PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26550796-10	2016	The alterations in furosemide pharmacokinetics and pharmacodynamics were explained by changes in the expression of renal organic anion transporters 1 and 3, and sodium-potassium-chloride cotransporter-2.	Furosemide	19-29	solute carrier family 22 member 6	Rattus norvegicus	115-155	
30120768-2	2018	Simultaneously, drug-drug interactions (DDIs) mediated by OAT1 occur at high altitude, severely affecting furosemide pharmacokinetics.	Furosemide	106-116	solute carrier family 22 member 6	Rattus norvegicus	58-62	
27282888-0	2017	Impact of the induced organic anion transporter 1 (Oat1) renal expression by furosemide on the pharmacokinetics of organic anions.	Furosemide	77-87	solute carrier family 22 member 6	Rattus norvegicus	22-49	
27282888-0	2017	Impact of the induced organic anion transporter 1 (Oat1) renal expression by furosemide on the pharmacokinetics of organic anions.	Furosemide	77-87	solute carrier family 22 member 6	Rattus norvegicus	51-55	
27282888-3	2017	This study was undertaken to simultaneously evaluate the effects of furosemide pretreatment on organic anion transporter 1 (Oat1) and multidrug resistance protein 2 (Mrp2) renal expressions, on p-aminohippurate (PAH) pharmacokinetics and on renal and urinary PAH levels in rats.	Furosemide	68-78	solute carrier family 22 member 6	Rattus norvegicus	95-122	
27282888-3	2017	This study was undertaken to simultaneously evaluate the effects of furosemide pretreatment on organic anion transporter 1 (Oat1) and multidrug resistance protein 2 (Mrp2) renal expressions, on p-aminohippurate (PAH) pharmacokinetics and on renal and urinary PAH levels in rats.	Furosemide	68-78	solute carrier family 22 member 6	Rattus norvegicus	124-128	
27282888-8	2017	RESULTS: Furosemide pretreatment increased both the expression of Oat1 and Mrp2.	Furosemide	9-19	solute carrier family 22 member 6	Rattus norvegicus	66-70	
16628676-2	2006	The objective of this work was to study, in rats with acute extrahepatic cholestasis, the cortical renal expression of the organic anion transporter 1 (OAT1) and the organic anion transporter 3 (OAT3), in association with the pharmacokinetics and renal excretion of furosemide (FS).	Furosemide	278-280	solute carrier family 22 member 6	Rattus norvegicus	123-150	
16628676-2	2006	The objective of this work was to study, in rats with acute extrahepatic cholestasis, the cortical renal expression of the organic anion transporter 1 (OAT1) and the organic anion transporter 3 (OAT3), in association with the pharmacokinetics and renal excretion of furosemide (FS).	Furosemide	278-280	solute carrier family 22 member 6	Rattus norvegicus	152-156	
16628676-12	2006	In conclusion, acute obstructive jaundice is associated with an upregulation of OAT1 and OAT3, which might explain, at least in part, the increased systemic and renal elimination of FS.	Furosemide	182-184	solute carrier family 22 member 6	Rattus norvegicus	80-84	
12897087-0	2003	Up-regulation of organic anion transporter 1 protein is induced by chronic furosemide or hydrochlorothiazide infusion in rat kidney.	Furosemide	75-85	solute carrier family 22 member 6	Rattus norvegicus	17-44	
12897087-9	2003	Although OAT1 protein abundance in cortical homogenates was increased by furosemide infusion (271 +/- 35 vs 100 +/- 15%, P < 0.05), Na-K-ATPase alpha1 subunit protein abundance was not affected (113 +/- 14 vs 100 +/- 8%, P = 0.42).	Furosemide	73-83	solute carrier family 22 member 6	Rattus norvegicus	9-13	
12897087-12	2003	CONCLUSION: Chronic furosemide or hydrochlorothiazide infusion caused increases in OAT1 protein abundance in rat kidney.	Furosemide	20-30	solute carrier family 22 member 6	Rattus norvegicus	83-87	
10991988-10	2000	Although the loop diuretics had little trans-stimulation effect on [(14)C]PAH efflux via rOAT1, the rOAT1-mediated furosemide uptake was observed.	Furosemide	115-125	solute carrier family 22 member 6	Rattus norvegicus	100-105	
10991988-4	2000	p-[(14)C]Aminohippurate (PAH) uptake by rOAT1-expressing oocytes was inhibited in the presence of a thiazide (chlorothiazide, cyclothiazide, hydrochlorothiazide), a loop diuretic (bumetanide, ethacrynic acid, furosemide), or a carbonic anhydrase inhibitor (acetazolamide, ethoxzolamide, methazolamide).	Furosemide	209-219	solute carrier family 22 member 6	Rattus norvegicus	40-45