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The protein encoded by SLC22A12 is a member of the organic anion transporter (OAT) family, and it acts as a urate transporter to regulate urate levels in blood. Additionally we are shipping Solute Carrier Family 22 (Organic Anion/urate Transporter), Member 12 Antibodies (28) and Solute Carrier Family 22 (Organic Anion/urate Transporter), Member 12 Kits (10) and many more products for this protein.
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Urat1-Uox double knockout mice are a suitable animal model for renal hypouricemia.
Immunostaining and highly-sensitive in situ hybridization was used to assess the distribution of UA transporters: GLUT9/URATv1, ABCG2, and URAT1. Immunostaining for GLUT9 was observed in ependymal cells, neurons, and brain capillaries. Immunostaining for ABCG2 was observed in the choroid plexus epithelium and brain capillaries, but not in ependymal cells. These results were validated by in situ hybridization.
The cause of obesity/metabolic syndrome-associated hyperuricemia appears to be associated with the urate reabsorption transporter Urat1 protein enhanced by fat.
Although the fractional excretion of urate of knockout mice was tend to higher than that of wildtype mice, the urate reabsorption ability remained in the kidney of knockout mice, indicating a urate reabsorptive transporter other than Urat1.
mouse RST mediates the efflux of organic anions including urate and works as exit for organic anions in the proximal tubules
NHERF-1 (show SLC9A3R1 Proteins) exerts a significant effect on the renal tubular reabsorption of uric acid in the mouse by modulating the brush Border membrane abundance of mURAT1.
A meta-analysis of all gout with Japanese, Caucasian and NZ Polynesian populations revealed that rs2285340 of SLC22A12 and rs1165196 of SLC17A1 showed a significant association but did not reach a genome-wide significance level.
The present proof-of-principle paper demonstrates that the multilocus profiles of ABCG2, SLC2A9 and SLC22A12 increase susceptibility to asymptomatic hyperuricaemia, gout and tophi.
The common dysfunction allelic variants of URAT1 exist in the general Roma population and thus renal hypouricemia should be kept in differential diagnostic algorithm on Roma patients with defect in renal tubular urate transport.
URAT1 nonfunctional variants are protective genetic factors for gout/hyperuricemia, and also demonstrated the sex-dependent effect size of these URAT1 variants on serum uric acid (P for interaction = 1.5 x 10(-12)).
These results suggest that URAT1 rs3825016 and rs1529909 polymorphisms influence the uricosuric action of losartan
Depletion of UA due to SLC22A12/URAT1 loss-of-function mutations causes endothelial dysfunction in hypouricemia patients.
not only loss-of-function mutation of URAT1 but also the dominant-negative effect cause RHUC through loss of UA absorption, partly due to protein misfolding caused by accumulation of URAT1 protein in the endoplasmic reticulum
Polymorphisms in GCKR, SLC17A1 and SLC22A12 were associated with phenotype gout in Han Chinese males.
protein expression of URAT1 and GLUT9 in renal tissues of patients with uric acid (UA) nephrolithiasis
There was no significant mutation found in SLC22A12 and SLC2A9 in this familial aggregation of Chinese female premenopausal gout.
The protein encoded by this gene is a member of the organic anion transporter (OAT) family, and it acts as a urate transporter to regulate urate levels in blood. This protein is an integral membrane protein primarily found in epithelial cells of the proximal tubule of the kidney. An elevated level of serum urate, hyperuricemia, is associated with increased incidences of gout, and mutations in this gene cause renal hypouricemia type 1. Alternative splicing results in multiple transcript variants.
, solute carrier family 22 (organic cation transporter)-like 2
, solute carrier family 22 member 12
, urate anion exchanger 1
, organic anion transporter 4-like protein
, solute carrier family 22 (organic anion/cation transporter), member 12
, urate transporter 1