PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31730632-5	2019	We then derived a mathematical model that can predict the conjugation capacities of mutant UGT1A1s by using results of substrate docking in silico and results of in vitro analysis of glucuronidation of acetaminophen and 17beta-estradiol by UGT1A1s.	Acetaminophen	202-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	91-97	
31730632-5	2019	We then derived a mathematical model that can predict the conjugation capacities of mutant UGT1A1s by using results of substrate docking in silico and results of in vitro analysis of glucuronidation of acetaminophen and 17beta-estradiol by UGT1A1s.	Acetaminophen	202-215	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	240-246	
28932176-2	2017	The present research was aimed to study the effect of 2 important single nucleotide polymorphisms (SNPs; rs8330 and rs10929303) of UGT1A1 gene on glucuronidation status of acetaminophen in healthy volunteers (n = 109).	Acetaminophen	172-185	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	131-137	
28932176-4	2017	The in vivo activity of UGT1A1 was investigated by high-performance liquid chromatography-based analysis of glucuronidation status (ie, acetaminophen and acetaminophen glucuronide) in human volunteers after oral intake of a single dose (1000 mg) of acetaminophen.	Acetaminophen	136-149	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30	
28932176-4	2017	The in vivo activity of UGT1A1 was investigated by high-performance liquid chromatography-based analysis of glucuronidation status (ie, acetaminophen and acetaminophen glucuronide) in human volunteers after oral intake of a single dose (1000 mg) of acetaminophen.	Acetaminophen	154-167	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	24-30	
27781231-4	2016	The control cells were treated with 10 mM acetaminophen without genistein to compare with the effects of the combination of acetaminophen and genistein on the expression of UGT1A1, 1A6 and 1A9, Nrf2 and Keap1 mRNAs, as well as the expression of Nrf2 and Keap1 proteins, which were tested by western blotting.	Acetaminophen	124-137	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	173-179	
23408116-7	2013	Cotransfection studies demonstrated an inhibitory effect of exon 5b containing cDNAs on acetaminophen glucuronidation by UGT1A1 and UGT1A6 cDNAs containing exon 5a.	Acetaminophen	88-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	121-127	
23279026-4	2012	It is well-known that UGT1A1, UGT1A6 and UGT1A9 enzymes glucuronidate acetaminophen.	Acetaminophen	70-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	22-28	
21235620-8	2011	Dasatinib and imatinib also inhibited UGT1A1-mediated paracetamol glucuronidation.	Acetaminophen	54-65	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	38-44	
15180166-2	2004	The underlying cause of GS is a polymorphism in the promotor region of the uridine diphosphate glucuronosyltransferase isoform 1A1 gene (UGT1A1*28), its encoded enzyme being responsible for the glucuronidation of bilirubin and presumably acetaminophen.	Acetaminophen	238-251	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143	
15180166-4	2004	Patients with GS might be more susceptible to unexpected side effects while taking acetaminophen and other drugs which are substrates of UGT1A1.	Acetaminophen	83-96	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	137-143	
15180166-9	2004	The metabolic ratios unchanged acetaminophen/acetaminophen glucuronide in UGT1A1-wildtypes, heterozygotes and mutants showed no statistically significant differences.	Acetaminophen	31-44	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80	
24104197-4	2014	The polymorphisms evaluated included those in genes encoding putative acetaminophen-metabolizing enzymes (UGT1A1, UGT1A6, UGT1A9, UGT2B15, SULT1A1, CYP2E1, and CYP3A5) as well as CD44 and BHMT1.	Acetaminophen	70-83	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	106-112	
21726413-8	2011	Glucuronidation activity towards acetaminophen of p.P364L-UGT1A1, 1A6, 1A7, 1A8, 1A9 and 1A10 was 50.3%, 46.4%, 17.2%, 44.1%, 5.0% and 42.8%, respectively, of wild-type.	Acetaminophen	33-46	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	58-64	
21245288-9	2011	Consistent with previous reports, APAP was glucuronidated by recombinant UGT1A1, UGT1A6, UGT1A9, and UGT2B15.	Acetaminophen	34-38	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	73-79	
11714888-9	2001	APAP-UGT activities correlated best with propofol-UGT (r = 0.85; UGT1A9) and bilirubin-UGT (r = 0.66; UGT1A1) activities, but poorly with UGT1A6 protein (r = 0.30).	Acetaminophen	0-4	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	102-108