis

    PMID:24409316

    Open questions at the time
    • Quantitative contribution of each isoform to net reabsorption not measured
    • Trafficking machinery recognizing the N-terminal sorting signal not identified
  7. 2014 Medium

    Identifying HNF4α and p53 as transcriptional regulators placed SLC2A9 within gene-regulatory networks controlling renal expression and oxidative-stress responses, the latter via urate's antioxidant import.

    Evidence Reporter assays, ChIP, HNF4α overexpression (renal promoter); siRNA, reporter assay, ROS measurement, probenecid (p53/oxidative stress)

    PMID:24858040 PMID:25209865

    Open questions at the time
    • p53 promoter occupancy by ChIP not demonstrated
    • Crosstalk between HNF4α and p53 regulation unexplored
  8. 2014 High

    Extending function beyond the kidney, intestinal SLC2A9 was shown to govern whole-body urate clearance, linking transport loss to hyperuricemia-driven metabolic and cardiovascular phenotypes.

    Evidence Whole-body knockout mouse, enterocyte urate transport kinetics, allopurinol pharmacological rescue

    PMID:25100214

    Open questions at the time
    • Relative renal vs intestinal contribution to systemic urate not quantified
    • Molecular link between urate and hypertension/dyslipidemia not defined
  9. 2018 High

    Inducible kidney-specific knockout established in vivo that renal SLC2A9 directly mediates urate reabsorption, while systematic variant analysis classified disease mutations into surface-expression versus intrinsic-activity defects and implicated specific residues in the binding pocket.

    Evidence Tetracycline-inducible kidney KO mouse with urate/creatinine and blood pressure readouts; oocyte 14C-urate uptake, TEVC, surface biotinylation across multiple variants

    PMID:29967582 PMID:30105595

    Open questions at the time
    • No urate variant conferred glucose transport, leaving substrate-switch determinants undefined at the time
    • Cause of blood-pressure phenotype in kiKO mice not mechanistically resolved
  10. 2025 High

    Cryo-EM structures in apo and urate-bound inward-open states defined the urate selectivity pocket and an alternating-access mechanism, providing the structural framework onto which disease mutations are mapped.

    Evidence Cryo-EM (3.3 Å apo, 4.1 Å urate-bound), modeling of outward-facing conformation; corroborated by oocyte/organoid variant studies and molecular dynamics

    PMID:34572357 PMID:36733941 PMID:38269090 PMID:39937868

    Open questions at the time
    • Outward-open state captured only by modeling, not experimentally
    • Structural basis for voltage dependence and potassium enhancement not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SLC2A9 activity is dynamically regulated across tissues (brain, liver, intestine) and how its antioxidant urate-import role integrates with its bulk reabsorptive function in disease remain open.
  • Functional role of brain SLC2A9 shown only by localization, not activity
  • Post-translational and trafficking regulation in vivo undefined
  • Mechanism linking urate transport to EMT/renal injury not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 5 GO:0140104 molecular carrier activity 3
Localization
GO:0005886 plasma membrane 2
Pathway
R-HSA-382551 Transport of small molecules 4 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-1430728 Metabolism 1
Partners
HNF4ATP53

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2008 SLC2A9 (GLUT9) mediates high-capacity urate transport in Xenopus laevis oocytes, with urate transported at rates 45- to 60-fold faster than glucose. Glucose and fructose facilitate SLC2A9-mediated urate transport, and the uricosuric drug benzbromarone inhibits transport dose-dependently (Ki = 27 µM). siRNA knockdown of SLC2A9 in a mammalian cell line diminished urate transport, confirming specificity. Xenopus laevis oocyte expression system, HEK cell overexpression, siRNA knockdown, radiolabeled urate flux assay PLoS medicine High 18842065
2008 SLC2A9 (GLUT9/URATv1) functions as a voltage-driven efflux transporter of urate on the basolateral side of renal proximal tubular cells. Transport in Xenopus oocytes is Na+-independent, saturable (Km ~365 µM), and enhanced by high extracellular potassium (negative-to-positive potential direction). A missense mutation in SLC2A9 found in a renal hypouricemia patient reduced urate transport in vitro, supporting the in vivo role. Xenopus laevis oocyte expression system, two-electrode voltage clamp, radiolabeled urate uptake, patient mutation functional assay The Journal of biological chemistry High 18701466
2008 SLC2A9 exhibits strong uric acid transport activity in Xenopus laevis oocytes. This established SLC2A9, previously known only as a fructose transporter, as a urate transporter influencing serum uric acid concentration and fractional excretion of uric acid. Xenopus laevis oocyte expression system, urate transport assay Nature genetics High 18327257
2008 Loss-of-function mutations in SLC2A9 (GLUT9) cause renal hypouricemia. Two heterozygous mutations in the 'sugar transport proteins signatures 1/2' region markedly reduced urate transport activity of both GLUT9 isoforms in Xenopus oocytes. The localization of GLUT9 on both sides of the renal proximal tubules suggests it regulates urate reabsorption on apical and basolateral membranes. Xenopus oocyte expression system, mutant transporter functional assay, sequencing of patient samples American journal of human genetics High 19026395
2009 Homozygous SLC2A9 mutations (L75R missense and a 36-kb deletion causing truncated protein) cause severe renal hypouricemia with fractional excretion of uric acid >150%. The L75R mutation dramatically impaired uric acid transport in vitro, establishing GLUT9 as essential for renal uric acid reabsorption. In vitro transport assay (patient mutation), genome-wide homozygosity screen, sequencing Journal of the American Society of Nephrology : JASN High 19926891
2014 SLC2A9 has two isoforms with distinct subcellular localizations in the kidney: SLC2A9-L (540 aa) localizes to the basolateral membrane of proximal tubules, while SLC2A9-S (512 aa) localizes to the apical membrane of collecting duct cells. In MDCK cells, SLC2A9-L is restricted to the basolateral membrane and SLC2A9-S is at both apical and basolateral membranes. N-terminal amino acids play a role in protein stability and trafficking. The unique N-terminus of SLC2A9-L (>30 aa deletion leads to mislocalization and lysosomal targeting) determines basolateral sorting. Isoform-specific antibody staining of human kidney sections, GFP-fusion protein expression in MDCK cells, N-terminal deletion/substitution mutagenesis PloS one High 24409316
2014 SLC2A9 is a direct transcriptional target of p53. Oxidative stress induces SLC2A9 expression in a p53-dependent manner. SLC2A9 reduces intracellular reactive oxygen species (ROS) by transporting uric acid (an antioxidant) into cells, and its inhibition (by siRNA or probenecid) increases ROS levels and sensitizes cancer cells to chemotherapeutic drugs. Expression of SLC2A9 protected against DNA damage and cell death. siRNA knockdown, reporter assay, p53-dependent gene expression analysis, ROS measurement, drug treatment (probenecid) Oncogene Medium 24858040
2014 The nuclear receptor HNF4α binds a site in the promoter of SLC2A9 isoform 1 and transcriptionally activates SLC2A9 expression. Mutation of the HNF4α binding site diminished promoter activation; HNF4α overexpression induced endogenous SLC2A9 expression in vitro; chromatin immunoprecipitation confirmed HNF4α binding at the SLC2A9 promoter in vivo. In silico promoter analysis, reporter gene assay, site-directed mutagenesis, HNF4α overexpression, ChIP assay, RT-qPCR in human kidney samples American journal of physiology. Renal physiology High 25209865
2011 Kidney-specific transgenic overexpression of URATv1 (SLC2A9) in mice decreased urate excretion compared to wild-type mice, indicating that increased SLC2A9 activity in the kidney enhances urate reabsorption. Plasma urate concentrations were not significantly different, suggesting compensatory mechanisms exist. Kidney-specific transgenic mouse model (URAT1 promoter-driven SLC2A9), plasma and urine urate measurement Nucleosides, nucleotides & nucleic acids Medium 22132990
2018 SLC2A9 mediates urate reabsorption in the mouse kidney in vivo. Inducible kidney-specific deletion of GLUT9 (kiKO mice) caused a major increase in urinary urate excretion and fractional excretion of urate within 4 days, without spontaneous kidney stones. kiKO mice also displayed lower blood pressure with increased heart rate. Tetracycline-inducible kidney-specific knockout mouse (Cre-lox), urate/creatinine ratio measurement, 24-hour urine collection, blood pressure monitoring Pflugers Archiv : European journal of physiology High 30105595
2014 Intestinal (enterocyte) SLC2A9/GLUT9 regulates whole-body uric acid clearance and metabolism. Glut9-deficient mice developed impaired enterocyte uric acid transport kinetics, hyperuricemia, hyperuricosuria, spontaneous hypertension, dyslipidemia, and elevated body fat. Treatment with allopurinol (xanthine oxidase inhibitor) reversed the hypertension and hypercholesterolemia, indicating these metabolic effects are mediated by elevated uric acid. Whole-body SLC2A9 knockout mouse model, urate transport kinetics assay, allopurinol pharmacological rescue Nature communications High 25100214
2008 A missense mutation (C188F) in the SLC2A9 gene, along with promoter mutations reducing expression of one isoform, causes hyperuricosuria and hyperuricemia in Dalmatian dogs and other dog breeds. This demonstrates SLC2A9 mediates uric acid transport in the liver and renal proximal tubules across mammalian species. Positional cloning, linkage mapping, sequence and expression analysis, breed-specific mutation verification PLoS genetics Medium 18989453
2018 Systematic functional analysis of human SLC2A9 (Glut9) disease-causing variants using 14C-urate uptake assay and two-electrode voltage clamp (TEVC) in Xenopus oocytes showed that most variants decreased urate transport. No variant permitted glucose transport. Two categories of dysfunction were identified: reduced cell-surface expression causing low activity, and full surface expression with decreased intrinsic activity. Residue N333S showed decreased urate affinity, suggesting it contributes to the urate binding pocket. C210F displayed lower transport ability. Xenopus oocyte expression, 14C-urate uptake flux assay, two-electrode voltage clamp, immunostaining, cell-surface biotinylation Frontiers in physiology High 29967582
2025 Cryo-EM structures of human SLC2A9 were determined in apo (3.3 Å) and urate-bound (4.1 Å) forms, both captured in inward-open conformation. Modeling of the outward-facing conformation revealed alternative salt bridge pairs on the cytoplasmic side that may balance energetics of the alternating access mechanism. The structures elucidate the molecular basis for urate selectivity and the locations of disease-causing mutations within the transporter. Cryo-EM structural determination, molecular modeling of outward-facing conformation Proceedings of the National Academy of Sciences of the United States of America High 39937868
2011 Two novel homozygous SLC2A9 missense mutations (R171C and T125M) dramatically reduced urate transport activity in Xenopus laevis oocytes. Molecular modeling showed both mutations are located within the inner channel that transports urate between cytoplasmic and extracellular regions, providing a structural basis for loss of function. Xenopus oocyte transport assay, molecular modeling Nephrology, dialysis, transplantation Medium 21810765
2021 The SLC2A9 variant p.Met126Val (in the short isoform; p.Met155Val in long isoform) significantly reduced uric acid transport in Xenopus oocytes without affecting protein expression level. Molecular dynamics simulation predicted the mutation hinders uric acid transport by disrupting the outward open geometry of the transporter. Xenopus oocyte expression and urate transport assay, molecular dynamics simulation, whole-exome sequencing Biomedicines Medium 34572357
2023 An intronic SLC2A9 variant (c.1419+1G>A) causes exon 11 skipping, producing a functionally null frameshift variant (p.Gly431GlufsTer28), confirmed as causal for renal hypouricemia type 2 by in vitro functional assays and identification in a second unrelated family. Whole exome sequencing, in vitro functional assay, mini-gene splicing assay, family segregation analysis Frontiers in genetics Medium 36733941
2016 GLUT9/SLC2A9 protein (immunoreactive) was detected in ependymal cells, neurons, and brain capillaries of mouse brain by immunostaining and in situ hybridization, suggesting urate transport by SLC2A9 occurs in the murine brain, potentially providing neuroprotection. Immunostaining, highly-sensitive in situ hybridization Fluids and barriers of the CNS Low 27955673
2024 SLC2A9 rs16890979 (V282I missense) reduces uric acid absorption in kidney organoids derived from gene-edited human embryonic stem cells. SLC2A9 overexpression increased urate absorption and SLC2A9 knockdown decreased it in the same system. Additionally, urate treatment of organoids with SLC2A9 overexpression induced epithelial-mesenchymal transition (EMT), suggesting a mechanism for hyperuricosuria-related renal injury. Human ESC-derived kidney organoids with CRISPR gene editing, SLC2A9 overexpression and shRNA knockdown, urate absorption assay, histopathological analysis Frontiers in cell and developmental biology Medium 38269090
2000 SLC2A9 (GLUT9) was identified as a novel member of the facilitative glucose transporter family encoding a predicted 540 amino acid protein with 12 transmembrane domains. Northern analysis revealed expression primarily in kidney and liver. The gene was localized to chromosome 4p15.3-p16. cDNA cloning, Northern blot analysis, hydropathic analysis, somatic cell hybrid mapping Genomics Medium 10860667

Source papers

Stage 0 corpus · 87 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 SLC2A9 is a newly identified urate transporter influencing serum urate concentration, urate excretion and gout. Nature genetics 614 18327257
2008 SLC2A9 influences uric acid concentrations with pronounced sex-specific effects. Nature genetics 332 18327256
2008 Mutations in glucose transporter 9 gene SLC2A9 cause renal hypouricemia. American journal of human genetics 303 19026395
2008 Plasma urate level is directly regulated by a voltage-driven urate efflux transporter URATv1 (SLC2A9) in humans. The Journal of biological chemistry 290 18701466
2008 SLC2A9 is a high-capacity urate transporter in humans. PLoS medicine 290 18842065
2009 Homozygous SLC2A9 mutations cause severe renal hypouricemia. Journal of the American Society of Nephrology : JASN 178 19926891
2000 Cloning and expression analysis of a novel member of the facilitative glucose transporter family, SLC2A9 (GLUT9). Genomics 165 10860667
2014 Early-onset metabolic syndrome in mice lacking the intestinal uric acid transporter SLC2A9. Nature communications 159 25100214
2008 Mutations in the SLC2A9 gene cause hyperuricosuria and hyperuricemia in the dog. PLoS genetics 88 18989453
2009 Role of the urate transporter SLC2A9 gene in susceptibility to gout in New Zealand Māori, Pacific Island, and Caucasian case-control sample sets. Arthritis and rheumatism 87 19877038
2008 Sex-specific association of the putative fructose transporter SLC2A9 variants with uric acid levels is modified by BMI. Diabetes care 83 18487473
2013 Sugar-sweetened beverage consumption: a risk factor for prevalent gout with SLC2A9 genotype-specific effects on serum urate and risk of gout. Annals of the rheumatic diseases 80 24026676
2014 The uric acid transporter SLC2A9 is a direct target gene of the tumor suppressor p53 contributing to antioxidant defense. Oncogene 76 24858040
2014 Expression of SLC2A9 isoforms in the kidney and their localization in polarized epithelial cells. PloS one 69 24409316
2013 Population-specific influence of SLC2A9 genotype on the acute hyperuricaemic response to a fructose load. Annals of the rheumatic diseases 58 23349133
2018 Human Mutations in SLC2A9 (Glut9) Affect Transport Capacity for Urate. Frontiers in physiology 56 29967582
2009 Associations of a non-synonymous variant in SLC2A9 with gouty arthritis and uric acid levels in Han Chinese subjects and Solomon Islanders. Annals of the rheumatic diseases 51 19723617
2011 Novel homozygous insertion in SLC2A9 gene caused renal hypouricemia. Molecular genetics and metabolism 45 21256783
2011 Two novel homozygous SLC2A9 mutations cause renal hypouricemia type 2. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 43 21810765
2010 Variation in the uric acid transporter gene SLC2A9 and its association with AAO of Parkinson's disease. Journal of molecular neuroscience : MN 41 20589538
2018 SLC2A9 (GLUT9) mediates urate reabsorption in the mouse kidney. Pflugers Archiv : European journal of physiology 40 30105595
2014 Complex analysis of urate transporters SLC2A9, SLC22A12 and functional characterization of non-synonymous allelic variants of GLUT9 in the Czech population: no evidence of effect on hyperuricemia and gout. PloS one 36 25268603
2010 Bayesian methods for instrumental variable analysis with genetic instruments ('Mendelian randomization'): example with urate transporter SLC2A9 as an instrumental variable for effect of urate levels on metabolic syndrome. International journal of epidemiology 36 20348110
2016 A Novel Homozygous SLC2A9 Mutation Associated with Renal-Induced Hypouricemia. American journal of nephrology 30 27116386
2013 Genome-wide association analysis confirms and extends the association of SLC2A9 with serum uric acid levels to Mexican Americans. Frontiers in genetics 30 24379826
2010 Variation in the uric acid transporter gene (SLC2A9) and memory performance. Human molecular genetics 29 20197412
2014 Recurrent exercise-induced acute kidney injury by idiopathic renal hypouricemia with a novel mutation in the SLC2A9 gene and literature review. BMC pediatrics 28 24628802
2011 Recurrent EIARF and PRES with severe renal hypouricemia by compound heterozygous SLC2A9 mutation. Pediatrics 27 21536615
2010 Association between SLC2A9 transporter gene variants and uric acid phenotypes in African American and white families. Rheumatology (Oxford, England) 25 21186168
2014 Recurrent exercise-induced acute renal failure in a young Pakistani man with severe renal hypouricemia and SLC2A9 compound heterozygosity. BMC medical genetics 23 24397858
2014 Abundant local interactions in the 4p16.1 region suggest functional mechanisms underlying SLC2A9 associations with human serum uric acid. Human molecular genetics 23 24821702
2013 Replication of the effect of SLC2A9 genetic variation on serum uric acid levels in American Indians. European journal of human genetics : EJHG 23 24301058
2021 Epigenome-wide association study of serum urate reveals insights into urate co-regulation and the SLC2A9 locus. Nature communications 20 34887389
2011 Significant association of serum uric acid levels with SLC2A9 rs11722228 among a Japanese population. Molecular genetics and metabolism 20 21511506
2015 Genetic analysis of ABCG2 and SLC2A9 gene polymorphisms in gouty arthritis in a Korean population. The Korean journal of internal medicine 19 26552468
2014 Transcriptional regulation of urate transportosome member SLC2A9 by nuclear receptor HNF4α. American journal of physiology. Renal physiology 19 25209865
2011 The rs1014290 polymorphism of the SLC2A9 gene is associated with type 2 diabetes mellitus in Han Chinese. Experimental diabetes research 18 21584282
2010 Association of an intronic SNP of SLC2A9 gene with serum uric acid levels in the Chinese male Han population by high-resolution melting method. Clinical rheumatology 18 20972595
2016 Association between SLC2A9 (GLUT9) gene polymorphisms and gout susceptibility: an updated meta-analysis. Rheumatology international 16 27255295
2016 Additive composite ABCG2, SLC2A9 and SLC22A12 scores of high-risk alleles with alcohol use modulate gout risk. Journal of human genetics 15 27225847
2016 Immunohistochemical and in situ hybridization study of urate transporters GLUT9/URATv1, ABCG2, and URAT1 in the murine brain. Fluids and barriers of the CNS 15 27955673
2015 Association of SLC2A9 genotype with phenotypic variability of serum urate in pre-menopausal women. Frontiers in genetics 15 26528330
2012 Polymorphisms in the presumptive promoter region of the SLC2A9 gene are associated with gout in a Chinese male population. PloS one 15 22393348
2010 Association of nephrolithiasis and gene for glucose transporter type 9 (SLC2A9): study of 145 patients. Croatian medical journal 15 20162745
2014 Copy number polymorphisms near SLC2A9 are associated with serum uric acid concentrations. BMC genetics 13 25007794
2014 Four pairs of gene-gene interactions associated with increased risk for type 2 diabetes (CDKN2BAS-KCNJ11), obesity (SLC2A9-IGF2BP2, FTO-APOA5), and hypertension (MC4R-IGF2BP2) in Chinese women. Meta gene 12 25606423
2011 Increased expression of SLC2A9 decreases urate excretion from the kidney. Nucleosides, nucleotides & nucleic acids 12 22132990
2021 Aotearoa New Zealand Māori and Pacific Population-amplified Gout Risk Variants: CLNK Is a Separate Risk Gene at the SLC2A9 Locus. The Journal of rheumatology 11 34210831
2013 Short communication: genetic variations of SLC2A9 in relation to Parkinson's disease. Translational neurodegeneration 11 23422251
2024 SLC2A9 rs16890979 reduces uric acid absorption by kidney organoids. Frontiers in cell and developmental biology 10 38269090
2012 Effects of SLC2A9 variants on uric acid levels in a Korean population. Rheumatology international 10 22212408
2010 Interactions between genetic variants in glucose transporter type 9 (SLC2A9) and dietary habits in serum uric acid regulation. Croatian medical journal 10 20162744
2024 Triglyceride-glucose index and its additive interaction with ABCG2/SLC2A9 polygenic risk score on hyperuricemia in middle age and older adults: findings from the DLCC and BHMC study. Annals of medicine 9 39607832
2023 Identification of a dysfunctional exon-skipping splice variant in GLUT9/SLC2A9 causal for renal hypouricemia type 2. Frontiers in genetics 9 36733941
2019 Amplicon targeted resequencing for SLC2A9 and SLC22A12 identified novel mutations in hypouricemia subjects. Molecular genetics & genomic medicine 9 31131560
2014 Identification of a hypouricemia patient with SLC2A9 R380W, a pathogenic mutation for renal hypouricemia type 2. Nucleosides, nucleotides & nucleic acids 9 24940677
2023 Pathogenic Variants of SLC22A12 (URAT1) and SLC2A9 (GLUT9) in Spanish Patients with Renal Hypouricemia: Founder Effect of SLC2A9 Variant c.374C>T; p.(T125M). International journal of molecular sciences 8 37176161
2018 Overexpression of Uric Acid Transporter SLC2A9 Inhibits Proliferation of Hepatocellular Carcinoma Cells. Oncology research 8 29523220
2017 Associations between SLC2A9 polymorphisms and gout susceptibility : A meta-analysis. Zeitschrift fur Rheumatologie 8 27052299
2015 Association of an Exon SNP of SLC2A9 Gene with Hyperuricemia Complicated with Type 2 Diabetes Mellitus in the Chinese Male Han Population. Cell biochemistry and biophysics 7 25476142
2015 Genome-Wide Association Identifies SLC2A9 and NLN Gene Regions as Associated with Entropion in Domestic Sheep. PloS one 7 26098909
2018 An Intron Variant of SLC2A9 Increases the Risk for Type 2 Diabetes Mellitus Complicated with Hyperuricemia in Chinese Male Population. Iranian journal of public health 6 30087870
2018 Long-term effects of the SLC2A9 G844A and SLC22A12 C246T variants on serum uric acid concentrations in children. BMC pediatrics 6 30189835
2015 SLC2A9 and ZNF518B polymorphisms correlate with gout-related metabolic indices in Chinese Tibetan populations. Genetics and molecular research : GMR 6 26345926
2012 Changes in uric acid levels following bariatric surgery are not associated with SLC2A9 variants in the Swedish Obese Subjects Study. PloS one 6 23272134
2017 The Single Nucleotide Polymorphism rs1014290 of the SLC2A9 Gene Is Associated with Uric Acid Metabolism in Parkinson's Disease. Parkinson's disease 5 29158942
2025 Red blood cell urate levels are linked to hemolysis in vitro and post-transfusion as a function of donor sex, population and genetic polymorphisms in SLC2A9 and ABCG2. Transfusion 4 39828898
2025 Structural basis of disease mutation and substrate recognition by the human SLC2A9 transporter. Proceedings of the National Academy of Sciences of the United States of America 4 39937868
2021 Characterization of a Compound Heterozygous SLC2A9 Mutation That Causes Hypouricemia. Biomedicines 4 34572357
2021 Mutation in the SLC2A9 Gene: A New Family with Familial Renal Hypouricemia Type 2. Case reports in nephrology 4 34603806
2015 Primary portal vein hypoplasia and SLC2A9 mutation associated with urate urolithiasis in a Spanish water dog. The Canadian veterinary journal = La revue veterinaire canadienne 4 26538670
2024 Polymorphism rs3733591 of the SLC2A9 gene and metabolic syndrome affect gout risk in Taiwan Biobank subjects. Frontiers in genetics 3 38689651
2024 Renal hypouricemia type 2 with SLC2A9 compound heterozygous variants: a case report of recurrent acute kidney injury triggered by low-intensity exercise. Frontiers in nephrology 3 39421323
2024 Mechanism of intestinal flora affecting SLC2A9 transport function to promote the formation of hyperuricemia. Heliyon 3 39698087
2022 Gene Dose-Dependent and Additive Effects of ABCG2 rs2231142 and SLC2A9 rs3733591 Genetic Polymorphisms on Serum Uric Acid Levels. Metabolites 3 36557230
2018 Association of solute carrier family 2, member 9 (SLC2A9) genetic variant rs3733591 with gout in a Malay sample set. The Medical journal of Malaysia 3 30350810
2016 [ROLE OF SLC2A9 AND ABCG2 GENE POLYMORPHISMS IN ORIGIN OF HYPERURICEMIA AND GOUT]. Georgian medical news 3 27119840
2025 Single Nucleotide Variants of the SLC2A9 Gene Are Associated with Hyperuricemia in Mexican Patients with Type 2 Diabetes. Archives of medical research 2 40373704
2021 Identification of two novel heterozygous SLC2A9 mutations in a Chinese woman and review of literature. Clinica chimica acta; international journal of clinical chemistry 2 34499869
2025 PCR-based detection of hereditary mutations in SLC2A9, BTBD17, and NECAP1 among native Korean dog breeds. Journal of veterinary science 1 40765230
2026 A potential association of SLC2A9 variant rs7442295 with uric acid at baseline and in interaction with iloperidone. The pharmacogenomics journal 0 41826282
2026 Mendelian Randomization Identified SLC2A9 as a Novel cis-eQTL-Mediated Susceptibility Gene in Suppressing Renal Cancer and Its Related Metabolic Mechanisms. Mediators of inflammation 0 41837832
2026 Associations between dietary micronutrient intake and serum urate concentrations are dependent on SLC2A9 polymorphism rs12498742: A UK Biobank cohort study. The Journal of nutrition 0 42235823
2025 Diagnostic Significance of SLC2A9 Gene Polymorphisms and Serum Biomarkers in Gout and Hyperuricemia. Clinical laboratory 0 40779481
2025 Prevalence of the SOD1, PRCD and SLC2A9 gene mutations responsible for degenerative myelopathy, progressive rod-cone degeneration, and hyperuricosuria in Polish population of Labrador Retriever dogs. Polish journal of veterinary sciences 0 40996129
2024 [First detection of the SLC2A9:p.C188F gene defect in a German Hunting Terrier with ammonium urate urolithiasis]. Tierarztliche Praxis. Ausgabe K, Kleintiere/Heimtiere 0 39173651
2018 Genetic analysis for rs2280205 (A>G) and rs2276961 (T>C) in SLC2A9 polymorphism for the susceptibility of gout in Cameroonians: a pilot study. BMC research notes 0 29615104

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