PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17576790-3	2007	The K(m) value of recombinant UGT2B10 for nicotine (0.29 mM) was similar to that determined for human liver microsomes (0.33 mM), whereas the K(m) value of UGT1A4 for nicotine was almost 10-fold greater (2.4 mM).	Nicotine	167-175	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	156-162	
20133892-6	2010	Nicotine was found to selectively inhibit UGT2B10 but not UGT1A4 activity.	Nicotine	0-8	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	58-64	
17909004-3	2007	In the present study, microsomes of UGT2B10-overexpressing HEK293 cells exhibited high N-glucuronidation activity against both nicotine and cotinine with apparent KM"s that were 37- and 3-fold lower than that observed for microsomes of UGT1A4-overexpressing cells against nicotine and cotinine, respectively.	Nicotine	127-135	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	236-242	
15470160-4	2005	Trans-3"-hydroxycotinine N-glucuronidation in human liver microsomes was significantly correlated with nicotine and cotinine N-glucuronidations, which are catalyzed mainly by UDP-glucuronosyltransferase (UGT)1A4 and was inhibited by imipramine and nicotine, which are substrates of UGT1A4.	Nicotine	103-111	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	204-211	
16141602-5	2005	Nicotine and cotinine are glucuronidated to N-glucuronides mainly by UGT1A4 and partly by UGT1A9.	Nicotine	0-8	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	69-75	
15470160-4	2005	Trans-3"-hydroxycotinine N-glucuronidation in human liver microsomes was significantly correlated with nicotine and cotinine N-glucuronidations, which are catalyzed mainly by UDP-glucuronosyltransferase (UGT)1A4 and was inhibited by imipramine and nicotine, which are substrates of UGT1A4.	Nicotine	103-111	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	282-288	
14570768-9	2003	The glucuronidation of nicotine and cotinine by heterologously expressed UGT1A3, UGT1A4, and UGT1A9 was also determined.	Nicotine	23-31	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	81-87	
14570768-13	2003	UGT1A4 Supersomes also catalyzed cotinine N-glucuronidation, but at one-tenth the rate of nicotine glucuronidation.	Nicotine	90-98	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	0-6	
14570768-15	2003	Both propofol, a UGT1A9 substrate, and imipramine, a UGT1A4 substrate, inhibited the glucuronidation of nicotine and cotinine by human liver microsomes.	Nicotine	104-112	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	53-59	
14570768-16	2003	Taken together, these data support a role for both UGT1A9 and UGT1A4 in the catalysis of nicotine and cotinine N-glucuronidation.	Nicotine	89-97	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	62-68	
12433823-7	2002	Nicotine and cotinine N-glucuronidations in pooled human liver microsomes were competitively inhibited by bilirubin as a substrate for UGT1A1 (K(i) = 3.9 and 3.3 micro M), imipramine as a substrate for UGT1A4 (K(i) = 6.1 and 2.7 micro M), and propofol as a substrate for UGT1A9 (K(i) = 6.0 and 12.0 micro M).	Nicotine	0-8	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	202-208	
12433823-10	2002	In conclusion, the involvement of UGT1A1 and UGT1A9 as well as UGT1A4 in nicotine and cotinine N-glucuronidations in human liver microsomes was suggested, although the contributions of each UGT isoform could not be determined conclusively.	Nicotine	73-81	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	63-69