PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
20613716-3	2010	Follow-up meta-analyses, including one with data from 28,141 individuals, implicated a total of nine additional loci influencing serum urate concentrations, including six other membrane transporters (SLC17A1, SLC17A3, SLC22A11, SLC22A12, SLC16A9, and ABCG2).	Uric Acid	135-140	solute carrier family 22 member 11	Homo sapiens	218-226
18609448-3	2008	The renal apical transport transport of zonampanel was examined in this study using HEK293 cells expressing human organic anion transporter 4 (OAT4/SLC22A11), and membrane vesicles prepared from Sf-9 insect cells expressing human multidrug resistance-associated protein 2 (MRP2/ABCC2), MRP4 (ABCC4), and breast cancer resistance protein (BCRP/ABCG2).	YM 872	40-50	solute carrier family 22 member 11	Homo sapiens	114-141
20360303-8	2010	Second, EE2-Sul uptake was also significantly higher in OAT4/HEK-293 cells and was inhibited by BSP, methotrexate, and probenecid.	ee2-sul	8-15	solute carrier family 22 member 11	Homo sapiens	56-60
20360303-8	2010	Second, EE2-Sul uptake was also significantly higher in OAT4/HEK-293 cells and was inhibited by BSP, methotrexate, and probenecid.	Methotrexate	101-113	solute carrier family 22 member 11	Homo sapiens	56-60
20360303-8	2010	Second, EE2-Sul uptake was also significantly higher in OAT4/HEK-293 cells and was inhibited by BSP, methotrexate, and probenecid.	Probenecid	119-129	solute carrier family 22 member 11	Homo sapiens	56-60
20140636-4	2010	METHODS: COS-7 cells expressing hOAT4 were treated with PKC activator phorbol 12-myristate 13-acetate (PMA) or transfected with dominant negative mutants of dynamin-2 or Eps15 or transfected with NHERF-1.	Tetradecanoylphorbol Acetate	70-101	solute carrier family 22 member 11	Homo sapiens	32-37
20140636-4	2010	METHODS: COS-7 cells expressing hOAT4 were treated with PKC activator phorbol 12-myristate 13-acetate (PMA) or transfected with dominant negative mutants of dynamin-2 or Eps15 or transfected with NHERF-1.	Tetradecanoylphorbol Acetate	103-106	solute carrier family 22 member 11	Homo sapiens	32-37
19371258-0	2009	Human organic anion transporter hOAT4 is a transporter of perfluorooctanoic acid.	perfluorooctanoic acid	58-80	solute carrier family 22 member 11	Homo sapiens	32-37
19282394-4	2009	In the current study, we characterized the inhibitory effects of novobiocin on the function of human OATs (hOAT)1, hOAT3, and hOAT4.	Novobiocin	65-75	solute carrier family 22 member 11	Homo sapiens	126-131
19282394-5	2009	Kinetic study revealed that novobiocin inhibited OAT-mediated uptake in a competitive manner, with K(i) of 14.87 +/- 0.40 microM for hOAT1, K(i) of 4.77 +/- 1.12 microM for hOAT3, and K(i) of 90.50 +/- 7.50 microM for hOAT4.	Novobiocin	28-38	solute carrier family 22 member 11	Homo sapiens	218-223
20015291-3	2010	In the present study, the impact of 10 nonsynonymous single nucleotide polymorphisms (SNPs) of hOAT4 on transport function in COS-7 cells was characterized.	carbonyl sulfide	126-129	solute carrier family 22 member 11	Homo sapiens	95-100
19643159-6	2009	Aristolochic acid I (AAI), the more cytotoxic and genotoxic AA congener, exhibited high affinity for hOAT1 (K(i)=0.6 microM) as well as hOAT3 (K(i)=0.5 microM), and lower affinity for hOAT4 (K(i)=20.6 microM).	aristolochic acid I	0-19	solute carrier family 22 member 11	Homo sapiens	184-189
19643159-6	2009	Aristolochic acid I (AAI), the more cytotoxic and genotoxic AA congener, exhibited high affinity for hOAT1 (K(i)=0.6 microM) as well as hOAT3 (K(i)=0.5 microM), and lower affinity for hOAT4 (K(i)=20.6 microM).	aristolochic acid I	21-24	solute carrier family 22 member 11	Homo sapiens	184-189
18985008-9	2008	When synthesized cRNA of hOAT4 along with scrambled- or antisense-oligodeoxynucleotide (ODN) of Xenopus caveolin-1 were co-injected to Xenopus oocytes, the [3H]estrone sulfate uptake was significantly decreased by the co-injection of antisense ODN but not by scrambled ODN.	Tritium	157-159	solute carrier family 22 member 11	Homo sapiens	25-30
18985008-9	2008	When synthesized cRNA of hOAT4 along with scrambled- or antisense-oligodeoxynucleotide (ODN) of Xenopus caveolin-1 were co-injected to Xenopus oocytes, the [3H]estrone sulfate uptake was significantly decreased by the co-injection of antisense ODN but not by scrambled ODN.	estrone sulfate	160-175	solute carrier family 22 member 11	Homo sapiens	25-30
18985008-9	2008	When synthesized cRNA of hOAT4 along with scrambled- or antisense-oligodeoxynucleotide (ODN) of Xenopus caveolin-1 were co-injected to Xenopus oocytes, the [3H]estrone sulfate uptake was significantly decreased by the co-injection of antisense ODN but not by scrambled ODN.	odn	244-247	solute carrier family 22 member 11	Homo sapiens	25-30
18985008-9	2008	When synthesized cRNA of hOAT4 along with scrambled- or antisense-oligodeoxynucleotide (ODN) of Xenopus caveolin-1 were co-injected to Xenopus oocytes, the [3H]estrone sulfate uptake was significantly decreased by the co-injection of antisense ODN but not by scrambled ODN.	odn	244-247	solute carrier family 22 member 11	Homo sapiens	25-30
18365245-0	2008	Organic anion transporters OAT1 and OAT4 mediate the high affinity transport of glutarate derivatives accumulating in patients with glutaric acidurias.	Glutarates	80-89	solute carrier family 22 member 11	Homo sapiens	36-40
18365245-0	2008	Organic anion transporters OAT1 and OAT4 mediate the high affinity transport of glutarate derivatives accumulating in patients with glutaric acidurias.	glutaric acidurias	132-150	solute carrier family 22 member 11	Homo sapiens	36-40
18365245-6	2008	In hOAT4-expressing cells and oocytes, ES uptake was strongly increased by intracellular GA derivatives.	Einsteinium	39-41	solute carrier family 22 member 11	Homo sapiens	3-8
18365245-6	2008	In hOAT4-expressing cells and oocytes, ES uptake was strongly increased by intracellular GA derivatives.	Glutarates	89-91	solute carrier family 22 member 11	Homo sapiens	3-8
18365245-7	2008	The data provide a model for the concerted action of OAT1 and NaDC3 mediating the basolateral uptake, and OAT4 mediating apical secretion of GA derivatives from proximal tubule cells and therefore contribute to the renal clearance of these compounds.	Glutarates	141-143	solute carrier family 22 member 11	Homo sapiens	106-110
18609448-3	2008	The renal apical transport transport of zonampanel was examined in this study using HEK293 cells expressing human organic anion transporter 4 (OAT4/SLC22A11), and membrane vesicles prepared from Sf-9 insect cells expressing human multidrug resistance-associated protein 2 (MRP2/ABCC2), MRP4 (ABCC4), and breast cancer resistance protein (BCRP/ABCG2).	YM 872	40-50	solute carrier family 22 member 11	Homo sapiens	143-147
18609448-3	2008	The renal apical transport transport of zonampanel was examined in this study using HEK293 cells expressing human organic anion transporter 4 (OAT4/SLC22A11), and membrane vesicles prepared from Sf-9 insect cells expressing human multidrug resistance-associated protein 2 (MRP2/ABCC2), MRP4 (ABCC4), and breast cancer resistance protein (BCRP/ABCG2).	YM 872	40-50	solute carrier family 22 member 11	Homo sapiens	148-156
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	glutaric acid	0-13	solute carrier family 22 member 11	Homo sapiens	90-94
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	glutaric acid	0-13	solute carrier family 22 member 11	Homo sapiens	142-146
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	malonic acid	23-36	solute carrier family 22 member 11	Homo sapiens	90-94
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	[(14)c]zonampanel	69-86	solute carrier family 22 member 11	Homo sapiens	90-94
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	[(14)c]zonampanel	69-86	solute carrier family 22 member 11	Homo sapiens	142-146
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	YM 872	76-86	solute carrier family 22 member 11	Homo sapiens	90-94
18609448-5	2008	Glutaric acid, a model dicarboxylate, trans-stimulated the uptake of [(14)C]zonampanel by OAT4, suggesting that zonampanel was transported by OAT4 via an exchange with dicarboxylate.	YM 872	76-86	solute carrier family 22 member 11	Homo sapiens	142-146
18609448-6	2008	Considering the endogenous dicarboxylate gradient, OAT4 seems to transport zonampanel in the direction of reabsorption rather than secretion.	malonic acid	27-40	solute carrier family 22 member 11	Homo sapiens	51-55
18609448-6	2008	Considering the endogenous dicarboxylate gradient, OAT4 seems to transport zonampanel in the direction of reabsorption rather than secretion.	YM 872	75-85	solute carrier family 22 member 11	Homo sapiens	51-55
18609448-10	2008	In conclusion, the data indicate that MRP4 was the apical efflux transporter that contributed to the active renal tubular secretion of zonampanel in humans, in concert with the apical reabsorption transporter OAT4 and basolateral uptake transporters.	YM 872	135-145	solute carrier family 22 member 11	Homo sapiens	209-213
18414001-4	2008	Among OATs, hOAT4 mediates high affinity transport of estrone sulfate and dehydroepiandrosterone sulfate.	estrone sulfate	54-69	solute carrier family 22 member 11	Homo sapiens	12-17
18501590-0	2008	Functional differences in steroid sulfate uptake of organic anion transporter 4 (OAT4) and organic anion transporting polypeptide 2B1 (OATP2B1) in human placenta.	steroid sulfate	26-41	solute carrier family 22 member 11	Homo sapiens	52-79
18501590-0	2008	Functional differences in steroid sulfate uptake of organic anion transporter 4 (OAT4) and organic anion transporting polypeptide 2B1 (OATP2B1) in human placenta.	steroid sulfate	26-41	solute carrier family 22 member 11	Homo sapiens	81-85
18414001-4	2008	Among OATs, hOAT4 mediates high affinity transport of estrone sulfate and dehydroepiandrosterone sulfate.	Dehydroepiandrosterone Sulfate	74-104	solute carrier family 22 member 11	Homo sapiens	12-17
18414001-11	2008	Uptake of [3H] estrone sulfate by oocytes injected with the hOAT4 E278K mutant was reduced compared with wild-type hOAT4.	[3h] estrone sulfate	10-30	solute carrier family 22 member 11	Homo sapiens	60-65
18414001-11	2008	Uptake of [3H] estrone sulfate by oocytes injected with the hOAT4 E278K mutant was reduced compared with wild-type hOAT4.	[3h] estrone sulfate	10-30	solute carrier family 22 member 11	Homo sapiens	115-120
17229912-5	2007	PAH and glutarate are not taken up by HEK293-hOAT4 cells, but they trans-stimulated 6-CF and [(3)H]ES uptake, indicating an asymmetric interaction of hOAT4 with these substrates.	Einsteinium	99-101	solute carrier family 22 member 11	Homo sapiens	150-155
17674156-3	2008	RESULTS: All ARBs inhibited uptake of uric acid or estrone-3-sulfate by OAT1, OAT3 and OAT4 in concentration dependent manners.	Uric Acid	38-47	solute carrier family 22 member 11	Homo sapiens	87-91
17674156-3	2008	RESULTS: All ARBs inhibited uptake of uric acid or estrone-3-sulfate by OAT1, OAT3 and OAT4 in concentration dependent manners.	estrone sulfate	51-68	solute carrier family 22 member 11	Homo sapiens	87-91
17674156-7	2008	No ARBs showed trans-stimulatory effects on the uptake of estrone-3-sulfate by OAT4.	estrone sulfate	58-75	solute carrier family 22 member 11	Homo sapiens	79-83
17602283-3	2008	The interaction of PDZK1 and NHERF1 with hOAT4 and hOAT4-Delta was investigated by measurement of [3H] estrone sulfate uptake, cell surface and total cell expression of hOAT4.	Tritium	99-101	solute carrier family 22 member 11	Homo sapiens	41-46
17602283-3	2008	The interaction of PDZK1 and NHERF1 with hOAT4 and hOAT4-Delta was investigated by measurement of [3H] estrone sulfate uptake, cell surface and total cell expression of hOAT4.	estrone sulfate	103-118	solute carrier family 22 member 11	Homo sapiens	41-46
17455113-3	2007	hOAT3 and hOAT4 transported pravastatin in a saturatable manner with Michaelis--Menten constants of 27.7 microM and 257 microM respectively.	Pravastatin	28-39	solute carrier family 22 member 11	Homo sapiens	10-15
17229912-5	2007	PAH and glutarate are not taken up by HEK293-hOAT4 cells, but they trans-stimulated 6-CF and [(3)H]ES uptake, indicating an asymmetric interaction of hOAT4 with these substrates.	p-Aminohippuric Acid	0-3	solute carrier family 22 member 11	Homo sapiens	150-155
17229912-5	2007	PAH and glutarate are not taken up by HEK293-hOAT4 cells, but they trans-stimulated 6-CF and [(3)H]ES uptake, indicating an asymmetric interaction of hOAT4 with these substrates.	Glutarates	8-17	solute carrier family 22 member 11	Homo sapiens	150-155
18409511-5	2008	Recently it has been shown that the proximal tubule apical membrane organic anion transporter OAT4 transports urate at low affinity and responsible for the hyperuricemia cased by thiazide diuretics.	Uric Acid	110-115	solute carrier family 22 member 11	Homo sapiens	94-98
17341544-3	2007	In the current study, we examined the regulation of hOAT4 by pregnancy-specific hormones progesterone (P(4)) and 17beta-estradiol (E(2)) and by protein kinase C (PKC) in human placental BeWo cells.	Progesterone	89-101	solute carrier family 22 member 11	Homo sapiens	52-57
17341544-3	2007	In the current study, we examined the regulation of hOAT4 by pregnancy-specific hormones progesterone (P(4)) and 17beta-estradiol (E(2)) and by protein kinase C (PKC) in human placental BeWo cells.	Estradiol	113-129	solute carrier family 22 member 11	Homo sapiens	52-57
17341544-6	2007	Activation of PKC by phorbol 12,13-dibutyrate also resulted in an inhibition of hOAT4 activity through a decreased cell surface expression of the transporter.	Phorbol 12,13-Dibutyrate	21-45	solute carrier family 22 member 11	Homo sapiens	80-85
17229912-6	2007	In chloride-free medium, HEK293-hOAT4-mediated [(3)H]PAH efflux was almost abolished, whereas addition of ES restored it comparable to Ringer solution, consistent with a physiologic ES/PAH or PAH/Cl(-) exchange mode of hOAT4.	Chlorides	3-11	solute carrier family 22 member 11	Homo sapiens	32-37
17229912-6	2007	In chloride-free medium, HEK293-hOAT4-mediated [(3)H]PAH efflux was almost abolished, whereas addition of ES restored it comparable to Ringer solution, consistent with a physiologic ES/PAH or PAH/Cl(-) exchange mode of hOAT4.	p-Aminohippuric Acid	53-56	solute carrier family 22 member 11	Homo sapiens	32-37
17229912-7	2007	Moreover, an acidification of the uptake medium increased 6-CF as well as [(3)H]ES uptake, which was reduced by nigericin, suggesting that hOAT4 also can operate as an OA/OH(-) exchanger.	Helium-3	74-82	solute carrier family 22 member 11	Homo sapiens	139-144
17229912-7	2007	Moreover, an acidification of the uptake medium increased 6-CF as well as [(3)H]ES uptake, which was reduced by nigericin, suggesting that hOAT4 also can operate as an OA/OH(-) exchanger.	Nigericin	112-121	solute carrier family 22 member 11	Homo sapiens	139-144
17229912-8	2007	hOAT4 facilitates substantial uptake of [(14)C]urate, which was elevated 2.6-fold by intracellular HCTZ.	c]urate	45-52	solute carrier family 22 member 11	Homo sapiens	0-5
17229912-8	2007	hOAT4 facilitates substantial uptake of [(14)C]urate, which was elevated 2.6-fold by intracellular HCTZ.	Hydrochlorothiazide	99-103	solute carrier family 22 member 11	Homo sapiens	0-5
17229912-9	2007	Thus, hOAT4 is the long-postulated, low-affinity apical urate anion exchanger that facilitates HCTZ-associated hyperuricemia.	Hydrochlorothiazide	95-99	solute carrier family 22 member 11	Homo sapiens	6-11
17132213-4	2006	The aim of this study was to examine the effects of various drugs on the OAT4-mediated transport of estrone-3-sulfate, a typical substrate of OAT4, by using human embryonic kidney cells stably transfected with OAT4 (HEK-OAT4).	estrone sulfate	100-117	solute carrier family 22 member 11	Homo sapiens	73-77
17132213-4	2006	The aim of this study was to examine the effects of various drugs on the OAT4-mediated transport of estrone-3-sulfate, a typical substrate of OAT4, by using human embryonic kidney cells stably transfected with OAT4 (HEK-OAT4).	estrone sulfate	100-117	solute carrier family 22 member 11	Homo sapiens	142-146
17132213-4	2006	The aim of this study was to examine the effects of various drugs on the OAT4-mediated transport of estrone-3-sulfate, a typical substrate of OAT4, by using human embryonic kidney cells stably transfected with OAT4 (HEK-OAT4).	estrone sulfate	100-117	solute carrier family 22 member 11	Homo sapiens	142-146
17132213-4	2006	The aim of this study was to examine the effects of various drugs on the OAT4-mediated transport of estrone-3-sulfate, a typical substrate of OAT4, by using human embryonic kidney cells stably transfected with OAT4 (HEK-OAT4).	estrone sulfate	100-117	solute carrier family 22 member 11	Homo sapiens	216-224
17132213-5	2006	HEK-OAT4 cells exhibited concentration-dependent uptake of estrone-3-sulfate, with a K(m) value of 20.9+/-3.53 microM.	estrone sulfate	59-76	solute carrier family 22 member 11	Homo sapiens	4-8
17132213-7	2006	We also searched for the potential inhibitors of OAT4 and identified candesartan, candesartan cilexetil, losartan, losartan carboxyl (EXP3174) and valsartan as inhibitors of OAT4, with K(i) values of 88.9, 135.2, 24.8, 13.8 and 19.6 microM, respectively.	candesartan	69-80	solute carrier family 22 member 11	Homo sapiens	174-178
17132213-7	2006	We also searched for the potential inhibitors of OAT4 and identified candesartan, candesartan cilexetil, losartan, losartan carboxyl (EXP3174) and valsartan as inhibitors of OAT4, with K(i) values of 88.9, 135.2, 24.8, 13.8 and 19.6 microM, respectively.	candesartan cilexetil	82-103	solute carrier family 22 member 11	Homo sapiens	174-178
17132213-7	2006	We also searched for the potential inhibitors of OAT4 and identified candesartan, candesartan cilexetil, losartan, losartan carboxyl (EXP3174) and valsartan as inhibitors of OAT4, with K(i) values of 88.9, 135.2, 24.8, 13.8 and 19.6 microM, respectively.	losartan carboxyl	115-132	solute carrier family 22 member 11	Homo sapiens	174-178
17132213-7	2006	We also searched for the potential inhibitors of OAT4 and identified candesartan, candesartan cilexetil, losartan, losartan carboxyl (EXP3174) and valsartan as inhibitors of OAT4, with K(i) values of 88.9, 135.2, 24.8, 13.8 and 19.6 microM, respectively.	Valsartan	147-156	solute carrier family 22 member 11	Homo sapiens	174-178
17132213-9	2006	Although pranlukast is devoid of anionic motifs other than the tetrazole group, it potently inhibited the OAT4-mediated uptake of estrone-3-sulfate, indicating that a tetrazole group may be one important structural feature in substrate recognition by OAT4.	pranlukast	9-19	solute carrier family 22 member 11	Homo sapiens	106-110
17132213-9	2006	Although pranlukast is devoid of anionic motifs other than the tetrazole group, it potently inhibited the OAT4-mediated uptake of estrone-3-sulfate, indicating that a tetrazole group may be one important structural feature in substrate recognition by OAT4.	pranlukast	9-19	solute carrier family 22 member 11	Homo sapiens	251-255
17132213-9	2006	Although pranlukast is devoid of anionic motifs other than the tetrazole group, it potently inhibited the OAT4-mediated uptake of estrone-3-sulfate, indicating that a tetrazole group may be one important structural feature in substrate recognition by OAT4.	estrone sulfate	130-147	solute carrier family 22 member 11	Homo sapiens	106-110
17132213-9	2006	Although pranlukast is devoid of anionic motifs other than the tetrazole group, it potently inhibited the OAT4-mediated uptake of estrone-3-sulfate, indicating that a tetrazole group may be one important structural feature in substrate recognition by OAT4.	estrone sulfate	130-147	solute carrier family 22 member 11	Homo sapiens	251-255
17132213-9	2006	Although pranlukast is devoid of anionic motifs other than the tetrazole group, it potently inhibited the OAT4-mediated uptake of estrone-3-sulfate, indicating that a tetrazole group may be one important structural feature in substrate recognition by OAT4.	1H-tetrazole	167-176	solute carrier family 22 member 11	Homo sapiens	106-110
15864504-5	2005	When human OAT3 (hOAT3) and hOAT4 were expressed in Xenopus laevis oocytes, only hOAT3 showed [3H]cortisol uptake in excess of that of water-injected control oocytes.	Hydrocortisone	98-106	solute carrier family 22 member 11	Homo sapiens	28-33
16934049-4	2006	RESULTS: In stably transfected HEK293 cells torsemide (100 microm) inhibited the uptake by human OAT1, OAT3 and OAT4 by 63.1, 58.1 and 68.0%, respectively.	Torsemide	44-53	solute carrier family 22 member 11	Homo sapiens	112-116
16934049-7	2006	AA carriers of the polymorphism rs11231809 in SLC22A11 had a torsemide renal clearance of 13.3 ml min(-1) (12.7-13.9) compared with 15.1 ml min(-1) (14.5-15.8) in AT and 18.0 ml min(-1) (16.7-19.5) in TT carriers (P = 0.002).	Torsemide	61-70	solute carrier family 22 member 11	Homo sapiens	46-54
16934049-8	2006	The two most frequent haplotypes at SLC22A11 showed an association with torsemide renal clearance.	Torsemide	72-81	solute carrier family 22 member 11	Homo sapiens	36-44
16934049-11	2006	CONCLUSIONS: Genetic variation in the gene encoding the luminally expressed OAT4 rather than in the basolaterally expressed OATs may affect the renal clearance of torsemide.	Torsemide	163-172	solute carrier family 22 member 11	Homo sapiens	76-80
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	p-Aminohippuric Acid	253-256	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-4	2006	hOAT4-mediated uptake of estrone sulfate, a protypical organic anion for hOAT4, was dose- and time-dependent, and saturable (Km=4.2 microM).	estrone sulfate	25-40	solute carrier family 22 member 11	Homo sapiens	0-5
16257192-4	2006	hOAT4-mediated uptake of estrone sulfate, a protypical organic anion for hOAT4, was dose- and time-dependent, and saturable (Km=4.2 microM).	estrone sulfate	25-40	solute carrier family 22 member 11	Homo sapiens	73-78
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	steroid sulfates	52-68	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	beta-estradiol-3,17-disulfate	78-107	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	estradiol-3-sulfate	109-136	solute carrier family 22 member 11	Homo sapiens	29-34
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	steroid sulfates	162-178	solute carrier family 22 member 11	Homo sapiens	6-33
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	steroid sulfates	162-178	solute carrier family 22 member 11	Homo sapiens	35-39
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	estrone sulfate	187-204	solute carrier family 22 member 11	Homo sapiens	6-33
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	estrone sulfate	187-204	solute carrier family 22 member 11	Homo sapiens	35-39
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	Estrone	206-209	solute carrier family 22 member 11	Homo sapiens	6-33
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	Estrone	206-209	solute carrier family 22 member 11	Homo sapiens	35-39
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	Dehydroepiandrosterone Sulfate	215-245	solute carrier family 22 member 11	Homo sapiens	6-33
16236806-1	2005	Human organic anion transporter 4 (OAT4) is an apical organic anion/dicarboxylate exchanger in the renal proximal tubules and mediates high-affinity transport of steroid sulfates such as estrone-3-sulfate (E1S) and dehydroepiandrosterone sulfate.	Dehydroepiandrosterone Sulfate	215-245	solute carrier family 22 member 11	Homo sapiens	35-39
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	beta-estradiol 3-sulfate	112-136	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	Dehydroepiandrosterone Sulfate	168-200	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	Dehydroepiandrosterone Sulfate	202-207	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	p-Aminohippuric Acid	231-251	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	Tetraethylammonium	262-280	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-5	2006	The substrate specificity of hOAT4 includes various steroid sulfates, such as beta-estradiol-3,17-disulfate, 17-beta-estradiol-3-sulfate, beta-estradiol-3-sulfate, and dehydroepiandrosterone-3-sulfate (DHEAS), but does not include p-aminohippuric acid (PAH) and tetraethylammonium (TEA).	Tetraethylammonium	282-285	solute carrier family 22 member 11	Homo sapiens	29-34
16257192-6	2006	Pre-incubation of hOAT4-expressing BeWo cells with phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), both of which are protein kinase C (PKC) activators, acutely inhibited the transport activity.	Tetradecanoylphorbol Acetate	51-82	solute carrier family 22 member 11	Homo sapiens	18-23
16257192-6	2006	Pre-incubation of hOAT4-expressing BeWo cells with phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), both of which are protein kinase C (PKC) activators, acutely inhibited the transport activity.	Tetradecanoylphorbol Acetate	84-87	solute carrier family 22 member 11	Homo sapiens	18-23
16257192-6	2006	Pre-incubation of hOAT4-expressing BeWo cells with phorbol 12-myristate 13-acetate (PMA) and phorbol 12,13-dibutyrate (PDBu), both of which are protein kinase C (PKC) activators, acutely inhibited the transport activity.	Phorbol 12,13-Dibutyrate	93-117	solute carrier family 22 member 11	Homo sapiens	18-23
15870380-4	2005	Oocytes expressing human (h)OAT1, rat (r)Oat1, and hOAT4 accumulated 6.5-, 7.1-, and 8.9-fold more EA, respectively, than did water-injected oocytes.	Water	126-131	solute carrier family 22 member 11	Homo sapiens	51-56
15377641-3	2004	The purpose of this study is to elucidate the molecular mechanism of the renal excretion of zonampanel using cells stably expressing human organic anion transporters (hOAT) 1, hOAT2, hOAT3, and hOAT4, as well as human organic cation transporters (hOCT) 1 and hOCT2.	YM 872	92-102	solute carrier family 22 member 11	Homo sapiens	194-199
15291761-0	2004	Mutational analysis of histidine residues in human organic anion transporter 4 (hOAT4).	Histidine	23-32	solute carrier family 22 member 11	Homo sapiens	51-78
15291761-0	2004	Mutational analysis of histidine residues in human organic anion transporter 4 (hOAT4).	Histidine	23-32	solute carrier family 22 member 11	Homo sapiens	80-85
15291761-2	2004	hOAT4-mediated transport of the organic anion oestrone sulphate in COS-7 cells was inhibited by the histidine-modifying reagent DEPC (diethyl pyrocarbonate).	estrone sulfate	46-63	solute carrier family 22 member 11	Homo sapiens	0-5
15291761-2	2004	hOAT4-mediated transport of the organic anion oestrone sulphate in COS-7 cells was inhibited by the histidine-modifying reagent DEPC (diethyl pyrocarbonate).	carbonyl sulfide	67-70	solute carrier family 22 member 11	Homo sapiens	0-5
15291761-2	2004	hOAT4-mediated transport of the organic anion oestrone sulphate in COS-7 cells was inhibited by the histidine-modifying reagent DEPC (diethyl pyrocarbonate).	Histidine	100-109	solute carrier family 22 member 11	Homo sapiens	0-5
15291761-2	2004	hOAT4-mediated transport of the organic anion oestrone sulphate in COS-7 cells was inhibited by the histidine-modifying reagent DEPC (diethyl pyrocarbonate).	Diethyl Pyrocarbonate	128-132	solute carrier family 22 member 11	Homo sapiens	0-5
15291761-2	2004	hOAT4-mediated transport of the organic anion oestrone sulphate in COS-7 cells was inhibited by the histidine-modifying reagent DEPC (diethyl pyrocarbonate).	Diethyl Pyrocarbonate	134-155	solute carrier family 22 member 11	Homo sapiens	0-5
15291761-3	2004	Therefore the role of histidine residues in the function of hOAT4 was examined by site-directed mutagenesis.	Histidine	22-31	solute carrier family 22 member 11	Homo sapiens	60-65
15291761-4	2004	All five histidine residues of hOAT4 were converted into alanine, singly or in combination.	Histidine	9-18	solute carrier family 22 member 11	Homo sapiens	31-36
15291761-4	2004	All five histidine residues of hOAT4 were converted into alanine, singly or in combination.	Alanine	57-64	solute carrier family 22 member 11	Homo sapiens	31-36
15291761-8	2004	We also showed that, although most of the histidine mutants of hOAT4 were sensitive to inhibition by DEPC, H469A (His-469-->Ala) was completely insensitive to inhibition by this reagent.	Histidine	42-51	solute carrier family 22 member 11	Homo sapiens	63-68
15291761-9	2004	Therefore modification of His-469 is responsible for the inhibition of hOAT4 by DEPC.	Histidine	26-29	solute carrier family 22 member 11	Homo sapiens	71-76
15576633-0	2005	The role of N-linked glycosylation in protein folding, membrane targeting, and substrate binding of human organic anion transporter hOAT4.	Nitrogen	12-13	solute carrier family 22 member 11	Homo sapiens	132-137
15576633-1	2005	We used a novel approach to evaluate how the addition/acquisition and processing/modification of N-linked oligosaccharides play a role in the functional maturation of human organic anion transporter hOAT4.	n-linked oligosaccharides	97-122	solute carrier family 22 member 11	Homo sapiens	199-204
15576633-2	2005	Inhibition of acquisition of oligosaccharides in hOAT4 by mutating asparagine to glutamine and by tunicamycin treatment was combined with the expression of wild-type hOAT4 in a series of mutant Chinese hamster ovary (CHO)-Lec cells defective in the different steps of glycosylation processing.	Oligosaccharides	29-45	solute carrier family 22 member 11	Homo sapiens	49-54
15576633-3	2005	We showed that both the disruption of the glycosylation sites by mutagenesis and the inhibition of glycosylation by tunicamycin treatment resulted in a nonglycosylated hOAT4, which was unable to target to the cell surface.	Tunicamycin	116-127	solute carrier family 22 member 11	Homo sapiens	168-173
15576633-4	2005	In contrast, hOAT4 synthesized in mutant CHO-Lec cells, carrying different structural forms of sugar moieties (mannose-rich in Lec1 cells, sialic acid-deficient in Lec2 cells, and sialic acid/galactose-deficient in Lec8 cells) were able to traffic to the cell surface.	Sugars	95-100	solute carrier family 22 member 11	Homo sapiens	13-18
15576633-4	2005	In contrast, hOAT4 synthesized in mutant CHO-Lec cells, carrying different structural forms of sugar moieties (mannose-rich in Lec1 cells, sialic acid-deficient in Lec2 cells, and sialic acid/galactose-deficient in Lec8 cells) were able to traffic to the cell surface.	Mannose	111-118	solute carrier family 22 member 11	Homo sapiens	13-18
15576633-4	2005	In contrast, hOAT4 synthesized in mutant CHO-Lec cells, carrying different structural forms of sugar moieties (mannose-rich in Lec1 cells, sialic acid-deficient in Lec2 cells, and sialic acid/galactose-deficient in Lec8 cells) were able to traffic to the cell surface.	N-Acetylneuraminic Acid	139-150	solute carrier family 22 member 11	Homo sapiens	13-18
15576633-4	2005	In contrast, hOAT4 synthesized in mutant CHO-Lec cells, carrying different structural forms of sugar moieties (mannose-rich in Lec1 cells, sialic acid-deficient in Lec2 cells, and sialic acid/galactose-deficient in Lec8 cells) were able to traffic to the cell surface.	N-Acetylneuraminic Acid	180-191	solute carrier family 22 member 11	Homo sapiens	13-18
15576633-6	2005	This study provided novel information that addition/acquisition of oligosaccharides but not the processing of the added oligosaccharides participates in the membrane insertion of hOAT4.	Oligosaccharides	67-83	solute carrier family 22 member 11	Homo sapiens	179-184
15576633-7	2005	Processing of added oligosaccharides from mannose-rich type to complex type is important for enhancing the binding affinity of hOAT4 for its substrates.	Oligosaccharides	20-36	solute carrier family 22 member 11	Homo sapiens	127-132
15576633-7	2005	Processing of added oligosaccharides from mannose-rich type to complex type is important for enhancing the binding affinity of hOAT4 for its substrates.	Mannose	42-49	solute carrier family 22 member 11	Homo sapiens	127-132
15377641-5	2004	Zonampanel inhibited the uptake of prototypical organic anion substrates, [14C]para-aminohippurate in hOAT1 and [3H]estrone sulfate in hOAT3 and hOAT4, in a competitive manner.	YM 872	0-10	solute carrier family 22 member 11	Homo sapiens	145-150
15377641-5	2004	Zonampanel inhibited the uptake of prototypical organic anion substrates, [14C]para-aminohippurate in hOAT1 and [3H]estrone sulfate in hOAT3 and hOAT4, in a competitive manner.	estrone sulfate	116-131	solute carrier family 22 member 11	Homo sapiens	145-150
15377641-6	2004	A time- and concentration-dependent increase in [14C]zonampanel uptake was observed in cells expressing hOAT1, hOAT3, and hOAT4.	Carbon-14	49-52	solute carrier family 22 member 11	Homo sapiens	122-127
15377641-6	2004	A time- and concentration-dependent increase in [14C]zonampanel uptake was observed in cells expressing hOAT1, hOAT3, and hOAT4.	YM 872	53-63	solute carrier family 22 member 11	Homo sapiens	122-127
15377641-7	2004	The Km values of zonampanel uptake by hOAT1, hOAT3, and hOAT4 were 1.4, 7.7, and 215 microM, respectively.	YM 872	17-27	solute carrier family 22 member 11	Homo sapiens	56-61
15377641-8	2004	Considering the localization of each transporter, results suggest that zonampanel is taken up via hOAT1 and hOAT3 from the blood into proximal tubular cells and then effluxed into the lumen via hOAT4.	YM 872	71-81	solute carrier family 22 member 11	Homo sapiens	194-199
15377641-9	2004	Probenecid and cimetidine competitively inhibited [14C]zonampanel uptake by the hOATs (hOAT1, hOAT3, and hOAT4 for probenecid; hOAT3 for cimetidine).	Probenecid	0-10	solute carrier family 22 member 11	Homo sapiens	105-110
15377641-9	2004	Probenecid and cimetidine competitively inhibited [14C]zonampanel uptake by the hOATs (hOAT1, hOAT3, and hOAT4 for probenecid; hOAT3 for cimetidine).	Cimetidine	15-25	solute carrier family 22 member 11	Homo sapiens	105-110
15377641-9	2004	Probenecid and cimetidine competitively inhibited [14C]zonampanel uptake by the hOATs (hOAT1, hOAT3, and hOAT4 for probenecid; hOAT3 for cimetidine).	14c]zonampanel	51-65	solute carrier family 22 member 11	Homo sapiens	105-110
15037815-1	2004	Human organic anion transporter OAT4 is expressed in the kidney and placenta and mediates high-affinity transport of estrone-3-sulfate (E1S).	estrone sulfate	117-134	solute carrier family 22 member 11	Homo sapiens	32-36
15102942-0	2004	The role of glycine residues in the function of human organic anion transporter 4.	Glycine	12-19	solute carrier family 22 member 11	Homo sapiens	54-81
15102942-2	2004	In this study, we investigated the role of conserved glycine residues in hOAT4 function.	Glycine	53-60	solute carrier family 22 member 11	Homo sapiens	73-78
14610216-6	2004	hOAT1, hOAT3, and hOAT4 but not hOAT2, mediated the uptake of bumetanide.	Bumetanide	62-72	solute carrier family 22 member 11	Homo sapiens	18-23
14610216-7	2004	hOAT3 and hOAT4, but not hOAT1 mediated the efflux of bumetanide.	Bumetanide	54-64	solute carrier family 22 member 11	Homo sapiens	10-15
14610216-10	2004	In addition, it was also suggested that bumetanide taken up by hOAT3 and/or hOAT1 is excreted into the urine by hOAT4.	Bumetanide	40-50	solute carrier family 22 member 11	Homo sapiens	112-117
15037815-1	2004	Human organic anion transporter OAT4 is expressed in the kidney and placenta and mediates high-affinity transport of estrone-3-sulfate (E1S).	Estrone	136-139	solute carrier family 22 member 11	Homo sapiens	32-36
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	42-51	solute carrier family 22 member 11	Homo sapiens	0-4
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	53-55	solute carrier family 22 member 11	Homo sapiens	0-4
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Carbon-14	77-80	solute carrier family 22 member 11	Homo sapiens	0-4
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Carbon-14	77-80	solute carrier family 22 member 11	Homo sapiens	98-102
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	81-83	solute carrier family 22 member 11	Homo sapiens	0-4
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	81-83	solute carrier family 22 member 11	Homo sapiens	98-102
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	81-83	solute carrier family 22 member 11	Homo sapiens	0-4
15037815-4	2004	OAT4-mediated E1S uptake was inhibited by glutarate (GA) (IC50:1.25 mM) and [14C]GA uptake via S2 OAT4 was significantly trans-stimulated by unlabeled GA (5 mM) (P<0.001).	Glutarates	81-83	solute carrier family 22 member 11	Homo sapiens	98-102
15037815-5	2004	[3H]E1S uptake via S2 OAT4 was significantly trans-stimulated by preloaded GA (P<0.001) and its [14C]GA efflux was significantly trans-stimulated by unlabeled E1S in the medium (P<0.05).	Tritium	1-3	solute carrier family 22 member 11	Homo sapiens	22-26
15037815-5	2004	[3H]E1S uptake via S2 OAT4 was significantly trans-stimulated by preloaded GA (P<0.001) and its [14C]GA efflux was significantly trans-stimulated by unlabeled E1S in the medium (P<0.05).	Estrone	4-7	solute carrier family 22 member 11	Homo sapiens	22-26
15037815-6	2004	In addition, both the uptake and efflux of [14C]p-aminohippuric acid (PAH) and [14C]GA via S2 OAT4 were significantly trans-stimulated by unlabeled GA or PAH.	[14c]p-aminohippuric acid	43-68	solute carrier family 22 member 11	Homo sapiens	94-98
15037815-6	2004	In addition, both the uptake and efflux of [14C]p-aminohippuric acid (PAH) and [14C]GA via S2 OAT4 were significantly trans-stimulated by unlabeled GA or PAH.	p-Aminohippuric Acid	70-73	solute carrier family 22 member 11	Homo sapiens	94-98
15037815-6	2004	In addition, both the uptake and efflux of [14C]p-aminohippuric acid (PAH) and [14C]GA via S2 OAT4 were significantly trans-stimulated by unlabeled GA or PAH.	p-Aminohippuric Acid	154-157	solute carrier family 22 member 11	Homo sapiens	94-98
15037815-8	2004	These results indicate that OAT4 is an apical organic anion/dicarboxylate exchanger and mainly functions as an apical pathway for the reabsorption of some organic anions in renal proximal tubules driven by an outwardly directed dicarboxylate gradient.	malonic acid	60-73	solute carrier family 22 member 11	Homo sapiens	28-32
12063169-0	2002	Role of human organic anion transporter 4 in the transport of ochratoxin A.	ochratoxin A	62-74	solute carrier family 22 member 11	Homo sapiens	14-41
12679137-3	2003	Indoxyl sulfate inhibited human-OAT1, human-OAT3 and human-OAT4, but not human-OAT2, human-OCT1 and human-OCT2.	Indican	0-15	solute carrier family 22 member 11	Homo sapiens	59-63
12679137-5	2003	Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate.	Indican	132-147	solute carrier family 22 member 11	Homo sapiens	75-79
12650826-8	2003	Cephaloridine significantly decreased the viability of cells stably expressing human-OAT2, human-OAT1, human-OAT3 and human-OAT4.	Cephaloridine	0-13	solute carrier family 22 member 11	Homo sapiens	124-128
12650826-9	2003	The decreased viability of cells stably expressing human-OAT1, human-OAT3 and human-OAT4 but not human-OAT2 was reversed by probenecid.	Probenecid	124-134	solute carrier family 22 member 11	Homo sapiens	84-88
12130730-5	2002	NSAIDs (salicylate, ibuprofen, ketoprofen, phenylbutazone, piroxicam, and indomethacin), probenecid, and penicillin G dose dependently inhibited methotrexate uptake mediated by hOAT1, hOAT3, and hOAT4.	Indomethacin	74-86	solute carrier family 22 member 11	Homo sapiens	195-200
12130730-5	2002	NSAIDs (salicylate, ibuprofen, ketoprofen, phenylbutazone, piroxicam, and indomethacin), probenecid, and penicillin G dose dependently inhibited methotrexate uptake mediated by hOAT1, hOAT3, and hOAT4.	Probenecid	89-99	solute carrier family 22 member 11	Homo sapiens	195-200
12130730-5	2002	NSAIDs (salicylate, ibuprofen, ketoprofen, phenylbutazone, piroxicam, and indomethacin), probenecid, and penicillin G dose dependently inhibited methotrexate uptake mediated by hOAT1, hOAT3, and hOAT4.	Penicillin G	105-117	solute carrier family 22 member 11	Homo sapiens	195-200
12130730-5	2002	NSAIDs (salicylate, ibuprofen, ketoprofen, phenylbutazone, piroxicam, and indomethacin), probenecid, and penicillin G dose dependently inhibited methotrexate uptake mediated by hOAT1, hOAT3, and hOAT4.	Methotrexate	145-157	solute carrier family 22 member 11	Homo sapiens	195-200
12130730-9	2002	In conclusion, these results suggest that methotrexate is taken up via hOAT3 and hOAT1 at the basolateral side of the proximal tubule and effluxed or taken up at the apical side via hOAT4.	Methotrexate	42-54	solute carrier family 22 member 11	Homo sapiens	182-187
12130730-10	2002	In addition, hOAT1, hOAT3, and hOAT4 are the sites of drug interactions between methotrexate and NSAIDs, probenecid, and penicillin G.	Methotrexate	80-92	solute carrier family 22 member 11	Homo sapiens	31-36
12130730-10	2002	In addition, hOAT1, hOAT3, and hOAT4 are the sites of drug interactions between methotrexate and NSAIDs, probenecid, and penicillin G.	Probenecid	105-115	solute carrier family 22 member 11	Homo sapiens	31-36
12130730-10	2002	In addition, hOAT1, hOAT3, and hOAT4 are the sites of drug interactions between methotrexate and NSAIDs, probenecid, and penicillin G.	Penicillin G	121-133	solute carrier family 22 member 11	Homo sapiens	31-36
14978359-2	2004	Pravastatin inhibited hOAT1/rOAT1, hOAT2/rOAT2, hOAT3/rOAT3, and hOAT4.	Pravastatin	0-11	solute carrier family 22 member 11	Homo sapiens	65-70
14978359-4	2004	Cimetidine also inhibited hOAT1/rOAT1, hOAT3/rOAT3, and hOAT4.	Cimetidine	0-10	solute carrier family 22 member 11	Homo sapiens	56-61
12409283-8	2003	Our results indicate that uptake of steroid sulfates by isolated MT is mediated by OATP-B and OAT-4 and suggest a physiological role of both carrier proteins in placental uptake of fetal-derived steroid sulfates.	steroid sulfates	36-52	solute carrier family 22 member 11	Homo sapiens	94-99
12388633-5	2002	HOAT1, hOAT2, hOAT3, and hOAT4 mediated the uptake of either ibuprofen, indomethacin, ketoprofen, or salicylate, but not acetylsalicylate.	Ibuprofen	61-70	solute carrier family 22 member 11	Homo sapiens	25-30
12388633-5	2002	HOAT1, hOAT2, hOAT3, and hOAT4 mediated the uptake of either ibuprofen, indomethacin, ketoprofen, or salicylate, but not acetylsalicylate.	Indomethacin	72-84	solute carrier family 22 member 11	Homo sapiens	25-30
12388633-5	2002	HOAT1, hOAT2, hOAT3, and hOAT4 mediated the uptake of either ibuprofen, indomethacin, ketoprofen, or salicylate, but not acetylsalicylate.	Ketoprofen	86-96	solute carrier family 22 member 11	Homo sapiens	25-30
12388633-5	2002	HOAT1, hOAT2, hOAT3, and hOAT4 mediated the uptake of either ibuprofen, indomethacin, ketoprofen, or salicylate, but not acetylsalicylate.	Salicylates	101-111	solute carrier family 22 member 11	Homo sapiens	25-30
12130730-4	2002	The K(m) values for hOAT1-, hOAT3-, and hOAT4-mediated methotrexate uptake were 553.8 microM, 21.1 microM, and 17.8 microM, respectively.	Methotrexate	55-67	solute carrier family 22 member 11	Homo sapiens	40-45
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Probenecid	0-10	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Piroxicam	12-21	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	octanoic acid	23-32	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Citrinin	37-45	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Probenecid	163-173	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Piroxicam	179-188	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	octanoic acid	194-203	solute carrier family 22 member 11	Homo sapiens	70-75
12063169-6	2002	Probenecid, piroxicam, octanoate and citrinin inhibited OTA uptake by hOAT4 in a competitive manner (K(i)=44.4-336.4 microM), with the following order of potency: probenecid > piroxicam > octanoate >citrinin.	Citrinin	208-216	solute carrier family 22 member 11	Homo sapiens	70-75
11909604-7	2002	The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4.	Ceftriaxone	66-77	solute carrier family 22 member 11	Homo sapiens	290-294
12023506-7	2002	In contrast, probenecid, KW-3902, and betamipron, but not cilastatin, inhibited hOAT4-mediated estrone sulfate (ES) uptake.	Probenecid	13-23	solute carrier family 22 member 11	Homo sapiens	80-85
12023506-7	2002	In contrast, probenecid, KW-3902, and betamipron, but not cilastatin, inhibited hOAT4-mediated estrone sulfate (ES) uptake.	rolofylline	25-32	solute carrier family 22 member 11	Homo sapiens	80-85
12023506-7	2002	In contrast, probenecid, KW-3902, and betamipron, but not cilastatin, inhibited hOAT4-mediated estrone sulfate (ES) uptake.	N-benzoylalanine	38-48	solute carrier family 22 member 11	Homo sapiens	80-85
12023506-7	2002	In contrast, probenecid, KW-3902, and betamipron, but not cilastatin, inhibited hOAT4-mediated estrone sulfate (ES) uptake.	estrone sulfate	95-110	solute carrier family 22 member 11	Homo sapiens	80-85
12023506-7	2002	In contrast, probenecid, KW-3902, and betamipron, but not cilastatin, inhibited hOAT4-mediated estrone sulfate (ES) uptake.	estrone sulfate	112-114	solute carrier family 22 member 11	Homo sapiens	80-85
12023506-9	2002	The K(i) value of probenecid for hOAT2 was 766 microM, whereas those of probenecid, KW-3902, and betamipron for hOAT4 were 54.9, 20.7, and 502 microM, respectively.	Probenecid	72-82	solute carrier family 22 member 11	Homo sapiens	112-117
12023506-9	2002	The K(i) value of probenecid for hOAT2 was 766 microM, whereas those of probenecid, KW-3902, and betamipron for hOAT4 were 54.9, 20.7, and 502 microM, respectively.	rolofylline	84-91	solute carrier family 22 member 11	Homo sapiens	112-117
12023506-9	2002	The K(i) value of probenecid for hOAT2 was 766 microM, whereas those of probenecid, KW-3902, and betamipron for hOAT4 were 54.9, 20.7, and 502 microM, respectively.	N-benzoylalanine	97-107	solute carrier family 22 member 11	Homo sapiens	112-117
12023506-10	2002	These results suggest that probenecid, KW-3902, and betamipron could inhibit hOAT4-mediated ES uptake in vitro, whereas probenecid alone could inhibit the hOAT2-mediated PGF(2alpha) uptake.	Probenecid	27-37	solute carrier family 22 member 11	Homo sapiens	77-82
12023506-10	2002	These results suggest that probenecid, KW-3902, and betamipron could inhibit hOAT4-mediated ES uptake in vitro, whereas probenecid alone could inhibit the hOAT2-mediated PGF(2alpha) uptake.	rolofylline	39-46	solute carrier family 22 member 11	Homo sapiens	77-82
12023506-10	2002	These results suggest that probenecid, KW-3902, and betamipron could inhibit hOAT4-mediated ES uptake in vitro, whereas probenecid alone could inhibit the hOAT2-mediated PGF(2alpha) uptake.	N-benzoylalanine	52-62	solute carrier family 22 member 11	Homo sapiens	77-82
12023506-10	2002	These results suggest that probenecid, KW-3902, and betamipron could inhibit hOAT4-mediated ES uptake in vitro, whereas probenecid alone could inhibit the hOAT2-mediated PGF(2alpha) uptake.	estrone sulfate	92-94	solute carrier family 22 member 11	Homo sapiens	77-82
12023506-11	2002	Comparing the K(i) values with the therapeutically relevant concentrations of unbound inhibitors in the plasma, probenecid alone was predicted to inhibit hOAT4-mediated organic anion transport in vivo.	Probenecid	112-122	solute carrier family 22 member 11	Homo sapiens	154-159
11907186-7	2002	In conclusion, considering the localization of these transporters, the results suggest that PGE(2) and PGF(2 alpha) transport in the basolateral membrane of the proximal tubule is mediated by multiple pathways including hOAT1, hOAT2, hOAT3, and hOCT2, whereas that in the apical side is mediated by hOAT4.	Prostaglandins F	103-106	solute carrier family 22 member 11	Homo sapiens	299-304
11909604-5	2002	All of these cephalosporin antibiotics significantly inhibited organic anion uptake mediated by human-OAT1, human-OAT3 and human-OAT4.	Cephalosporins	13-26	solute carrier family 22 member 11	Homo sapiens	129-133
11909604-7	2002	The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4.	Cefoperazone	41-53	solute carrier family 22 member 11	Homo sapiens	290-294
11909604-7	2002	The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4.	Cefazolin	55-64	solute carrier family 22 member 11	Homo sapiens	290-294
11907186-4	2002	A time- and dose-dependent increase in PGE(2) and PGF(2 alpha) uptake was observed in cells expressing hOAT1, hOAT2, hOAT3, hOAT4, hOCT1, and hOCT2.	Prostaglandins E	39-42	solute carrier family 22 member 11	Homo sapiens	124-129
11907186-4	2002	A time- and dose-dependent increase in PGE(2) and PGF(2 alpha) uptake was observed in cells expressing hOAT1, hOAT2, hOAT3, hOAT4, hOCT1, and hOCT2.	Prostaglandins F	50-53	solute carrier family 22 member 11	Homo sapiens	124-129
11907186-5	2002	The K(m) values of PGE(2) uptake by hOAT1, hOAT2, hOAT3, hOAT4, hOCT1, and hOCT2 were 970, 713, 345, 154, 657, and 28.9 nM, respectively, whereas those of PGF(2 alpha) uptake by hOAT1, hOAT3, hOAT4, hOCT1, and hOCT2 were 575, 1092, 692, 477, and 334 nM, respectively.	Prostaglandins E	19-23	solute carrier family 22 member 11	Homo sapiens	57-62
11907186-5	2002	The K(m) values of PGE(2) uptake by hOAT1, hOAT2, hOAT3, hOAT4, hOCT1, and hOCT2 were 970, 713, 345, 154, 657, and 28.9 nM, respectively, whereas those of PGF(2 alpha) uptake by hOAT1, hOAT3, hOAT4, hOCT1, and hOCT2 were 575, 1092, 692, 477, and 334 nM, respectively.	Prostaglandins E	19-23	solute carrier family 22 member 11	Homo sapiens	192-197
11907186-7	2002	In conclusion, considering the localization of these transporters, the results suggest that PGE(2) and PGF(2 alpha) transport in the basolateral membrane of the proximal tubule is mediated by multiple pathways including hOAT1, hOAT2, hOAT3, and hOCT2, whereas that in the apical side is mediated by hOAT4.	Prostaglandins E	92-95	solute carrier family 22 member 11	Homo sapiens	299-304
11909604-7	2002	The inhibition constant (K(i)) values of cefoperazone, cefazolin, ceftriaxone and cephaloridine for human-OAT1 were much lower than those for human-OAT3 and human-OAT4, whereas the K(i) values of cephalothin and cefotaxime for human-OAT3 were much lower than those for human-OAT1 and human-OAT4.	Cephaloridine	82-95	solute carrier family 22 member 11	Homo sapiens	290-294
11909604-8	2002	Human-OAT4 mediated the bidirectional transport of estrone sulfate, an optimal substrate for human-OAT4.	estrone sulfate	51-66	solute carrier family 22 member 11	Homo sapiens	6-10
11909604-8	2002	Human-OAT4 mediated the bidirectional transport of estrone sulfate, an optimal substrate for human-OAT4.	estrone sulfate	51-66	solute carrier family 22 member 11	Homo sapiens	99-103
11909604-9	2002	These results suggest that human-OAT1, human-OAT3 and human-OAT4 interact with various cephalosporin antibiotics, and that human-OAT1 and human-OAT3 play a distinct role in the basolateral uptake of cephalosporin antibiotics.	Cephalosporins	87-100	solute carrier family 22 member 11	Homo sapiens	60-64
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	24-37	solute carrier family 22 member 11	Homo sapiens	48-52
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	24-37	solute carrier family 22 member 11	Homo sapiens	167-171
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	193-206	solute carrier family 22 member 11	Homo sapiens	48-52
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	193-206	solute carrier family 22 member 11	Homo sapiens	167-171
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	193-206	solute carrier family 22 member 11	Homo sapiens	48-52
11909604-10	2002	Since the K(i) value of cephaloridine for human-OAT4-mediated organic uptake was much higher than that for human-OAT1, the results indicate the possibility that human-OAT4 limits the efflux of cephaloridine, leading to the accumulation of cephaloridine and the induction of nephrotoxicity.	Cephaloridine	193-206	solute carrier family 22 member 11	Homo sapiens	167-171
11861798-9	2002	In conclusion, these results suggest that hOAT1 and hOCT1 mediate renal ACV and GCV transport, whereas hOAT1, hOAT2, hOAT3, and hOAT4 mediate renal AZT transport.	Zidovudine	148-151	solute carrier family 22 member 11	Homo sapiens	128-133
11861798-5	2002	On the other hand, AZT uptake was observed in hOAT1-, hOAT2-, hOAT3-, and hOAT4-expressing cells.	Zidovudine	19-22	solute carrier family 22 member 11	Homo sapiens	74-79
11855680-2	2002	The cells stably expressing hOAT1, hOAT2, hOAT3 and hOAT4 exhibited a higher amount of [3H]tetracycline uptake compared with mock cells.	3h]tetracycline	88-103	solute carrier family 22 member 11	Homo sapiens	52-57
11861798-7	2002	On the other hand, the Km values of AZT uptake by hOAT1, hOAT2, hOAT3, and hOAT4 were 45.9, 26.8, 145.1, and 151.8 microM, respectively.	Zidovudine	36-39	solute carrier family 22 member 11	Homo sapiens	75-80
11855680-7	2002	HOAT1 and hOAT4 mediated the efflux of tetracycline, but hOAT2 and hOAT3 did not.	Tetracycline	39-51	solute carrier family 22 member 11	Homo sapiens	10-15
11855680-8	2002	These results suggest that hOAT1, hOAT2 and hOAT3 mediate the basolateral uptake and/or efflux of tetracycline, whereas hOAT4 is responsible for the reabsorption as well as the efflux of tetracycline in the apical side of the proximal tubule.	Tetracycline	187-199	solute carrier family 22 member 11	Homo sapiens	120-125
11855680-3	2002	The apparent Km values for hOAT2-, hOAT3- and hOAT4-mediated tetracycline uptakes were 439.9 +/- 23.0, 566.2 +/- 28.4 and 122.7 +/- 16.0 microM, respectively.	Tetracycline	61-73	solute carrier family 22 member 11	Homo sapiens	46-51
11855680-4	2002	Tetracycline significantly inhibited the organic anion uptake by hOAT1, hOAT2 and hOAT4, but not hOAT3.	Tetracycline	0-12	solute carrier family 22 member 11	Homo sapiens	82-87
33617845-4	2021	We concluded from a comparison of E3S and uric acid transport that SLC22A11 does not translocate E3S into the cytosol, but into the plasma membrane.	estrone sulfate	34-37	solute carrier family 22 member 11	Homo sapiens	67-75
10660625-5	2000	When expressed in Xenopus oocytes, OAT4 mediated the high affinity transport of estrone sulfate (K(m) = 1.01 microM) and dehydroepiandrosterone sulfate (K(m) = 0.63 microM) in a sodium-independent manner.	estrone sulfate	80-95	solute carrier family 22 member 11	Homo sapiens	35-39
10660625-5	2000	When expressed in Xenopus oocytes, OAT4 mediated the high affinity transport of estrone sulfate (K(m) = 1.01 microM) and dehydroepiandrosterone sulfate (K(m) = 0.63 microM) in a sodium-independent manner.	Dehydroepiandrosterone Sulfate	121-151	solute carrier family 22 member 11	Homo sapiens	35-39
10660625-5	2000	When expressed in Xenopus oocytes, OAT4 mediated the high affinity transport of estrone sulfate (K(m) = 1.01 microM) and dehydroepiandrosterone sulfate (K(m) = 0.63 microM) in a sodium-independent manner.	Sodium	178-184	solute carrier family 22 member 11	Homo sapiens	35-39
10660625-6	2000	OAT4 also mediated the transport of ochratoxin A.	ochratoxin A	36-48	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	estrone sulfate	27-42	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	Sulfates	35-42	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	4-nitrophenyl sulfate	96-117	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	naphthyl sulfate	119-141	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	beta-estradiol sulfate	143-165	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-7	2000	OAT4-mediated transport of estrone sulfate was inhibited by several sulfate conjugates, such as p-nitrophenyl sulfate, alpha-naphthyl sulfate, beta-estradiol sulfate, and 4-methylumbelliferyl sulfate.	4-methylumbelliferyl sulfate	171-199	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-9	2000	OAT4 interacted with chemically heterogeneous anionic compounds, such as nonsteroidal anti-inflammatory drugs, diuretics, sulfobromophthalein, penicillin G, and bile salts, whereas tetraethylammonium, an organic cation, did not.	Sulfobromophthalein	122-141	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-9	2000	OAT4 interacted with chemically heterogeneous anionic compounds, such as nonsteroidal anti-inflammatory drugs, diuretics, sulfobromophthalein, penicillin G, and bile salts, whereas tetraethylammonium, an organic cation, did not.	Penicillin G	143-155	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-9	2000	OAT4 interacted with chemically heterogeneous anionic compounds, such as nonsteroidal anti-inflammatory drugs, diuretics, sulfobromophthalein, penicillin G, and bile salts, whereas tetraethylammonium, an organic cation, did not.	Bile Acids and Salts	161-171	solute carrier family 22 member 11	Homo sapiens	0-4
10660625-9	2000	OAT4 interacted with chemically heterogeneous anionic compounds, such as nonsteroidal anti-inflammatory drugs, diuretics, sulfobromophthalein, penicillin G, and bile salts, whereas tetraethylammonium, an organic cation, did not.	Tetraethylammonium	181-199	solute carrier family 22 member 11	Homo sapiens	0-4
34842392-9	2021	<i>ABCC1</i> expression was induced by all treatments while <i>ABCG2</i> and <i>SLC22A11 </i>were induced only by 500 mug mL<sup>1</sup> PI-MeOH and PI-EtOH.	Methanol	140-144	solute carrier family 22 member 11	Homo sapiens	80-88
34842392-9	2021	<i>ABCC1</i> expression was induced by all treatments while <i>ABCG2</i> and <i>SLC22A11 </i>were induced only by 500 mug mL<sup>1</sup> PI-MeOH and PI-EtOH.	Ethanol	152-156	solute carrier family 22 member 11	Homo sapiens	80-88
34597623-0	2022	Role of uptake transporters OAT4, OATP2A1, and OATP1A2 in human placental bio-disposition of pravastatin.	Pravastatin	93-104	solute carrier family 22 member 11	Homo sapiens	28-32
34597623-5	2022	Preloading placental membrane vesicles with glutarate increased the uptake of pravastatin suggesting involvement of glutarate-dependent transporters such as OAT4.	Glutarates	44-53	solute carrier family 22 member 11	Homo sapiens	157-161
34597623-5	2022	Preloading placental membrane vesicles with glutarate increased the uptake of pravastatin suggesting involvement of glutarate-dependent transporters such as OAT4.	Pravastatin	78-89	solute carrier family 22 member 11	Homo sapiens	157-161
34597623-5	2022	Preloading placental membrane vesicles with glutarate increased the uptake of pravastatin suggesting involvement of glutarate-dependent transporters such as OAT4.	Glutarates	116-125	solute carrier family 22 member 11	Homo sapiens	157-161
34597623-6	2022	In the HEK293 cells overexpressing individual uptake transporters, OATP2A1, OATP1A2 and OAT4 were determined to accept pravastatin as a substrate at physiological pH, while the uptake of pravastatin by OATP2B1 (known to interact with pravastatin at acidic pH) and OATP5A1 was not detected at pH 7.4.	Pravastatin	119-130	solute carrier family 22 member 11	Homo sapiens	88-92
34290818-8	2021	OAT4 (SLC22A11) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia.	Uric Acid	29-34	solute carrier family 22 member 11	Homo sapiens	0-4
34290818-8	2021	OAT4 (SLC22A11) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia.	Uric Acid	29-34	solute carrier family 22 member 11	Homo sapiens	6-14
34290818-15	2021	In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3).	Uric Acid	30-35	solute carrier family 22 member 11	Homo sapiens	145-149
33617845-4	2021	We concluded from a comparison of E3S and uric acid transport that SLC22A11 does not translocate E3S into the cytosol, but into the plasma membrane.	Uric Acid	42-51	solute carrier family 22 member 11	Homo sapiens	67-75
33485002-9	2021	For PFSAs, their binding affinities to organic anion transporter 4 (OAT4) were increased with the chain length except for the sodium perfluoro-1-heptanesulfonate (PFHpS) and sodium perfluoro-1-nonanesulfonate (PFNS).	pfsas	4-9	solute carrier family 22 member 11	Homo sapiens	39-66
33189558-1	2021	Organic anion transporter (OAT) 4, which is localized at the apical membrane of human renal proximal tubules, transports olmesartan, an angiotensin II receptor blocker (ARB).	olmesartan	121-131	solute carrier family 22 member 11	Homo sapiens	0-33
33189558-2	2021	Many ARBs, including olmesartan, undergo partial tubular secretion as active forms, and inhibit OAT4-mediated uptake activity.	olmesartan	21-31	solute carrier family 22 member 11	Homo sapiens	96-100
33189558-4	2021	Concentration-dependent OAT4-mediated uptake of azilsartan, candesartan, carboxylosartan, losartan, and valsartan was observed with Km values of 6.6, 31, 7.2, 13, and 1.7 muM, respectively, in the absence of extracellular Cl-.	azilsartan	48-58	solute carrier family 22 member 11	Homo sapiens	24-28
33189558-4	2021	Concentration-dependent OAT4-mediated uptake of azilsartan, candesartan, carboxylosartan, losartan, and valsartan was observed with Km values of 6.6, 31, 7.2, 13, and 1.7 muM, respectively, in the absence of extracellular Cl-.	candesartan	60-71	solute carrier family 22 member 11	Homo sapiens	24-28
33189558-4	2021	Concentration-dependent OAT4-mediated uptake of azilsartan, candesartan, carboxylosartan, losartan, and valsartan was observed with Km values of 6.6, 31, 7.2, 13, and 1.7 muM, respectively, in the absence of extracellular Cl-.	losartan carboxylic acid	73-88	solute carrier family 22 member 11	Homo sapiens	24-28
33189558-4	2021	Concentration-dependent OAT4-mediated uptake of azilsartan, candesartan, carboxylosartan, losartan, and valsartan was observed with Km values of 6.6, 31, 7.2, 13, and 1.7 muM, respectively, in the absence of extracellular Cl-.	Losartan	80-88	solute carrier family 22 member 11	Homo sapiens	24-28
33189558-4	2021	Concentration-dependent OAT4-mediated uptake of azilsartan, candesartan, carboxylosartan, losartan, and valsartan was observed with Km values of 6.6, 31, 7.2, 13, and 1.7 muM, respectively, in the absence of extracellular Cl-.	Valsartan	104-113	solute carrier family 22 member 11	Homo sapiens	24-28
33189558-5	2021	In the presence of extracellular Cl-, OAT4-mediated uptake of dianionic ARBs (azilsartan, candesartan, carboxylosartan, and valsartan) was lower and reached a steady state faster than in the absence of extracellular Cl-.	azilsartan	78-88	solute carrier family 22 member 11	Homo sapiens	38-42
33189558-5	2021	In the presence of extracellular Cl-, OAT4-mediated uptake of dianionic ARBs (azilsartan, candesartan, carboxylosartan, and valsartan) was lower and reached a steady state faster than in the absence of extracellular Cl-.	candesartan	90-101	solute carrier family 22 member 11	Homo sapiens	38-42
33189558-5	2021	In the presence of extracellular Cl-, OAT4-mediated uptake of dianionic ARBs (azilsartan, candesartan, carboxylosartan, and valsartan) was lower and reached a steady state faster than in the absence of extracellular Cl-.	losartan carboxylic acid	103-118	solute carrier family 22 member 11	Homo sapiens	38-42
33189558-5	2021	In the presence of extracellular Cl-, OAT4-mediated uptake of dianionic ARBs (azilsartan, candesartan, carboxylosartan, and valsartan) was lower and reached a steady state faster than in the absence of extracellular Cl-.	Valsartan	124-133	solute carrier family 22 member 11	Homo sapiens	38-42
33189558-7	2021	Our results suggest that OAT4 may play a role in the excretion of azilsartan, candesartan, carboxylosartan, and valsartan, as well as olmesartan.	azilsartan	66-76	solute carrier family 22 member 11	Homo sapiens	25-29
33189558-7	2021	Our results suggest that OAT4 may play a role in the excretion of azilsartan, candesartan, carboxylosartan, and valsartan, as well as olmesartan.	candesartan	78-89	solute carrier family 22 member 11	Homo sapiens	25-29
33189558-7	2021	Our results suggest that OAT4 may play a role in the excretion of azilsartan, candesartan, carboxylosartan, and valsartan, as well as olmesartan.	losartan carboxylic acid	91-106	solute carrier family 22 member 11	Homo sapiens	25-29
33189558-7	2021	Our results suggest that OAT4 may play a role in the excretion of azilsartan, candesartan, carboxylosartan, and valsartan, as well as olmesartan.	Valsartan	112-121	solute carrier family 22 member 11	Homo sapiens	25-29
33189558-7	2021	Our results suggest that OAT4 may play a role in the excretion of azilsartan, candesartan, carboxylosartan, and valsartan, as well as olmesartan.	olmesartan	134-144	solute carrier family 22 member 11	Homo sapiens	25-29
33189558-8	2021	In contrast, OAT4-mediated uptake of losartan, a monoanionic ARB, was little affected by extracellular Cl-, suggesting that only OAT4-mediated dianion transport is Cl--sensitive.	Losartan	37-45	solute carrier family 22 member 11	Homo sapiens	13-17
33485002-9	2021	For PFSAs, their binding affinities to organic anion transporter 4 (OAT4) were increased with the chain length except for the sodium perfluoro-1-heptanesulfonate (PFHpS) and sodium perfluoro-1-nonanesulfonate (PFNS).	pfsas	4-9	solute carrier family 22 member 11	Homo sapiens	68-72
33485002-9	2021	For PFSAs, their binding affinities to organic anion transporter 4 (OAT4) were increased with the chain length except for the sodium perfluoro-1-heptanesulfonate (PFHpS) and sodium perfluoro-1-nonanesulfonate (PFNS).	pfns	210-214	solute carrier family 22 member 11	Homo sapiens	39-66
33485002-9	2021	For PFSAs, their binding affinities to organic anion transporter 4 (OAT4) were increased with the chain length except for the sodium perfluoro-1-heptanesulfonate (PFHpS) and sodium perfluoro-1-nonanesulfonate (PFNS).	pfns	210-214	solute carrier family 22 member 11	Homo sapiens	68-72
30941173-5	2019	Among the drugs tested, only epirubicin hydrochloride and dabrafenib mesylate exhibited &gt; 50% cis-inhibitory effect, in COS-7 cells, on hOAT4-mediated uptake of estrone sulfate, a prototypical substrate for the transporter.	Epirubicin	29-53	solute carrier family 22 member 11	Homo sapiens	139-144
32506648-2	2020	Arhalofenate (Arha) has been proved to have uricosuric activity as an inhibitor of URAT1, organic anion transporter 4 (OAT4) and OAT10.	arhalofenate	0-12	solute carrier family 22 member 11	Homo sapiens	90-117
32506648-2	2020	Arhalofenate (Arha) has been proved to have uricosuric activity as an inhibitor of URAT1, organic anion transporter 4 (OAT4) and OAT10.	arhalofenate	0-12	solute carrier family 22 member 11	Homo sapiens	119-123
32506648-2	2020	Arhalofenate (Arha) has been proved to have uricosuric activity as an inhibitor of URAT1, organic anion transporter 4 (OAT4) and OAT10.	arhalofenate	0-4	solute carrier family 22 member 11	Homo sapiens	90-117
32506648-2	2020	Arhalofenate (Arha) has been proved to have uricosuric activity as an inhibitor of URAT1, organic anion transporter 4 (OAT4) and OAT10.	arhalofenate	0-4	solute carrier family 22 member 11	Homo sapiens	119-123
30941173-8	2019	Our results established that epirubicin hydrochloride and dabrafenib mesylate are inhibitors of hOAT4.	Epirubicin	29-53	solute carrier family 22 member 11	Homo sapiens	96-101
30941173-5	2019	Among the drugs tested, only epirubicin hydrochloride and dabrafenib mesylate exhibited &gt; 50% cis-inhibitory effect, in COS-7 cells, on hOAT4-mediated uptake of estrone sulfate, a prototypical substrate for the transporter.	Dabrafenib mesylate	58-77	solute carrier family 22 member 11	Homo sapiens	139-144
30941173-8	2019	Our results established that epirubicin hydrochloride and dabrafenib mesylate are inhibitors of hOAT4.	Dabrafenib mesylate	58-77	solute carrier family 22 member 11	Homo sapiens	96-101
30941173-5	2019	Among the drugs tested, only epirubicin hydrochloride and dabrafenib mesylate exhibited &gt; 50% cis-inhibitory effect, in COS-7 cells, on hOAT4-mediated uptake of estrone sulfate, a prototypical substrate for the transporter.	carbonyl sulfide	123-126	solute carrier family 22 member 11	Homo sapiens	139-144
30941173-9	2019	Furthermore, by comparing our data with clinically relevant exposures of these drugs, we conclude that although the tendency for dabrafenib mesylate to cause drug-drug interaction through hOAT4 is insignificant in the kidney, the propensity for epirubicin hydrochloride to cause drug-drug interaction is high.	Dabrafenib mesylate	129-148	solute carrier family 22 member 11	Homo sapiens	188-193
30941173-5	2019	Among the drugs tested, only epirubicin hydrochloride and dabrafenib mesylate exhibited &gt; 50% cis-inhibitory effect, in COS-7 cells, on hOAT4-mediated uptake of estrone sulfate, a prototypical substrate for the transporter.	estrone sulfate	164-179	solute carrier family 22 member 11	Homo sapiens	139-144
29272511-8	2018	Arhalofenate, another emerging uricosuric, also interacts with URAT1 and organic anion transporter 4.	arhalofenate	0-12	solute carrier family 22 member 11	Homo sapiens	73-100
30453017-7	2019	We further showed that insulin phosphorylated serine 327 on Nedd4-2 and weakened the interaction between hOAT4 and Nedd4-2.	Serine	46-52	solute carrier family 22 member 11	Homo sapiens	105-110
30453017-9	2019	In addition, the stimulatory effect of insulin on hOAT4 was blocked by wortmannin and buparlisib, two PI3K inhibitors.	Wortmannin	71-81	solute carrier family 22 member 11	Homo sapiens	50-55
30453017-9	2019	In addition, the stimulatory effect of insulin on hOAT4 was blocked by wortmannin and buparlisib, two PI3K inhibitors.	NVP-BKM120	86-96	solute carrier family 22 member 11	Homo sapiens	50-55
30167756-8	2018	Intracellular accumulation of actinomycin D was greater compared to vector control in OAT4-transfected cells by 1.5- and 1.4-fold at 10 min (p = 0.01) and 20 min (p = 0.03), and in PEPT2-transfected cells by 1.5- and 1.7-fold at 10 min (p = 0.047) and 20 min (p = 0.043), respectively.	Dactinomycin	30-43	solute carrier family 22 member 11	Homo sapiens	86-90
30167756-10	2018	CONCLUSION: Transport of actinomycin D was mediated by OAT4 and PEPT2 in vitro.	Dactinomycin	25-38	solute carrier family 22 member 11	Homo sapiens	55-59
29725345-11	2018	The identified variants localize to genes including neuroblast differentiation-associated protein (AHNAK), previously associated with blood biomarkers in COPD, phospholipase C Beta 3 (PLCB3), shown to increase airway hyper-responsiveness, solute carrier family 22-A11 (SLC22A11), involved in amino acid metabolism and ion transport, and metallothionein-like protein 5 (MTL5), involved in nicotinate and nicotinamide metabolism.	Niacin	388-398	solute carrier family 22 member 11	Homo sapiens	239-267
29725345-11	2018	The identified variants localize to genes including neuroblast differentiation-associated protein (AHNAK), previously associated with blood biomarkers in COPD, phospholipase C Beta 3 (PLCB3), shown to increase airway hyper-responsiveness, solute carrier family 22-A11 (SLC22A11), involved in amino acid metabolism and ion transport, and metallothionein-like protein 5 (MTL5), involved in nicotinate and nicotinamide metabolism.	Niacin	388-398	solute carrier family 22 member 11	Homo sapiens	269-277
29725345-11	2018	The identified variants localize to genes including neuroblast differentiation-associated protein (AHNAK), previously associated with blood biomarkers in COPD, phospholipase C Beta 3 (PLCB3), shown to increase airway hyper-responsiveness, solute carrier family 22-A11 (SLC22A11), involved in amino acid metabolism and ion transport, and metallothionein-like protein 5 (MTL5), involved in nicotinate and nicotinamide metabolism.	Niacinamide	403-415	solute carrier family 22 member 11	Homo sapiens	239-267
29725345-11	2018	The identified variants localize to genes including neuroblast differentiation-associated protein (AHNAK), previously associated with blood biomarkers in COPD, phospholipase C Beta 3 (PLCB3), shown to increase airway hyper-responsiveness, solute carrier family 22-A11 (SLC22A11), involved in amino acid metabolism and ion transport, and metallothionein-like protein 5 (MTL5), involved in nicotinate and nicotinamide metabolism.	Niacinamide	403-415	solute carrier family 22 member 11	Homo sapiens	269-277
29162614-8	2018	Moreover, transporter profiling assessed using stable cell lines constitutively expressing transporters demonstrated that PDA and HVA are substrates for human OAT1, OAT3, OAT2 (HVA), and OAT4 (PDA), but not OCT2, MATE1, MATE2K, OATP1B1, OATP1B3, and sodium taurocholate cotransporting polypeptide.	Taurocholic Acid	250-269	solute carrier family 22 member 11	Homo sapiens	187-191
28951782-2	2017	The aim of this study was to determine whether variation in SLC2A9 or SLC22A11 influences acute renal handling of uric acid in response to frusemide.	Uric Acid	114-123	solute carrier family 22 member 11	Homo sapiens	70-78
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	lesinurad	0-9	solute carrier family 22 member 11	Homo sapiens	70-74
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	lesinurad	11-19	solute carrier family 22 member 11	Homo sapiens	70-74
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	Uric Acid	75-84	solute carrier family 22 member 11	Homo sapiens	70-74
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	Uric Acid	86-88	solute carrier family 22 member 11	Homo sapiens	70-74
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	Uric Acid	140-142	solute carrier family 22 member 11	Homo sapiens	70-74
28425024-1	2017	Lesinurad (Zurampic ) is an oral selective inhibitor of the URAT1 and OAT4 uric acid (UA) transporters of the kidney, via which it inhibits UA reabsorption and thus increases renal UA excretion and lowers serum UA (sUA) levels.	sua	215-218	solute carrier family 22 member 11	Homo sapiens	70-74
28385546-0	2017	Cellular Uptake of Levocetirizine by Organic Anion Transporter 4.	levocetirizine	19-33	solute carrier family 22 member 11	Homo sapiens	37-64
28385546-2	2017	In this study, we aimed to investigate the transport mechanism of levocetirizine, the pharmacologically active enantiomer of cetirizine, via human organic anion transporter 4 (OAT4) expressed in the apical membrane of renal proximal tubules and the basal plasma membrane of placental syncytiotrophoblasts.	levocetirizine	66-80	solute carrier family 22 member 11	Homo sapiens	147-174
28385546-2	2017	In this study, we aimed to investigate the transport mechanism of levocetirizine, the pharmacologically active enantiomer of cetirizine, via human organic anion transporter 4 (OAT4) expressed in the apical membrane of renal proximal tubules and the basal plasma membrane of placental syncytiotrophoblasts.	levocetirizine	66-80	solute carrier family 22 member 11	Homo sapiens	176-180
28385546-2	2017	In this study, we aimed to investigate the transport mechanism of levocetirizine, the pharmacologically active enantiomer of cetirizine, via human organic anion transporter 4 (OAT4) expressed in the apical membrane of renal proximal tubules and the basal plasma membrane of placental syncytiotrophoblasts.	Cetirizine	70-80	solute carrier family 22 member 11	Homo sapiens	147-174
28385546-2	2017	In this study, we aimed to investigate the transport mechanism of levocetirizine, the pharmacologically active enantiomer of cetirizine, via human organic anion transporter 4 (OAT4) expressed in the apical membrane of renal proximal tubules and the basal plasma membrane of placental syncytiotrophoblasts.	Cetirizine	70-80	solute carrier family 22 member 11	Homo sapiens	176-180
28385546-3	2017	In cells expressing human OAT4 under the control of tetracycline, levocetirizine uptake was increased by tetracycline treatment.	Tetracycline	52-64	solute carrier family 22 member 11	Homo sapiens	26-30
28385546-3	2017	In cells expressing human OAT4 under the control of tetracycline, levocetirizine uptake was increased by tetracycline treatment.	levocetirizine	66-80	solute carrier family 22 member 11	Homo sapiens	26-30
28385546-3	2017	In cells expressing human OAT4 under the control of tetracycline, levocetirizine uptake was increased by tetracycline treatment.	Tetracycline	105-117	solute carrier family 22 member 11	Homo sapiens	26-30
28385546-5	2017	The OAT4-mediated levocetirizine uptake was concentration-dependent with a Km of 38 muM.	levocetirizine	18-32	solute carrier family 22 member 11	Homo sapiens	4-8
28385546-6	2017	The uptake rate of levocetirizine via OAT4 was approximately twice that of racemic cetirizine, indicating stereoselective uptake of levocetirizine.	levocetirizine	19-33	solute carrier family 22 member 11	Homo sapiens	38-42
28385546-6	2017	The uptake rate of levocetirizine via OAT4 was approximately twice that of racemic cetirizine, indicating stereoselective uptake of levocetirizine.	Cetirizine	23-33	solute carrier family 22 member 11	Homo sapiens	38-42
28385546-6	2017	The uptake rate of levocetirizine via OAT4 was approximately twice that of racemic cetirizine, indicating stereoselective uptake of levocetirizine.	levocetirizine	132-146	solute carrier family 22 member 11	Homo sapiens	38-42
28385546-7	2017	On the other hand, OAT4-mediated [3H]dehydroepiandrosterone sulfate uptake was inhibited by dextrocetirizine and levocetirizine.	CCG-204473	33-67	solute carrier family 22 member 11	Homo sapiens	19-23
28385546-7	2017	On the other hand, OAT4-mediated [3H]dehydroepiandrosterone sulfate uptake was inhibited by dextrocetirizine and levocetirizine.	(S)-cetirizine	92-108	solute carrier family 22 member 11	Homo sapiens	19-23
28385546-7	2017	On the other hand, OAT4-mediated [3H]dehydroepiandrosterone sulfate uptake was inhibited by dextrocetirizine and levocetirizine.	levocetirizine	113-127	solute carrier family 22 member 11	Homo sapiens	19-23
28385546-8	2017	Overall, our findings indicate that OAT4 mediates levocetirizine uptake but is unlikely to mediate the efflux.	levocetirizine	50-64	solute carrier family 22 member 11	Homo sapiens	36-40
28951782-2	2017	The aim of this study was to determine whether variation in SLC2A9 or SLC22A11 influences acute renal handling of uric acid in response to frusemide.	Furosemide	139-148	solute carrier family 22 member 11	Homo sapiens	70-78
28951782-8	2017	The presence of the urate-lowering and gout-protective alleles for SLC2A9 (rs11942223 and rs13129697) and SLC22A11 (rs207826) did not significantly alter the FEUA following a frusemide load.	Uric Acid	20-25	solute carrier family 22 member 11	Homo sapiens	106-114
27716403-8	2016	At concentrations achieved in the clinic, lesinurad inhibited activity of URAT1 and OAT4 in vitro, did not inhibit GLUT9, and had no effect on ABCG2.	lesinurad	42-51	solute carrier family 22 member 11	Homo sapiens	84-88
28027879-0	2017	A novel mode of operation of SLC22A11: Membrane insertion of estrone sulfate versus translocation of uric acid and glutamate.	estrone sulfate	61-76	solute carrier family 22 member 11	Homo sapiens	29-37
28027879-0	2017	A novel mode of operation of SLC22A11: Membrane insertion of estrone sulfate versus translocation of uric acid and glutamate.	Uric Acid	101-110	solute carrier family 22 member 11	Homo sapiens	29-37
28027879-0	2017	A novel mode of operation of SLC22A11: Membrane insertion of estrone sulfate versus translocation of uric acid and glutamate.	Glutamic Acid	115-124	solute carrier family 22 member 11	Homo sapiens	29-37
28027879-3	2017	Here we scrutinized the mechanism of transport of E3S by SLC22A11 (alias OAT4), by direct comparison with uric acid (UA), an important physiological substrate.	Uric Acid	106-115	solute carrier family 22 member 11	Homo sapiens	57-65
28027879-3	2017	Here we scrutinized the mechanism of transport of E3S by SLC22A11 (alias OAT4), by direct comparison with uric acid (UA), an important physiological substrate.	Uric Acid	106-115	solute carrier family 22 member 11	Homo sapiens	73-77
28027879-3	2017	Here we scrutinized the mechanism of transport of E3S by SLC22A11 (alias OAT4), by direct comparison with uric acid (UA), an important physiological substrate.	Uric Acid	117-119	solute carrier family 22 member 11	Homo sapiens	57-65
28027879-4	2017	Heterologous expression of SLC22A11 in human 293 cells gave rise to a huge unidirectional efflux of glutamate (Glu) and aspartate, as determined by LC-MS/MS.	Glutamic Acid	100-109	solute carrier family 22 member 11	Homo sapiens	27-35
28027879-4	2017	Heterologous expression of SLC22A11 in human 293 cells gave rise to a huge unidirectional efflux of glutamate (Glu) and aspartate, as determined by LC-MS/MS.	Glutamic Acid	111-114	solute carrier family 22 member 11	Homo sapiens	27-35
28027879-4	2017	Heterologous expression of SLC22A11 in human 293 cells gave rise to a huge unidirectional efflux of glutamate (Glu) and aspartate, as determined by LC-MS/MS.	Aspartic Acid	120-129	solute carrier family 22 member 11	Homo sapiens	27-35
28027879-9	2017	These results establish that SLC22A11 provides entirely different transport mechanisms for E3S and UA.	estrone sulfate	91-94	solute carrier family 22 member 11	Homo sapiens	29-37
28027879-9	2017	These results establish that SLC22A11 provides entirely different transport mechanisms for E3S and UA.	Uric Acid	99-101	solute carrier family 22 member 11	Homo sapiens	29-37
28357121-5	2017	We report here that tranilast is a potent inhibitor of [14C]-urate transport mediated by the major reabsorptive urate transporters (URAT1, GLUT9, OAT4, and OAT10) in Xenopus oocytes; this provides an unequivocal molecular mechanism for the drug"s uricosuric effect.	Carbon-14	56-59	solute carrier family 22 member 11	Homo sapiens	146-150
28357121-5	2017	We report here that tranilast is a potent inhibitor of [14C]-urate transport mediated by the major reabsorptive urate transporters (URAT1, GLUT9, OAT4, and OAT10) in Xenopus oocytes; this provides an unequivocal molecular mechanism for the drug"s uricosuric effect.	Uric Acid	61-66	solute carrier family 22 member 11	Homo sapiens	146-150
27716403-11	2016	CONCLUSION: The pharmacodynamic effects and in vitro activity of lesinurad are consistent with inhibition of URAT1 and OAT4, major apical transporters for uric acid.	Uric Acid	155-164	solute carrier family 22 member 11	Homo sapiens	119-123
27103454-4	2016	Loss-of-function mutations in SLC2A9, SLC22A11, and SLC22A12 cause hereditary hypouricaemia, while their overexpression may increase the reabsorption of uric acid.	Uric Acid	153-162	solute carrier family 22 member 11	Homo sapiens	38-46
27335682-5	2016	Among these drugs, only chlorambucil and cabazitaxel demonstrated more than 50% cis-inhibitory effect on hOAT4-mediated uptake of (3)H-labeled estrone sulfate, a prototypical substrate for the transporter.	Chlorambucil	24-36	solute carrier family 22 member 11	Homo sapiens	105-110
27335682-5	2016	Among these drugs, only chlorambucil and cabazitaxel demonstrated more than 50% cis-inhibitory effect on hOAT4-mediated uptake of (3)H-labeled estrone sulfate, a prototypical substrate for the transporter.	cabazitaxel	41-52	solute carrier family 22 member 11	Homo sapiens	105-110
27335682-5	2016	Among these drugs, only chlorambucil and cabazitaxel demonstrated more than 50% cis-inhibitory effect on hOAT4-mediated uptake of (3)H-labeled estrone sulfate, a prototypical substrate for the transporter.	estrone sulfate	143-158	solute carrier family 22 member 11	Homo sapiens	105-110
27335682-8	2016	Our results demonstrated that chlorambucil and cabazitaxel were inhibitors of hOAT4.	Chlorambucil	30-42	solute carrier family 22 member 11	Homo sapiens	78-83
27335682-8	2016	Our results demonstrated that chlorambucil and cabazitaxel were inhibitors of hOAT4.	cabazitaxel	47-58	solute carrier family 22 member 11	Homo sapiens	78-83
27335682-9	2016	Furthermore, by comparing our data with clinically relevant exposures of these drugs, we conclude that the propensity for chlorambucil and cabazitaxel to cause drug-drug interaction through inhibition of hOAT4 is low.	Chlorambucil	122-134	solute carrier family 22 member 11	Homo sapiens	204-209
27335682-9	2016	Furthermore, by comparing our data with clinically relevant exposures of these drugs, we conclude that the propensity for chlorambucil and cabazitaxel to cause drug-drug interaction through inhibition of hOAT4 is low.	cabazitaxel	139-150	solute carrier family 22 member 11	Homo sapiens	204-209
26714763-8	2016	It is concluded that the disposition of DF-AG, once formed, can be mediated by various candidate transporters known to be expressed in the kidney (basolateral, OAT1, OAT2, and OAT3; apical, MRP2, BCRP, and OAT4) and liver (canalicular, MRP2 and BCRP; basolateral, OATP1B1, OATP2B1, OAT2, and MRP3).	df-ag	40-45	solute carrier family 22 member 11	Homo sapiens	206-210
26861027-2	2016	It reduces serum uric acid (sUA) levels by inhibiting the function of the transporter proteins (URAT1 and organic anion transporter 4) involved in uric acid reabsorption in the kidney.	Uric Acid	17-26	solute carrier family 22 member 11	Homo sapiens	106-133
26861027-2	2016	It reduces serum uric acid (sUA) levels by inhibiting the function of the transporter proteins (URAT1 and organic anion transporter 4) involved in uric acid reabsorption in the kidney.	sua	28-31	solute carrier family 22 member 11	Homo sapiens	106-133
26902266-3	2016	Association of five known variants in SLC2A9 and SLC22A11 genes with SUA level in 4,834 normoglycemics (1,109 in discovery and 3,725 in validation phase) was revealed with different effect size in Indians compared to other major ethnic population of the world.	sua	69-72	solute carrier family 22 member 11	Homo sapiens	49-57
26861027-2	2016	It reduces serum uric acid (sUA) levels by inhibiting the function of the transporter proteins (URAT1 and organic anion transporter 4) involved in uric acid reabsorption in the kidney.	Uric Acid	147-156	solute carrier family 22 member 11	Homo sapiens	106-133
26902266-8	2016	Our results extends association of SLC2A9, SLC22A11 and ABCG2 genes with SUA level in Indians and enrich the assemblages of evidence for SUA level and T2DM interrelationship.	sua	73-76	solute carrier family 22 member 11	Homo sapiens	43-51
26277985-8	2015	However, glutamate efflux was trans-stimulated by an OAT4 and OATP2B1 substrate (bromosulphothalein).	Glutamic Acid	9-18	solute carrier family 22 member 11	Homo sapiens	53-57
25319728-0	2015	Transport of the soy isoflavone daidzein and its conjugative metabolites by the carriers SOAT, NTCP, OAT4, and OATP2B1.	Isoflavones	21-31	solute carrier family 22 member 11	Homo sapiens	101-105
25319728-0	2015	Transport of the soy isoflavone daidzein and its conjugative metabolites by the carriers SOAT, NTCP, OAT4, and OATP2B1.	daidzein	32-40	solute carrier family 22 member 11	Homo sapiens	101-105
25319728-6	2015	DAI monosulfates were transported by the carriers NTCP and SOAT in a sodium-dependent manner, while OAT4-HEK293 cells revealed a partly sodium-dependent transport for these compounds.	Sodium	136-142	solute carrier family 22 member 11	Homo sapiens	100-104
26277985-8	2015	However, glutamate efflux was trans-stimulated by an OAT4 and OATP2B1 substrate (bromosulphothalein).	bromosulphothalein	81-99	solute carrier family 22 member 11	Homo sapiens	53-57
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	[(14)c]glutamate	103-119	solute carrier family 22 member 11	Homo sapiens	63-67
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	[(14)c]glutamate	103-119	solute carrier family 22 member 11	Homo sapiens	189-193
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	[(14)c]glutamate	103-119	solute carrier family 22 member 11	Homo sapiens	189-193
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	Glutamic Acid	110-119	solute carrier family 22 member 11	Homo sapiens	63-67
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	Glutamic Acid	110-119	solute carrier family 22 member 11	Homo sapiens	189-193
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	Glutamic Acid	110-119	solute carrier family 22 member 11	Homo sapiens	189-193
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	estrone sulfate	196-212	solute carrier family 22 member 11	Homo sapiens	63-67
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	bromosulphothalein	217-235	solute carrier family 22 member 11	Homo sapiens	63-67
26277985-11	2015	Our data demonstrate that in Xenopus oocytes expressing either OAT4 or OATP2B1 efflux of intracellular [(14)C]glutamate could be stimulated by conditions including extracellular glutamate (OAT4), estrone-sulphate and bromosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).	Pravastatin	263-274	solute carrier family 22 member 11	Homo sapiens	63-67
26277985-12	2015	Cycling of glutamate across the placenta involving efflux via OAT4 and OATP2B1 and subsequent reuptake will drive placental uptake of organic anions from the fetal circulation.	Glutamic Acid	11-20	solute carrier family 22 member 11	Homo sapiens	62-66
26640952-10	2015	Preloading OAT4-transfected HEK293 cells with ICA stimulated ES uptake by 18.3 +- 3.8%.	ica	46-49	solute carrier family 22 member 11	Homo sapiens	11-15
26303760-0	2015	Organic anion transporter 4 (OAT 4) modifies placental transfer of perfluorinated alkyl acids PFOS and PFOA in human placental ex vivo perfusion system.	alkyl acids pfos	82-98	solute carrier family 22 member 11	Homo sapiens	0-27
26303760-0	2015	Organic anion transporter 4 (OAT 4) modifies placental transfer of perfluorinated alkyl acids PFOS and PFOA in human placental ex vivo perfusion system.	alkyl acids pfos	82-98	solute carrier family 22 member 11	Homo sapiens	29-34
26303760-0	2015	Organic anion transporter 4 (OAT 4) modifies placental transfer of perfluorinated alkyl acids PFOS and PFOA in human placental ex vivo perfusion system.	perfluorooctanoic acid	103-107	solute carrier family 22 member 11	Homo sapiens	0-27
26303760-0	2015	Organic anion transporter 4 (OAT 4) modifies placental transfer of perfluorinated alkyl acids PFOS and PFOA in human placental ex vivo perfusion system.	perfluorooctanoic acid	103-107	solute carrier family 22 member 11	Homo sapiens	29-34
26303760-4	2015	METHODS: To evaluate the contribution of OAT4 and ATP-binding cassette transporter G2 (ABCG2) proteins in the transplacental transfer of perfluoro octane sulfonate (PFOS) and perfluoro octanoate (PFOA) an ex vivo dual recirculating human placental perfusion was used.	perfluorooctane sulfonic acid	137-163	solute carrier family 22 member 11	Homo sapiens	41-45
26303760-4	2015	METHODS: To evaluate the contribution of OAT4 and ATP-binding cassette transporter G2 (ABCG2) proteins in the transplacental transfer of perfluoro octane sulfonate (PFOS) and perfluoro octanoate (PFOA) an ex vivo dual recirculating human placental perfusion was used.	perfluorooctane sulfonic acid	165-169	solute carrier family 22 member 11	Homo sapiens	41-45
26303760-4	2015	METHODS: To evaluate the contribution of OAT4 and ATP-binding cassette transporter G2 (ABCG2) proteins in the transplacental transfer of perfluoro octane sulfonate (PFOS) and perfluoro octanoate (PFOA) an ex vivo dual recirculating human placental perfusion was used.	perfluorooctanoic acid	175-194	solute carrier family 22 member 11	Homo sapiens	41-45
26303760-8	2015	The expression of OAT4 was in negative correlation with TI % of PFOA (R(2) = 0.92, p = 0.043) and PFOS (R(2) = 0.99, p = 0.007) at 120 min while at 240 min the correlation was statistically significant only with PFOA.	perfluorooctanoic acid	64-68	solute carrier family 22 member 11	Homo sapiens	18-22
26303760-8	2015	The expression of OAT4 was in negative correlation with TI % of PFOA (R(2) = 0.92, p = 0.043) and PFOS (R(2) = 0.99, p = 0.007) at 120 min while at 240 min the correlation was statistically significant only with PFOA.	perfluorooctane sulfonic acid	98-102	solute carrier family 22 member 11	Homo sapiens	18-22
26303760-8	2015	The expression of OAT4 was in negative correlation with TI % of PFOA (R(2) = 0.92, p = 0.043) and PFOS (R(2) = 0.99, p = 0.007) at 120 min while at 240 min the correlation was statistically significant only with PFOA.	perfluorooctanoic acid	212-216	solute carrier family 22 member 11	Homo sapiens	18-22
26303760-11	2015	Placental passage of PFOS and PFOA is modified by the transporter protein OAT4 but not by ABCG2.	perfluorooctane sulfonic acid	21-25	solute carrier family 22 member 11	Homo sapiens	74-78
26303760-11	2015	Placental passage of PFOS and PFOA is modified by the transporter protein OAT4 but not by ABCG2.	perfluorooctanoic acid	30-34	solute carrier family 22 member 11	Homo sapiens	74-78
25919187-0	2015	Role of OAT4 in Uptake of Estriol Precursor 16alpha-Hydroxydehydroepiandrosterone Sulfate Into Human Placental Syncytiotrophoblasts From Fetus.	Estriol	26-33	solute carrier family 22 member 11	Homo sapiens	8-12
25919187-0	2015	Role of OAT4 in Uptake of Estriol Precursor 16alpha-Hydroxydehydroepiandrosterone Sulfate Into Human Placental Syncytiotrophoblasts From Fetus.	16alpha-hydroxydehydroepiandrosterone sulfate	44-89	solute carrier family 22 member 11	Homo sapiens	8-12
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	[(3)h]16alpha-oh dheas	10-32	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	Dehydroepiandrosterone Sulfate	103-133	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	Sulfobromophthalein	158-177	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	Cyclosporine	189-202	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	Tetraethylammonium	204-222	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	p-Aminohippuric Acid	224-244	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-5	2015	Uptake of [(3)H]16alpha-OH DHEAS by BM vesicles was significantly inhibited by OAT4 substrates such as dehydroepiandrosterone sulfate, estrone-3-sulfate, and bromosulfophthalein but not by cyclosporin A, tetraethylammonium, p-aminohippuric acid, or cimetidine.	Cimetidine	249-259	solute carrier family 22 member 11	Homo sapiens	79-83
25919187-6	2015	These characteristics of vesicular [(3)H]16alpha-OH DHEAS uptake are in good agreement with those of human OAT4-transfected COS-7 cells as well as forskolin-differentiated JEG-3 cells.	[(3)h]16alpha-oh dheas	35-57	solute carrier family 22 member 11	Homo sapiens	107-111
25919187-6	2015	These characteristics of vesicular [(3)H]16alpha-OH DHEAS uptake are in good agreement with those of human OAT4-transfected COS-7 cells as well as forskolin-differentiated JEG-3 cells.	carbonyl sulfide	124-127	solute carrier family 22 member 11	Homo sapiens	107-111
25919187-8	2015	Our results indicate that OAT4 at the BM of human placental syncytiotrophoblasts plays a predominant role in the uptake of 16alpha-OH DHEAS for placental estriol synthesis.	16alpha-oh dheas	123-139	solute carrier family 22 member 11	Homo sapiens	26-30
25919187-8	2015	Our results indicate that OAT4 at the BM of human placental syncytiotrophoblasts plays a predominant role in the uptake of 16alpha-OH DHEAS for placental estriol synthesis.	Estriol	154-161	solute carrier family 22 member 11	Homo sapiens	26-30
25710938-4	2015	Cellular uptake of tanshinol was mediated by human organic anion transporter 1 (OAT1) (Km, 121 muM), OAT2 (859 muM), OAT3 (1888 muM), and OAT4 (1880 muM) and rat Oat1 (117 microM), Oat2 (1207 muM), and Oat3 (1498 muM).	tanshinol	19-28	solute carrier family 22 member 11	Homo sapiens	138-142
25820021-4	2015	In tetracycline-inducible OAT4-expressing cells, [(3) H]olmesartan uptake was increased by tetracycline treatment.	Tetracycline	3-15	solute carrier family 22 member 11	Homo sapiens	26-30
25820021-4	2015	In tetracycline-inducible OAT4-expressing cells, [(3) H]olmesartan uptake was increased by tetracycline treatment.	[(3) h]olmesartan	49-66	solute carrier family 22 member 11	Homo sapiens	26-30
25820021-4	2015	In tetracycline-inducible OAT4-expressing cells, [(3) H]olmesartan uptake was increased by tetracycline treatment.	Tetracycline	91-103	solute carrier family 22 member 11	Homo sapiens	26-30
25820021-5	2015	Olmesartan uptake via OAT4 was concentration dependent with a Km of 20 muM, and was increased in the absence of chloride.	olmesartan	0-10	solute carrier family 22 member 11	Homo sapiens	22-26
25820021-6	2015	[(3) H]Olmesartan efflux via OAT4 was also observed and was trans-stimulated by extracellular chloride and DHEAS.	olmesartan	7-17	solute carrier family 22 member 11	Homo sapiens	29-33
25820021-6	2015	[(3) H]Olmesartan efflux via OAT4 was also observed and was trans-stimulated by extracellular chloride and DHEAS.	Chlorides	94-102	solute carrier family 22 member 11	Homo sapiens	29-33
25820021-8	2015	Efflux transport of olmesartan via OAT4 from syncytiotrophoblasts to the fetal circulation might be facilitated in the presence of an inwardly directed physiological chloride gradient and extracellular DHEAS.	olmesartan	20-30	solute carrier family 22 member 11	Homo sapiens	35-39
25820021-8	2015	Efflux transport of olmesartan via OAT4 from syncytiotrophoblasts to the fetal circulation might be facilitated in the presence of an inwardly directed physiological chloride gradient and extracellular DHEAS.	Chlorides	166-174	solute carrier family 22 member 11	Homo sapiens	35-39
25502344-4	2015	A weighted genetic urate score was calculated using the SLC2A9, ABCG2, SLC17A1, SLC22A11, and SLC22A12 single-nucleotide polymorphisms (SNPs) that explains 3.4% of the variance in serum urate.	Uric Acid	19-24	solute carrier family 22 member 11	Homo sapiens	80-88
25477469-5	2015	Melphalan had no significant inhibitory effect on any OAT, whereas chlorambucil reduced OAT1-, OAT3-, and OAT4-mediated uptake of PAH or ES down to 14.6%, 16.3%, and 66.0% of control, respectively.	Chlorambucil	67-79	solute carrier family 22 member 11	Homo sapiens	106-110
25477469-5	2015	Melphalan had no significant inhibitory effect on any OAT, whereas chlorambucil reduced OAT1-, OAT3-, and OAT4-mediated uptake of PAH or ES down to 14.6%, 16.3%, and 66.0% of control, respectively.	p-Aminohippuric Acid	130-133	solute carrier family 22 member 11	Homo sapiens	106-110
25477469-5	2015	Melphalan had no significant inhibitory effect on any OAT, whereas chlorambucil reduced OAT1-, OAT3-, and OAT4-mediated uptake of PAH or ES down to 14.6%, 16.3%, and 66.0% of control, respectively.	Einsteinium	137-139	solute carrier family 22 member 11	Homo sapiens	106-110
26640952-6	2015	METHOD: To demonstrate interaction of ICA with human OAT1, OAT2, OAT3 and OAT4, ICA was tested on these transporters stably transfected in HEK293 cells by using p-aminohippurate (PAH), cGMP and estrone-3-sulfate (ES) as reference substrates, respectively.	ica	38-41	solute carrier family 22 member 11	Homo sapiens	74-78
26640952-10	2015	Preloading OAT4-transfected HEK293 cells with ICA stimulated ES uptake by 18.3 +- 3.8%.	estrone sulfate	61-63	solute carrier family 22 member 11	Homo sapiens	11-15
26640952-11	2015	CONCLUSION: The uptake of ICA across the basolateral membrane of PCTs occurs mainly by OAT1 and the efflux into the tubular lumen by OAT4.	ica	26-29	solute carrier family 22 member 11	Homo sapiens	133-137
24717977-0	2014	Transport of the placental estriol precursor 16alpha-hydroxy-dehydroepiandrosterone sulfate (16alpha-OH-DHEAS) by stably transfected OAT4-, SOAT-, and NTCP-HEK293 cells.	16alpha-hydroxy-dehydroepiandrosterone sulfate	45-91	solute carrier family 22 member 11	Homo sapiens	133-137
25354943-10	2014	Preincubation of OAT4-transfected human embryonic kidney-293 cells with NCG showed an increased uptake of estrone sulfate, the reference substrate of OAT4, indicating efflux of NCG by OAT4.	estrone sulfate	106-121	solute carrier family 22 member 11	Homo sapiens	17-21
25354943-10	2014	Preincubation of OAT4-transfected human embryonic kidney-293 cells with NCG showed an increased uptake of estrone sulfate, the reference substrate of OAT4, indicating efflux of NCG by OAT4.	estrone sulfate	106-121	solute carrier family 22 member 11	Homo sapiens	150-154
25354943-10	2014	Preincubation of OAT4-transfected human embryonic kidney-293 cells with NCG showed an increased uptake of estrone sulfate, the reference substrate of OAT4, indicating efflux of NCG by OAT4.	estrone sulfate	106-121	solute carrier family 22 member 11	Homo sapiens	150-154
24717977-0	2014	Transport of the placental estriol precursor 16alpha-hydroxy-dehydroepiandrosterone sulfate (16alpha-OH-DHEAS) by stably transfected OAT4-, SOAT-, and NTCP-HEK293 cells.	16alpha-oh-dheas	93-109	solute carrier family 22 member 11	Homo sapiens	133-137
24717977-4	2014	To identify these carriers, uptake of 16alpha-OH-DHEAS by the candidate carriers organic anion transporter OAT4, sodium-dependent organic anion transporter SOAT, Na(+)-taurocholate cotransporting polypeptide NTCP, and organic anion transporting polypeptide OATP2B1 was measured in stably transfected HEK293 cells by LC-MS-MS.	16alpha-oh-dheas	38-54	solute carrier family 22 member 11	Homo sapiens	107-111
24717977-9	2014	In conclusion, OAT4, SOAT, and NTCP were identified as carriers for the estriol precursor 16alpha-OH-DHEAS.	Estriol	72-79	solute carrier family 22 member 11	Homo sapiens	15-19
24717977-9	2014	In conclusion, OAT4, SOAT, and NTCP were identified as carriers for the estriol precursor 16alpha-OH-DHEAS.	16alpha-oh-dheas	90-106	solute carrier family 22 member 11	Homo sapiens	15-19
22877817-0	2012	Potential for food-drug interactions by dietary phenolic acids on human organic anion transporters 1 (SLC22A6), 3 (SLC22A8), and 4 (SLC22A11).	phenolic acid	48-62	solute carrier family 22 member 11	Homo sapiens	132-140
23402939-1	2013	Effects of 96 h aflatoxin B1 (AFB1) exposure at concentrations from 0.2 muM to 6 muM on the mRNA and protein expression levels of the following transporters ABCB1/B4, ABCC1, ABCC2, ABCG2, OAT4 and the mRNA expression of steroid-metabolizing enzymes CYP1A1, CYP19A1, HSD3B1 and HSD17B1, and conjugating enzyme family UGT1A were evaluated in trophoblastic JEG-3 cells.	Aflatoxin B1	16-28	solute carrier family 22 member 11	Homo sapiens	188-192
23402939-1	2013	Effects of 96 h aflatoxin B1 (AFB1) exposure at concentrations from 0.2 muM to 6 muM on the mRNA and protein expression levels of the following transporters ABCB1/B4, ABCC1, ABCC2, ABCG2, OAT4 and the mRNA expression of steroid-metabolizing enzymes CYP1A1, CYP19A1, HSD3B1 and HSD17B1, and conjugating enzyme family UGT1A were evaluated in trophoblastic JEG-3 cells.	Aflatoxin B1	30-34	solute carrier family 22 member 11	Homo sapiens	188-192
23573138-0	2013	Interaction of Natural Dietary and Herbal Anionic Compounds and Flavonoids with Human Organic Anion Transporters 1 (SLC22A6), 3 (SLC22A8), and 4 (SLC22A11).	Flavonoids	64-74	solute carrier family 22 member 11	Homo sapiens	146-154
23573138-6	2013	Only catechin inhibited hOAT4.	Catechin	5-13	solute carrier family 22 member 11	Homo sapiens	24-29
22877817-6	2012	Only sinapinic acid inhibited hOAT4 (~35%).	sinapinic acid	5-19	solute carrier family 22 member 11	Homo sapiens	30-35
24969759-2	2014	Forskolin, a PKA activator, significantly increased [(3)H]DHEAS uptake and the mRNA expression levels of organic anion transporter (OAT) 4 and CYP19A1 in choriocarcinoma JEG-3 cells, while other steroid sulfate transporters present in the placenta showed no change in expression level.	Colforsin	0-9	solute carrier family 22 member 11	Homo sapiens	105-138
24025986-4	2014	Since human organic anion transporter 4 (OAT4/SLC22A11) is expressed in the kidney and mediates urate transport, we investigated the effects of a common variant of OAT4/SLC22A11 on the susceptibility to gout.	Uric Acid	96-101	solute carrier family 22 member 11	Homo sapiens	12-39
24025986-4	2014	Since human organic anion transporter 4 (OAT4/SLC22A11) is expressed in the kidney and mediates urate transport, we investigated the effects of a common variant of OAT4/SLC22A11 on the susceptibility to gout.	Uric Acid	96-101	solute carrier family 22 member 11	Homo sapiens	41-45
24025986-4	2014	Since human organic anion transporter 4 (OAT4/SLC22A11) is expressed in the kidney and mediates urate transport, we investigated the effects of a common variant of OAT4/SLC22A11 on the susceptibility to gout.	Uric Acid	96-101	solute carrier family 22 member 11	Homo sapiens	46-54
22875277-0	2012	alpha-Ketoglutarate-related inhibitors of HIF prolyl hydroxylases are substrates of renal organic anion transporters 1 (OAT1) and 4 (OAT4).	Ketoglutaric Acids	0-19	solute carrier family 22 member 11	Homo sapiens	133-137
22875277-9	2012	All compounds trans-stimulated ES uptake by OAT4, but only PDCA stabilized HIF-1alpha.	estrone sulfate	31-33	solute carrier family 22 member 11	Homo sapiens	44-48
22634047-6	2012	The accumulation of quercetin-3"-O-sulfate was further evaluated in HEK293 cells expressing OAT2, OAT4 and OATP4C1.	quercetin 3'-sulfate	20-42	solute carrier family 22 member 11	Homo sapiens	98-102
22634047-7	2012	Uptake of quercetin-3"-O-sulfate was 2.3- and 1.4-fold higher in cells expressing OAT4 and OATP4C1 at pH 6.0, respectively, than in control HEK293 cells.	quercetin 3'-sulfate	10-32	solute carrier family 22 member 11	Homo sapiens	82-86
22160269-5	2012	Most of the CpG dinucleotides around the TSSs of OAT1 and OAT3 were highly methylated in the liver compared with kidney cortex, being consistent with their tissue specificity, whereas the difference in the DNA methylation status was less remarkable between the two tissues for OAT4 and URAT1.	cytidylyl-3'-5'-guanosine	12-29	solute carrier family 22 member 11	Homo sapiens	277-281
21103968-3	2011	OAT4 in the apical membrane of human proximal tubule cells is related to drug exit into the lumen and to uptake of estrone sulfate and urate from the lumen into the cell.	estrone sulfate	115-130	solute carrier family 22 member 11	Homo sapiens	0-4
23097748-6	2012	Activation of PKA by Bt2-cAMP also resulted in a stimulation of hOAT4 activity through an increased cell surface expression of the transporter.	Bucladesine	21-29	solute carrier family 22 member 11	Homo sapiens	64-69
21538853-6	2011	Hydroxycinnamic acid sulfates are substrates of OAT4 and were capable of trans-stimulating 5-carboxyfluorescein uptake mediated by OAT4.	hydroxycinnamic acid sulfates	0-29	solute carrier family 22 member 11	Homo sapiens	48-52
21538853-6	2011	Hydroxycinnamic acid sulfates are substrates of OAT4 and were capable of trans-stimulating 5-carboxyfluorescein uptake mediated by OAT4.	hydroxycinnamic acid sulfates	0-29	solute carrier family 22 member 11	Homo sapiens	131-135
21538853-6	2011	Hydroxycinnamic acid sulfates are substrates of OAT4 and were capable of trans-stimulating 5-carboxyfluorescein uptake mediated by OAT4.	4-carboxyfluorescein	91-111	solute carrier family 22 member 11	Homo sapiens	48-52
21538853-6	2011	Hydroxycinnamic acid sulfates are substrates of OAT4 and were capable of trans-stimulating 5-carboxyfluorescein uptake mediated by OAT4.	4-carboxyfluorescein	91-111	solute carrier family 22 member 11	Homo sapiens	131-135
21538853-9	2011	CONCLUSION: Concerted action of OAT1, OAT3, and OAT4 is involved in the elimination of hydroxycinnamic acid conjugates into urine, whereas MRP2 and breast cancer resistance protein are not involved in the disposition of these conjugates.	Coumaric Acids	87-107	solute carrier family 22 member 11	Homo sapiens	48-52
21103968-3	2011	OAT4 in the apical membrane of human proximal tubule cells is related to drug exit into the lumen and to uptake of estrone sulfate and urate from the lumen into the cell.	Uric Acid	135-140	solute carrier family 22 member 11	Homo sapiens	0-4
20884846-6	2010	Single-nucleotide polymorphisms at 8 genetic loci achieved genome-wide significance with serum urate levels (P=4x10(-8) to 2x10(-242) in SLC22A11, GCKR, R3HDM2-INHBC region, RREB1, PDZK1, SLC2A9, ABCG2, and SLC17A1).	Uric Acid	95-100	solute carrier family 22 member 11	Homo sapiens	137-145
20639259-0	2010	Characterization of cellular uptake of perfluorooctanoate via organic anion-transporting polypeptide 1A2, organic anion transporter 4, and urate transporter 1 for their potential roles in mediating human renal reabsorption of perfluorocarboxylates.	perfluorooctanoic acid	39-57	solute carrier family 22 member 11	Homo sapiens	106-133
20639259-2	2010	In the present study, PFO uptake kinetics of human organic anion-transporting polypeptide (OATP) 1A2, organic anion transporter (OAT) 4, and urate transporter 1 (URAT1) in stably transfected cell lines was investigated.	perfluorooctanoic acid	22-25	solute carrier family 22 member 11	Homo sapiens	102-135
20639259-3	2010	OAT4 and URAT1, but not OATP1A2, were shown to mediate saturable PFO cellular uptake.	perfluorooctanoic acid	65-68	solute carrier family 22 member 11	Homo sapiens	0-4
20639259-4	2010	OAT4-mediated PFO uptake was stimulated by a low extracellular pH, which was evidenced as a lower Michaelis constant (K(m)) at pH 6 (172.3 +- 45.9muM) than that at pH 7.4 (310.3 +- 30.2muM).	perfluorooctanoic acid	14-17	solute carrier family 22 member 11	Homo sapiens	0-4
20639259-6	2010	The inhibition of OATP1A2- or OAT4-mediated estrone-3-sulfate uptake or URAT1-mediated urate uptake has been compared for linear perfluorocarboxylates (PFCs) with carbon chain lengths from 4 to 12.	estrone sulfate	44-61	solute carrier family 22 member 11	Homo sapiens	30-34
20639259-8	2010	Our results suggest that OAT4 and URAT1 are key transporters in renal reabsorption of PFCs in humans and, as a result, may contribute significantly to the long half-life of PFO in humans.	perfluorooctanoic acid	173-176	solute carrier family 22 member 11	Homo sapiens	25-29