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The first genome-wide association study for serum uric acid level in Indians revealed association of SLC2A9, SLC22A11 and ABCG2 gene variants at genome wide significance level in Type 2 diabetes patients.
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modifies placental passage of perfluorinated alkyl acids, may decrease fetal exposure
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The regulation of hOAT4 activity was mediated by sgk2 acting through Nedd4-2.
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SLC22A11 at the basal plasma membrane of human placental syncytiotrophoblasts plays a predominant role in the uptake of 16alpha-OH DHEAS for placental estriol synthesis.
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A common variant of OAT4/SLC22A11 is associated with renal underexcretion type gout in Japanese men.
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Our analysis provides evidence for multiple ancestral-specific effects across the SLC22A11/SLC22A12 locus that presumably influence the activity of OAT4 and URAT1 and risk of gout.
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When investigating the genes separately, SLC22A11 and SLC2A9 showed a significant interaction, consistent with the former encoding an organic anion/dicarboxylate exchanger, which mediates diuretic transport in the kidney.
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Genetic variants of human organic anion transporter 4 demonstrate altered transport of endogenous substrates.
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The down-regulation of hOAT4 activity by activation of protein kinase C and the up-regulation of hOAT4 activity by NHERF-1 are mediated through alteration of hOAT4 internalization.
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Several naturally occurring SNPs encode variant hOAT4s that may impair the renal tubular re-absorption of important drug substrates.
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elucidation of the molecular mechanism for renal tetracycline transport by human organic anion transporters (hOATs) using proximal tubular cells stably expressing hOATs
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Glycosylation serves as a means to specifically regulate hOAT4 function in vivo.
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hOAT4 is the long-postulated, low-affinity apical urate anion exchanger that facilitates hydrochlorothiazide-associated hyperuricemia.
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The interaction of PDZ proteins with hOAT4 may be cell-specific. In placenta, a different set of interacting proteins from PDZK1 and NHERF1 may be required to modulate hOAT4 activity.
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The present study demonstrates that hOAT4 variants can causing inter-individual variation in anionic drug uptake and, therefore, could be used as markers for certain diseases including osteoporosis.
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Findings suggest that hOAT4 and caveolin-1 share a cellular expression in the plasma membrane and caveolin-1 up-regulates the organic anionic compound uptake by hOAT4 under the normal physiological condition.
