anti-Solute Carrier Family 22 (Organic Cation Transporter), Member 11 (SLC22A11) Antibodies

Human Solute Carrier Family 22 (Organic Cation Transporter), Member 11 (SLC22A11) interaction partners

1. 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.

2. modifies placental passage of perfluorinated alkyl acids, may decrease fetal exposure

3. The regulation of hOAT4 activity was mediated by sgk2 acting through Nedd4-2.

4. 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.

5. A common variant of OAT4/SLC22A11 is associated with renal underexcretion type gout in Japanese men.

6. 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.

7. 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.

8. Genetic variants of human organic anion transporter 4 demonstrate altered transport of endogenous substrates.

9. 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.

10. Several naturally occurring SNPs encode variant hOAT4s that may impair the renal tubular re-absorption of important drug substrates.

11. elucidation of the molecular mechanism for renal tetracycline transport by human organic anion transporters (hOATs) using proximal tubular cells stably expressing hOATs

12. Glycosylation serves as a means to specifically regulate hOAT4 function in vivo.

13. hOAT4 is the long-postulated, low-affinity apical urate anion exchanger that facilitates hydrochlorothiazide-associated hyperuricemia.

14. 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.

15. 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.

16. 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.