| Literature DB >> 20544513 |
M Hosoyamada1, Y Takiue, H Morisaki, J Cheng, M Ikawa, M Okabe, T Morisaki, K Ichida, T Hosoya, T Shibasaki.
Abstract
In order to elucidate the mechanisms of post-exercise acute renal failure, one of the complications of hereditary renal hypouricemia, we have targeted the mouse Slc22a12 gene by the exchange of exons 1-4 with pMC1neo-polyA. The knockout mice revealed no gross anomalies. The concentration ratio of urinary urate/creatinine of the knockout mice was significantly higher than that of wildtype mice, indicating an attenuated renal reabsorption of urate. The plasma levels of urate were around 11 muM and were similar among the genotypes. 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.Entities:
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Year: 2010 PMID： 20544513 DOI： 10.1080/15257771003738634
Source DB: PubMed Journal: Nucleosides Nucleotides Nucleic Acids ISSN： 1525-7770 Impact factor: 1.381