PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	40-43	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	119-125
22227166-0	2012	The association of the UGT1A8, SLCO1B3 and ABCC2/ABCG2 genetic polymorphisms with the pharmacokinetics of mycophenolic acid and its phenolic glucuronide metabolite in Chinese individuals.	Mycophenolic Acid	106-123	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	23-29
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	48-51	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	119-125
22269145-10	2012	Taken together, these data suggest that ETR and ETR metabolites are substrates of CYP2C19, CYP3A4, CYP2C9, UGT1A3, and UGT1A8 and that ETR is a PXR-dependent modulator of CYP3A4 mRNA levels.	etravirine	48-51	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	119-125
21189330-9	2011	We conclude that limited in vivo metabolism of AR-67 by UGT1A1 may partly explain the absence of AR-67 glucuronides in plasma and hypothesize that UGT1A8- and CYP3A-mediated biotransformation within the gastrointestinal epithelium may provide protective mechanisms against AR-67 gastrointestinal toxicity.	Argon	47-49	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	147-153
22031623-9	2012	Inhibition studies using typical UGT substrates suggested that darexaban glucuronidation in both HLM and HIM was mainly catalyzed by UGT1A8, -1A9, and -1A10.	darexaban	63-72	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	133-139
21524190-7	2011	In addition, both mycophenolic acid (substrate of UGT1A9) and emodin (substrate of UGT1A8 and UGT1A10) could inhibit the glucuronidation of Picroside II with the half maximal inhibitory concentration (IC(50)) values of 173.6 and 76.2 muM, respectively.	Mycophenolic Acid	18-35	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	83-89
21524190-7	2011	In addition, both mycophenolic acid (substrate of UGT1A9) and emodin (substrate of UGT1A8 and UGT1A10) could inhibit the glucuronidation of Picroside II with the half maximal inhibitory concentration (IC(50)) values of 173.6 and 76.2 muM, respectively.	Emodin	62-68	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	83-89
21524190-7	2011	In addition, both mycophenolic acid (substrate of UGT1A9) and emodin (substrate of UGT1A8 and UGT1A10) could inhibit the glucuronidation of Picroside II with the half maximal inhibitory concentration (IC(50)) values of 173.6 and 76.2 muM, respectively.	picroside II	140-152	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	83-89
21953915-6	2012	Among the tested human UGT isoforms, UGT1A7, UGT1A8, and UGT1A9 showed the highest activity for the conjugation of hydroxylated TCC metabolites followed by UGT1A1, UGT1A3, and UGT1A10.	triclocarban	128-131	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	45-51
21191764-5	2010	Jaceosidin glucuronidation was catalyzed by UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, and UGT1A10.	jaceosidin glucuronidation	0-26	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	68-74
20297805-4	2010	The results also indicated that UGT1A1, UGT1A7, UGT1A8, UGT1A9, UGT1A10 and UGT2B7 are the most important six UGT isoforms for metabolizing the chosen flavones.	Flavones	151-159	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	48-54
20797434-10	2010	The apparent K(m) or S(50) values were high: 1.2mM+-0.23 for 1R,2R-O-desmethyltramadol with UGT1A8 and 1.84+-1.2 and 4.6+-2.0mM for 1S,2S- and 1R,2R-O-desmethyltramadol enantiomers with UGT2B7, respectively.	2r-o-desmethyltramadol	64-86	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	92-98
20565459-5	2010	When patients were divided according to the immunosuppressive co-treatment, a significant effect of UGT1A8 2 was found in those co-treated with CsA (HR = 2.414; 95%CI (1.089, 5.354); P = 0.0301) but not TAC or SIR (P = 0.4331).	Cyclosporine	144-147	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	100-106
20565459-6	2010	CONCLUSION: These results suggest that a possible inhibition of biliary excretion of MPA metabolites by CsA and a decreased intestinal production of these metabolites in UGT1A8 2 carriers may be protective factors against MMF-induced diarrhoea.	Mycophenolic Acid	222-225	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	170-176
20053997-4	2010	Xenobiotic (XRE) and antioxidant (ARE) response elements were detected in the promoters of UGT1A8, UGT1A9, and UGT1A10.	xre	12-15	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	91-97
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	hesperetin	76-86	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	7-o-glucuronide	130-145	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
20056724-4	2010	UGT1A9, UGT1A1, UGT1A7, UGT1A8, and UGT1A3 are the major enzymes catalyzing hesperetin glucuronidation, the latter only producing 7-O-glucuronide, whereas UGT1A7 produced mainly 3"-O-glucuronide.	3"-o-glucuronide	178-194	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
20053997-5	2010	Reporter gene experiments demonstrated XRE-mediated induction by dioxin in addition to tert-butylhydroquinone (ARE)-mediated induction of UGT1A8 and UGT1A10, which are expressed in extrahepatic tissue in humans in vivo.	2-tert-butylhydroquinone	87-109	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	138-144
20053997-5	2010	Reporter gene experiments demonstrated XRE-mediated induction by dioxin in addition to tert-butylhydroquinone (ARE)-mediated induction of UGT1A8 and UGT1A10, which are expressed in extrahepatic tissue in humans in vivo.	ACARBOSE DERIVED PENTASACCHARIDE	111-114	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	138-144
19494809-7	2009	Cyclosporine-treated UGT1A8*2/*2 (518GG) patients had an 18% higher MPA AUC(0-12) compared with noncarriers.	Cyclosporine	0-12	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	21-27
19082692-7	2009	UGT1A9, and to a lesser extent UGT1A6, UGT1A7 and UGT1A8, catalyzed the O-glucuronidation of gaboxadol in vitro.	gaboxadol	93-102	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	50-56
19318555-5	2009	Whereas the UGT1A8p.Ala173Gly variant exhibited a 3-fold (P<0.005) decrease in glucuronidation activity against SAHA compared with wild-type UGT1A8, the UGT1A8p.Cys277Tyr variant exhibited no detectable glucuronidation activity; a similar lack of detectable glucuronidation activity was observed for the UGT1A10p.Gly139Lys variant.	Vorinostat	115-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	12-19
19318555-5	2009	Whereas the UGT1A8p.Ala173Gly variant exhibited a 3-fold (P<0.005) decrease in glucuronidation activity against SAHA compared with wild-type UGT1A8, the UGT1A8p.Cys277Tyr variant exhibited no detectable glucuronidation activity; a similar lack of detectable glucuronidation activity was observed for the UGT1A10p.Gly139Lys variant.	Vorinostat	115-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	12-18
19318555-5	2009	Whereas the UGT1A8p.Ala173Gly variant exhibited a 3-fold (P<0.005) decrease in glucuronidation activity against SAHA compared with wild-type UGT1A8, the UGT1A8p.Cys277Tyr variant exhibited no detectable glucuronidation activity; a similar lack of detectable glucuronidation activity was observed for the UGT1A10p.Gly139Lys variant.	Vorinostat	115-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	156-163
19545173-2	2009	The results indicated that these isoflavones are metabolized most rapidly at three different concentrations by one of these four UGT isoforms: UGT1A1, UGT1A8, UGT1A9 and UGT1A10.	Isoflavones	33-44	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	151-157
19486934-5	2009	It has been reported that UDP-glucuronosyltransferase (UGT) 1A1, UGT1A8, UGT1A9, and UGT1A10 are enzymes for raloxifene glucuronidation, and UGT1A8 and UGT1A10 are absent in the human liver, whereas UGT1A1, UGT1A8, UGT1A9, and UGT1A10 are present in the human intestine.	Raloxifene Hydrochloride	109-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	65-71
19486934-5	2009	It has been reported that UDP-glucuronosyltransferase (UGT) 1A1, UGT1A8, UGT1A9, and UGT1A10 are enzymes for raloxifene glucuronidation, and UGT1A8 and UGT1A10 are absent in the human liver, whereas UGT1A1, UGT1A8, UGT1A9, and UGT1A10 are present in the human intestine.	Raloxifene Hydrochloride	109-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	141-147
19486934-5	2009	It has been reported that UDP-glucuronosyltransferase (UGT) 1A1, UGT1A8, UGT1A9, and UGT1A10 are enzymes for raloxifene glucuronidation, and UGT1A8 and UGT1A10 are absent in the human liver, whereas UGT1A1, UGT1A8, UGT1A9, and UGT1A10 are present in the human intestine.	Raloxifene Hydrochloride	109-119	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	141-147
19244109-8	2009	These results suggest that functional polymorphisms in TAM-metabolizing UGTs, including UGT2B7 and potentially UGT1A8, may be important in interindividual variability in TAM metabolism and response to TAM therapy.	Tamoxifen	55-58	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	111-117
19244109-8	2009	These results suggest that functional polymorphisms in TAM-metabolizing UGTs, including UGT2B7 and potentially UGT1A8, may be important in interindividual variability in TAM metabolism and response to TAM therapy.	Tamoxifen	170-173	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	111-117
19244109-8	2009	These results suggest that functional polymorphisms in TAM-metabolizing UGTs, including UGT2B7 and potentially UGT1A8, may be important in interindividual variability in TAM metabolism and response to TAM therapy.	Tamoxifen	170-173	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	111-117
17591679-8	2007	Kinetic and inhibition analyses suggested that the thyroxine glucuronidation in human jejunum microsomes was mainly catalyzed by UGT1A8 and UGT1A10 and to a lesser extent by UGT1A1, and the activity in human kidney microsomes was mainly catalyzed by UGT1A7, UGT1A9, and UGT1A10.	Thyroxine	51-60	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	129-135
18838507-12	2009	UGT1A4, UGT1A8, and UGT1A10 also were found to catalyze the formation of VPAG in vitro.	valproic acid glucuronide	73-77	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	8-14
18946804-1	2008	The aim was to investigate the effect of UGT1A9, UGT1A8, UGT2B7 and ABCC2 polymorphism on the pharmacokinetics of mycophenolic acid (MPA) and its metabolites phenolic glucuronide (MPAG) and acyl glucuronide (AcMPAG) in Chinese renal transplant recipients.	Mycophenolic Acid	114-131	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	49-55
18602884-5	2008	All of the chimeras and UGT1A8 and UGT1A9 had 7-hydroxy-(4-trifluoromethyl)coumarin (HFC) O-glucuronidating activity.	7-hydroxy-(4-trifluoromethyl)coumarin	46-83	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
17921187-7	2008	Studies with extrahepatic UGT isoforms showed that UGT1A8 metabolized 7- and 8-hydroxywarfarin and that UGT1A10 glucuronidated 4"-, 6-, 7-, and 8-hydroxywarfarin.	7- and 8-hydroxywarfarin	70-94	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	51-57
18832479-8	2009	It is interesting to note that only Mut 4 was active toward 3-hydroxydesloratadine O-glucuronidation that is specific for UGT1A8.	3-hydroxydesloratadine	60-82	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	122-128
18568343-8	2008	RESULTS: Mycophenolic acid dose-corrected trough concentrations were 60% higher in subjects heterozygous or homozygous for UGT1A8*2 than in those with the wild type (p = 0.02); however, this effect was dependent on concomitant calcineurin inhibitor.	Mycophenolic Acid	9-26	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	123-129
18568343-9	2008	When subjects were stratified by calcineurin inhibitor status, the UGT1A8*2 effect was only apparent in the tacrolimus group (p < 0.01).	Tacrolimus	108-118	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	67-73
18430559-4	2008	Recombinant human UGT1A8 also metabolised both genistein and daidzein, whereas UGT1A6 was specific to genistein and UGTs 2B7 and 2B15 were inactive, or only marginally active, with either isoflavone as substrate.	Genistein	47-56	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	18-24
18430559-4	2008	Recombinant human UGT1A8 also metabolised both genistein and daidzein, whereas UGT1A6 was specific to genistein and UGTs 2B7 and 2B15 were inactive, or only marginally active, with either isoflavone as substrate.	daidzein	61-69	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	18-24
18187562-11	2008	The results strongly suggest that UGT1A1 and UGT1A8 are isozymes involved in morphine-6-glucuronidation in vivo, as is UGT2B7 in humans.	Morphine	77-85	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	45-51
17875670-5	2007	All the UGTs examined catalyzed the formation of T4 phenolic glucuronide except UGT1A4; the highest activity was detected with UGT1A3, UGT1A8, and UGT1A10, followed by UGT1A1 and UGT2B4.	Glucuronides	61-72	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	135-141
17875670-6	2007	Formation of T3 phenolic glucuronide was observed in the order of UGT1A8 > UGT1A10 > UGT1A3 > UGT1A1; trace activity was observed with UGT1A6 and UGT1A9.	t3 phenolic glucuronide	13-36	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	66-72
17211619-1	2007	OBJECTIVE: UGT1A8 and UGT2B7 are important uridine diphosphate-glucuronosyltransferase isoforms for the glucuronidation of mycophenolic acid (MPA).	Mycophenolic Acid	123-140	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	11-17
17628876-4	2007	The phenolic glucuronidation of the curcuminoids was predominantly catalyzed by hepatic UGT1A1 and intestinal UGT1A8 and 1A10, whereas UGT1A9, 2B7, and 1A8 exhibited high activities for hexahydro-curcuminoids.	curcuminoids	36-48	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	110-125
17339869-0	2007	The impact of UGT1A8, UGT1A9, and UGT2B7 genetic polymorphisms on the pharmacokinetic profile of mycophenolic acid after a single oral dose in healthy volunteers.	Mycophenolic Acid	97-114	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	14-20
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	mycophenolic acid glucuronide	110-114	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	Glucuronides	134-146	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	Mycophenolic Acid	150-167	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	Mycophenolic Acid	110-113	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	Mycophenolic Acid	237-258	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17339869-1	2007	We studied whether polymorphisms in the UGT1A8, UGT1A9, and UGT2B7 genes, the enzymes producing the phenolic (MPAG) and acyl (AcMPAG) glucuronides of mycophenolic acid (MPA), could contribute to the interindividual variation observed in mycophenolate mofetil (MMF) pharmacokinetics (PKs).	Mycophenolic Acid	260-263	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	40-46
17151191-4	2007	Although UGT1A8 and 1A3 also catalyzed the glucuronidation of etoposide, their activities were approximately 10 and 1% of UGT1A1.	Etoposide	62-71	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	9-15
17211619-1	2007	OBJECTIVE: UGT1A8 and UGT2B7 are important uridine diphosphate-glucuronosyltransferase isoforms for the glucuronidation of mycophenolic acid (MPA).	Mycophenolic Acid	142-145	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	11-17
16790554-0	2006	Influence of nonsynonymous polymorphisms of UGT1A8 and UGT2B7 metabolizing enzymes on the formation of phenolic and acyl glucuronides of mycophenolic acid.	phenolic and acyl glucuronides	103-133	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	44-50
16790554-0	2006	Influence of nonsynonymous polymorphisms of UGT1A8 and UGT2B7 metabolizing enzymes on the formation of phenolic and acyl glucuronides of mycophenolic acid.	Mycophenolic Acid	137-154	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	44-50
16790554-2	2006	This study examines the role of the genetic variants of UDP-glucuronosyltransferase (UGT) 1A8 and 2B7 enzymes involved in the formation of the primary metabolite of MPA, the inactive phenolic glucuronide (MPAG), and the reactive acyl glucuronide (AcMPAG).	Glucuronides	192-203	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	56-101
16790554-2	2006	This study examines the role of the genetic variants of UDP-glucuronosyltransferase (UGT) 1A8 and 2B7 enzymes involved in the formation of the primary metabolite of MPA, the inactive phenolic glucuronide (MPAG), and the reactive acyl glucuronide (AcMPAG).	mycophenolic acid glucuronide	205-209	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	56-101
16790554-2	2006	This study examines the role of the genetic variants of UDP-glucuronosyltransferase (UGT) 1A8 and 2B7 enzymes involved in the formation of the primary metabolite of MPA, the inactive phenolic glucuronide (MPAG), and the reactive acyl glucuronide (AcMPAG).	acyl glucuronide	229-245	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	56-101
16790554-2	2006	This study examines the role of the genetic variants of UDP-glucuronosyltransferase (UGT) 1A8 and 2B7 enzymes involved in the formation of the primary metabolite of MPA, the inactive phenolic glucuronide (MPAG), and the reactive acyl glucuronide (AcMPAG).	mycophenolic acid acyl glucuronide	247-253	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	56-101
16595710-3	2006	In contrast, the activity of DHT monoglucuronidation was high and was found in UGT2B17, UGT2B15, UGT1A8, and UGT1A4 in descending order.	Dihydrotestosterone	29-32	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	97-103
16790554-6	2006	Upon stable expression in human embryonic kidney 293 cells, the UGT1A8*3 (C277Y), *5 (G173A240), *7 (A231T), *8 (S43L), and *9 (N53G) proteins were associated with the most profound decreases in the formation of MPAG and AcMPAG, indicating that these amino acids are critical for substrate binding and enzyme function.	mycophenolic acid glucuronide	212-216	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	64-70
16790554-6	2006	Upon stable expression in human embryonic kidney 293 cells, the UGT1A8*3 (C277Y), *5 (G173A240), *7 (A231T), *8 (S43L), and *9 (N53G) proteins were associated with the most profound decreases in the formation of MPAG and AcMPAG, indicating that these amino acids are critical for substrate binding and enzyme function.	mycophenolic acid acyl glucuronide	221-227	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	64-70
16595710-0	2006	Human UDP-glucuronosyltransferase, UGT1A8, glucuronidates dihydrotestosterone to a monoglucuronide and further to a structurally novel diglucuronide.	Dihydrotestosterone	58-77	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	35-41
16595710-4	2006	Among the 12 UGT isoforms tested, only UGT1A8 was capable of producing DHT diglucuronide from DHT.	dihydrotestosterone glucuronide	71-88	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	39-45
16595710-0	2006	Human UDP-glucuronosyltransferase, UGT1A8, glucuronidates dihydrotestosterone to a monoglucuronide and further to a structurally novel diglucuronide.	monoglucuronide	83-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	35-41
16595710-0	2006	Human UDP-glucuronosyltransferase, UGT1A8, glucuronidates dihydrotestosterone to a monoglucuronide and further to a structurally novel diglucuronide.	diglucuronide	135-148	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	35-41
16595710-4	2006	Among the 12 UGT isoforms tested, only UGT1A8 was capable of producing DHT diglucuronide from DHT.	Dihydrotestosterone	71-74	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	39-45
12642472-9	2003	UGT1A8, an intestine-specific UGT, had the highest V(max)/K(m) for EGCG but low activity with EGC.	epigallocatechin gallate	67-71	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	dht monoglucuronide	18-37	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	211-217
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	5"-diphosphoglucuronic acid	104-131	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	211-217
16595710-2	2006	Incubation of the DHT monoglucuronide with 12 cDNA-expressed recombinant human UGT isoforms and uridine 5"-diphosphoglucuronic acid resulted in a low but measurable DHT diglucuronidation activity primarily with UGT1A8, a gastrointestinal UGT, and to a lesser extent with UGT1A1 and UGT1A9.	Dihydrotestosterone	18-21	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	211-217
16480962-6	2006	Only UGT1A4 catalyzed the N-linked glucuronidation of 4-HO-TAM among recombinant human UGT isoforms (UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, UGT2B4, UGT2B7, UGT2B15, and UGT2B17) expressed in insect cells.	4-ho-tam	54-62	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	141-147
16092069-4	2005	The identification of the metabolites formed was elucidated using HPLC with diode array detection as well as HPLC/API-ES MS. XN was efficiently glucuronidated by UGT 1 A 8, 1 A 9, and 1 A 10; further important UGTs were UGT 1 A 1, 1 A 7, and 2 B 7.	xanthohumol	125-127	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	162-178
15949398-9	2005	The levels of UGT1A1, UGT1A8, and UGT1A10 mRNA expression were significantly increased in the cells treated with 25 micromol/L sulforaphane compared to that in the controls (P = 0.006, P = 0.017, and P = 0.008 respectively).	sulforaphane	127-139	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
12920167-10	2003	Furthermore, the high activity of UGT1A8 and 1A10 toward some of the substrates indicates that extrahepatic enzymes might play a role in the metabolism of anabolic androgenic steroids.	Steroids	175-183	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	34-40
16821585-4	2006	RESULTS: Three independent lines of enquiry indicated that, in the tumour specimens, SN-38 was glucuronidated primarily by UGT1A1, the isozyme generally recognised as being responsible for hepatic detoxification of this compound, while with NU/ICRF 505 two candidate isoforms emerged - UGT1A8 and/or UGT1A10 - both of which are not normally expressed in the liver.	Irinotecan	85-90	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	286-292
16715376-9	2006	Incubations with various cDNA-expressed UDP-glucuronosyltransferases indicated that the isozymes UGT1A1, UGT1A6, UGT1A8, and UGT1A9 were responsible for glucuronidation of 8-PN.	8-prenylnaringenin	172-176	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	113-119
16339389-5	2006	The four UGT1A-fulvestrant conjugating enzymes glucuronidate this substrate at position 3, whereas only UGT1A8 also produces fulvestrant-17-glucuronide.	fulvestrant-17-glucuronide	125-151	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	104-110
16620709-11	2006	(2) The mRNA expression of Nrf2, UGT1A8, and UGT1A10 increased by 1.8-9.2 times after the addition of EGCG (all P < 0.05).	epigallocatechin gallate	102-106	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	33-39
16620709-16	2006	(4) The basal levels of UGT1A8 and UGT1A10 mRNA expression in the Caco-2-siNrf2 and HT-29-siNrf2 cells were lower by 15%-65% in comparison with those in control, and the induction of genes by EGCG was largely attenuated in them (all P > 0.05).	epigallocatechin gallate	192-196	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
16620709-19	2006	EGCG induces the expression of UGT1A, UGT1A8 and UGT1A10 genes via a Nrf2-dependent mechanism.	epigallocatechin gallate	0-4	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	38-44
16397224-0	2006	Characterization of common UGT1A8, UGT1A9, and UGT2B7 variants with different capacities to inactivate mutagenic 4-hydroxylated metabolites of estradiol and estrone.	Estradiol	143-152	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	27-33
16397224-0	2006	Characterization of common UGT1A8, UGT1A9, and UGT2B7 variants with different capacities to inactivate mutagenic 4-hydroxylated metabolites of estradiol and estrone.	Estrone	157-164	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	27-33
16397224-2	2006	In this study, we conducted functional analyses of genetic variants in the UDP-glucuronosyltransferase UGT1A8, UGT1A9, and UGT2B7 enzymes primarily involved in the inactivation of 4-OHCEs.	4-ohces	180-187	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	103-109
15788539-7	2005	The major UGT isoforms identified were UGT1A6, UGT1A7, and UGT1A9 for 4-methylumbelliferone; UGT1A6 and UGT1A8 for 1-naphthol; UGT2B7 for naloxone; UGT1A3 and UGT2B7 for ketoprofen; and UGT1A4 for trifluoperazine.	1-naphthol	115-125	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	104-110
15334623-5	2004	Out of ten recombinant human UDP-glucuronosyltransferases (UGTs), UGT1A1, UGT1A3, UGT1A8 and UGT2B15 exhibited catalytic activity with respect to the formation of 3-hydroxydesloratadine-glucuronide.	3-hydroxydesloratadine-glucuronide	163-197	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	82-88
12642472-9	2003	UGT1A8, an intestine-specific UGT, had the highest V(max)/K(m) for EGCG but low activity with EGC.	gallocatechol	67-70	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
12018987-7	2002	Human UGT1A1, UGT1A8, and UGT1A9 were shown to be especially active in conjugation of both flavonoids, whereas UGT1A4 and UGT1A10 and the isoenzymes from the UGTB family, UGT2B7 and UGT2B15, were less efficient.	Flavonoids	91-101	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	14-20
12433820-0	2002	Troglitazone glucuronidation in human liver and intestine microsomes: high catalytic activity of UGT1A8 and UGT1A10.	Troglitazone	0-12	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	97-103
12433820-14	2002	The troglitazone glucuronosyltransferase activity in human jejunum microsomes was strongly inhibited by emodin (IC(50) = 15.6 micro M), a typical substrate of UGT1A8 and UGT1A10, rather than by bilirubin (IC(50) = 154.0 micro M).	Bilirubin	194-203	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	159-165
12433820-15	2002	Therefore, it is suggested that the troglitazone glucuronidation in human intestine might be mainly catalyzed by UGT1A8 and UGT1A10.	Troglitazone	36-48	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	113-119
12019197-6	2002	Based on rates of raloxifene glucuronidation and known extrahepatic expression, UGT1A8 and 1A10 appear to be primary contributors to raloxifene glucuronidation in human jejunum microsomes.	Raloxifene Hydrochloride	133-143	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	80-86
9605424-6	1998	The glucuronidation of propofol is catalysed by UGT1A8/9 suggesting higher levels of this isoform in the kidney.	Propofol	23-31	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	48-54
10497143-7	1999	The catalytic activity of stably expressed UGT1A8 toward catechol estrogens, coumarins, flavonoids, anthraquinones, and phenolic compounds was much higher than that of UGT1A10.	catechol	57-65	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	43-49
10497143-7	1999	The catalytic activity of stably expressed UGT1A8 toward catechol estrogens, coumarins, flavonoids, anthraquinones, and phenolic compounds was much higher than that of UGT1A10.	Coumarins	77-86	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	43-49
10497143-7	1999	The catalytic activity of stably expressed UGT1A8 toward catechol estrogens, coumarins, flavonoids, anthraquinones, and phenolic compounds was much higher than that of UGT1A10.	Flavonoids	88-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	43-49
10497143-7	1999	The catalytic activity of stably expressed UGT1A8 toward catechol estrogens, coumarins, flavonoids, anthraquinones, and phenolic compounds was much higher than that of UGT1A10.	Anthraquinones	100-114	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	43-49
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	Bile Acids and Salts	67-77	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	Fatty Acids	79-90	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	Retinoids	92-101	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	ciprofibrate	140-152	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	Furosemide	154-164	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
10497143-8	1999	UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal.	Diflunisal	170-180	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	Coumarins	73-82	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	Anthraquinones	84-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	Flavonoids	100-110	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	catechol	132-140	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	17-hydroxyandrogens	152-171	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9705221-4	1998	Transiently expressed human UGT1A8 shows glucuronidation activities with coumarins, anthraquinones, flavonoids, phenolic compounds, catechol estrogens, 17-hydroxyandrogens, primary amines such as the carcinogen 4-aminobiphenyl, and certain opioids.	Amines	181-187	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	28-34
9647757-6	1998	UGT1A8 was most active towards the 10- and 11-hydroxy benzo(alpha)pyrenes and the preferred 2-acetylaminofluorene metabolites were the 1-, 2-, and 8-hydroxy derivatives.	10- and 11-hydroxy benzo(alpha)pyrenes	35-73	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
9647757-6	1998	UGT1A8 was most active towards the 10- and 11-hydroxy benzo(alpha)pyrenes and the preferred 2-acetylaminofluorene metabolites were the 1-, 2-, and 8-hydroxy derivatives.	2-Acetylaminofluorene	92-113	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
11179460-5	2001	Using microsome preparations from human embryonic kidney 293 cells stably expressing each of the 12 human and 11 monkey UGT enzymes cloned to date, the two EM-652-monoglucuronides were detected after incubation with microsomes containing human UGT1A1, UGT1A3, UGT1A8, UGT1A9, and monkey monUGT1A01, monUGT1A03, and monUGT1A09.	em-652-monoglucuronides	156-179	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	260-266
10688250-4	2000	Two UDP glucuronosyltransferase forms, UGT1A8 and UGT1A10, were active in the glucuronidation of mycophenolic acid.	Mycophenolic Acid	97-114	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	39-45
9316860-6	1997	Riluzole glucuronidation was inhibited most potently by propofol, a substrate for the human hepatic UGT HP4 (UGT1.8/9) isoenzyme.	Riluzole	0-8	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
9316860-6	1997	Riluzole glucuronidation was inhibited most potently by propofol, a substrate for the human hepatic UGT HP4 (UGT1.8/9) isoenzyme.	Propofol	56-64	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
34192355-6	2021	RESULTS: Our data indicated that dabrafenib had a broad inhibitory effect on 4-MU glucuronidation by inhibiting the activities of UGTs, especially on UGT1A1, UGT1A7, UGT1A8, and UGT1A9, and dabrafenib can increase the area under curve (AUC) of co-administered drug.	dabrafenib	33-43	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	166-172
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	Ticagrelor	173-183	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	132-138
34721047-7	2021	Study with recombinant human UGTs suggested that multiple UGT isoforms including UGT1A9, UGT1A7, UGT1A3, UGT1A4, UGT1A1, UGT2B7 and UGT1A8 are involved in the conversion of ticagrelor to ticagrelor-O-glucuronide with UGT1A9 showing highest catalytic activity.	ticagrelor-o-glucuronide	187-211	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	132-138
35148019-6	2022	Our aim is to study the effect of PEG400 on the absorption of baicalein on the Caco-2 monolayer, and confirm the interaction of PEG400 with UGTs (UGT1A8 and UGT1A9) and efflux transports.	polyethylene glycol 400	128-134	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	146-152
35148019-7	2022	We initially found that baicalein in the Caco-2 monolayer would be metabolized into glucuronide conjugates BG and B6G under the action of UGT1A8 and UGT1A9 on the endoplasmic reticulum membrane, and then mainly excreted to different sides by acting of MRP and BCRP.	baicalein	24-33	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	138-144
35148019-7	2022	We initially found that baicalein in the Caco-2 monolayer would be metabolized into glucuronide conjugates BG and B6G under the action of UGT1A8 and UGT1A9 on the endoplasmic reticulum membrane, and then mainly excreted to different sides by acting of MRP and BCRP.	caco-2	41-47	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	138-144
35148019-7	2022	We initially found that baicalein in the Caco-2 monolayer would be metabolized into glucuronide conjugates BG and B6G under the action of UGT1A8 and UGT1A9 on the endoplasmic reticulum membrane, and then mainly excreted to different sides by acting of MRP and BCRP.	Glucuronides	84-95	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	138-144
35148019-10	2022	In the in vitro intestinal microsome regeneration system, low concentration PEG400 decreased the Km value of UGT1A8 and UGT1A9 (key enzymes that mediate the production of BG and B6G); high concentration PEG400 enhanced the Vmax value of UGT1A8 and UGT1A9.	polyethylene glycol 400	76-82	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
35148019-10	2022	In the in vitro intestinal microsome regeneration system, low concentration PEG400 decreased the Km value of UGT1A8 and UGT1A9 (key enzymes that mediate the production of BG and B6G); high concentration PEG400 enhanced the Vmax value of UGT1A8 and UGT1A9.	polyethylene glycol 400	76-82	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	237-243
35148019-10	2022	In the in vitro intestinal microsome regeneration system, low concentration PEG400 decreased the Km value of UGT1A8 and UGT1A9 (key enzymes that mediate the production of BG and B6G); high concentration PEG400 enhanced the Vmax value of UGT1A8 and UGT1A9.	O(6)-benzylguanine	171-173	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
35148019-10	2022	In the in vitro intestinal microsome regeneration system, low concentration PEG400 decreased the Km value of UGT1A8 and UGT1A9 (key enzymes that mediate the production of BG and B6G); high concentration PEG400 enhanced the Vmax value of UGT1A8 and UGT1A9.	polyethylene glycol 400	203-209	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
35148019-10	2022	In the in vitro intestinal microsome regeneration system, low concentration PEG400 decreased the Km value of UGT1A8 and UGT1A9 (key enzymes that mediate the production of BG and B6G); high concentration PEG400 enhanced the Vmax value of UGT1A8 and UGT1A9.	polyethylene glycol 400	203-209	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	237-243
32648321-12	2020	CONCLUSIONS: CYP1A1 and CYP2C9, UGT1A1, UGT1A7, UGT1A8 and UGT1A9, and MRP4 all played important roles in the metabolism and disposition of bavachin.	bavachin	140-148	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	48-54
31979355-3	2020	Empagliflozin is metabolized and inactivated by UGT1A9 and by other related isoforms UGT2B7, UGT1A3, and UGT1A8.	empagliflozin	0-13	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	105-111
32446839-7	2020	The quantitative prediction of risks showed that the coadministration of piceatannol with drugs primarily cleared by UGT1A6, UGT1A7, UGT1A8, and UGT1A9 may result in potential food-drug interaction.	3,3',4,5'-tetrahydroxystilbene	73-84	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	133-139
31812603-4	2020	Our data indicated that PT exhibited potent inhibition against HLM, UGT1A6, UGT1A9, UGT2B7, and UGT2B15, moderate inhibition against UGT1A1, UGT1A3, UGT1A8, and UGT2B4, negligible inhibition against UGT1A4, UGT1A7, UGT1A10, and UGT2B17.	pterostilbene	24-26	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	149-155
31936432-6	2020	Stereoselective interaction was found for both UGT1A8 and CYP3A4, demonstrating that 24S-PDQ was more susceptible to glucuronidation, whereas 24R-PDQ was more prone to oxidation catalyzed by CYP3A4.	propylene diquat	85-92	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	47-53
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	perfluorodecanoic acid	64-68	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	pifithrin	70-74	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	Perfluorooctadecanoic acid	76-102	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	pfocda	104-110	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	perfluorododecanoic acid	113-118	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-8	2019	UGT1A8 was inhibited by 97.6%, 94.8%, 86.3%, 83.4% and 77.1% by PFDA, PFTA, perfluorooctadecanoic acid (PFOcDA), PFDoA and PFOS, respectively.	perfluorooctane sulfonic acid	123-127	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
31472452-11	2019	PFDA and PFOS exhibited competitive inhibition towards UGT1A1, and PFDA and PFTA showed competitive inhibition towards UGT1A8.	perfluorodecanoic acid	67-71	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	119-125
31472452-11	2019	PFDA and PFOS exhibited competitive inhibition towards UGT1A1, and PFDA and PFTA showed competitive inhibition towards UGT1A8.	pifithrin	76-80	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	119-125
31472452-13	2019	The values were calculated to be 0.3 mumoL/L and 1.3 mumoL/L for the in vivo inhibition of PFDA towards UGT1A1-and UGT1A8-catalyzed metabolism of substances, and 0.2 mumoL/L and 2.0 mumoL/L for the inhibition of PFOS towards UGT1A1 and the inhibition of PFTA towards UGT1A8, respectively.	perfluorodecanoic acid	91-95	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	115-121
31472452-13	2019	The values were calculated to be 0.3 mumoL/L and 1.3 mumoL/L for the in vivo inhibition of PFDA towards UGT1A1-and UGT1A8-catalyzed metabolism of substances, and 0.2 mumoL/L and 2.0 mumoL/L for the inhibition of PFOS towards UGT1A1 and the inhibition of PFTA towards UGT1A8, respectively.	perfluorodecanoic acid	91-95	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	267-273
31421085-6	2019	KEY FINDINGS: At 100 muM, licoricidin strongly inhibited CYP2C9, CYP2C19, CYP3A4, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15, and UGT2B17.	licoricidin	26-37	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	106-112
31515991-3	2019	Auriculasin inhibited UGT1A6, UGT1A8, UGT1A10, UGT2B7, CYP2C9, and CYP3A4 strongly at a concentration of 100 muM.	auriculasin	0-11	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	30-36
29357726-7	2019	TSI could be reduced to a relatively unstable hydroquinone intermediate by NAD(P)H: quinone oxidoreductase 1 (NQO1), and then immediately conjugated with glucuronic acid by a panel of UGTs, especially UGT1A9, UGT1A1 and UGT1A8.	Glucuronic Acid	154-169	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	220-226
30044687-7	2019	UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, UGT1A10 and UGT2B7 participated in the formation of 4-O-glucuronide, with UGT1A9 exhibiting the highest catalytic activity in this biotransformation.	4-o-glucuronide	92-107	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	24-30
30736072-8	2019	Glucuronidation of isoscopoletin and scopoletin was catalyzed by the human UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, and UGT2B17.	isoscopoletin	19-32	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	99-105
30736072-8	2019	Glucuronidation of isoscopoletin and scopoletin was catalyzed by the human UGT1A1, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, and UGT2B17.	Scopoletin	22-32	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	99-105
29025387-0	2018	In Vitro Study on Influences of UGT1A8 Gene Polymorphisms on Mycophenolate Mofetil Metabolism.	Mycophenolic Acid	61-82	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	32-38
29025387-8	2018	RESULTS: Mutations of UGT1A8 157C>A and 518C>G vectors can lead to increased activity of UDP glucuronosyltransferase enzymes and increased production of the 7-O-mycophenolic acid glucuronide metabolite, which showed 116% (P < .001) and 107% (P = .0191) production changes of 157C>A and 518C>G mutations, respectively, relative to wild-type UGT1A8.	7-o-mycophenolic acid glucuronide	163-196	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
29025387-8	2018	RESULTS: Mutations of UGT1A8 157C>A and 518C>G vectors can lead to increased activity of UDP glucuronosyltransferase enzymes and increased production of the 7-O-mycophenolic acid glucuronide metabolite, which showed 116% (P < .001) and 107% (P = .0191) production changes of 157C>A and 518C>G mutations, respectively, relative to wild-type UGT1A8.	7-o-mycophenolic acid glucuronide	163-196	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	355-361
29025387-11	2018	CONCLUSIONS: Our results showed that UGT1A8 gene polymorphisms can affect the activity of UDP glucuronosyltransferase enzyme, which may influence the elimination of mycophenolate mofetil in different patients.	Mycophenolic Acid	165-186	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	37-43
29025387-2	2018	The UDP glucuronosyltransferase enzyme is the key metabolic enzyme for mycophenolate mofetil, and UGT1A8 gene polymorphisms may affect the elimination of mycophenolate mofetil in patients.	Mycophenolic Acid	154-175	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	98-104
29025387-3	2018	Here, we conducted an in vitro study to explore the relation between UGT1A8 gene polymorphisms and mycophenolate mofetil metabolism.	Mycophenolic Acid	99-120	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	69-75
29025387-8	2018	RESULTS: Mutations of UGT1A8 157C>A and 518C>G vectors can lead to increased activity of UDP glucuronosyltransferase enzymes and increased production of the 7-O-mycophenolic acid glucuronide metabolite, which showed 116% (P < .001) and 107% (P = .0191) production changes of 157C>A and 518C>G mutations, respectively, relative to wild-type UGT1A8.	Uridine Diphosphate	95-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
29025387-8	2018	RESULTS: Mutations of UGT1A8 157C>A and 518C>G vectors can lead to increased activity of UDP glucuronosyltransferase enzymes and increased production of the 7-O-mycophenolic acid glucuronide metabolite, which showed 116% (P < .001) and 107% (P = .0191) production changes of 157C>A and 518C>G mutations, respectively, relative to wild-type UGT1A8.	Uridine Diphosphate	95-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	355-361
29328989-4	2018	100 muM phthalate monoesters exhibited negligible inhibition towards the activity of UGT1A1, UGT1A3, UGT1A6, UGT1A8, UGT1A10, UGT2B4, UGT2B7, UGT2B15 and UGT2B17.	phthalic acid	8-17	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
27916843-5	2016	Deglycosylation of AST to CAG could strongly increase the inhibitory effects towards almost all of the tested UGT isoforms, with an IC50 of 0.84 muM and 11.28 muM for UGT1A8 and UGT2B7, respectively.	GUANOSINE 5'-TRIPHOSPHATE P3-[1-(2-NITROPHENYL)ETHYL ESTER]	26-29	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	167-173
29562678-6	2018	Five UGTs (UGT1A3, UGT2B4, UGT2B7, UGT1A9 and UGT1A8) were identified that produced abundant Ib monoglucuronide, especially UGT1A3.	ib monoglucuronide	93-111	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	46-52
27496319-7	2016	The impact of 1-alpha,25-dihydroxyvitamin D3 (D3) on UGT1A8 and UGT1A10 transcription and on MPA glucuronidation was tested in human intestinal cell lines LS180, Caco-2 and HCT-116.	Calcitriol	14-44	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	53-59
27916843-8	2016	From the second plot drawn with the slopes from the Lineweaver-Burk plot versus the concentrations of CAG, the inhibition constant (Ki) was calculated to be 0.034 muM and 20.98 muM for the inhibition of UGT1A8 and UGT2B7, respectively.	GUANOSINE 5'-TRIPHOSPHATE P3-[1-(2-NITROPHENYL)ETHYL ESTER]	102-105	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	203-209
27546373-9	2016	Of the four studied SNPs, the rs1042597 variant in the UGT1A8 gene was associated with a different treatment response in negative symptoms with raloxifene treatment, whereas the rs2234693 variant in the ESR1 gene was associated with a distinct response in general psychopathology.	Raloxifene Hydrochloride	144-154	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	55-61
27546373-10	2016	In conclusion, our study suggests that genetic variants in UGT1A8 and ESR1 genes modulate the treatment response to adding raloxifene to antipsychotic treatment in postmenopausal women with schizophrenia.	Raloxifene Hydrochloride	123-133	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	59-65
29874021-9	2016	The sciadopitysin competitively inhibited the formation of 4-MU-O-glucuronide by UGT1A1, UGT1A3, UGT1A8, and UGT1A10.	4-mu-o-glucuronide	59-77	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	97-103
26632033-10	2016	ABT-751 is metabolized by UGT1A8 and to a lesser extent UGT1A4 and UGT1A1.	ABT751	0-7	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	26-32
26547877-5	2016	DPhP and DNOP weakly inhibited the activities of UGT1A1, UGT1A7, and UGT1A8.	dphp	0-4	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	69-75
26547877-5	2016	DPhP and DNOP weakly inhibited the activities of UGT1A1, UGT1A7, and UGT1A8.	di-n-octyl phthalate	9-13	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	69-75
25903196-5	2015	(R)-zaltoprofen exhibited noncompetitive inhibition towards UGT1A8 and competitive inhibition towards UGT2B7.	(R)-Zaltoprofen	0-15	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	60-66
26317684-7	2015	Tilianin and acacetin were metabolized into different glucuronides, with UGT1A8 produced as the main isoform.	tilianin	0-8	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	73-79
26317684-7	2015	Tilianin and acacetin were metabolized into different glucuronides, with UGT1A8 produced as the main isoform.	acacetin	13-21	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	73-79
26317684-7	2015	Tilianin and acacetin were metabolized into different glucuronides, with UGT1A8 produced as the main isoform.	Glucuronides	54-66	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	73-79
26317684-8	2015	Assessment of enzyme kinetics in UGT1A8, human liver microsomes and human intestinal microsomes revealed that compared with tilianin, acacetin displayed lower Km (0.6-, 0.7- and 0.6-fold, respectively), higher Vmax (20-, 60- and 230-fold, respectively) and higher clearance (30-, 80- and 300-fold, respectively).	acacetin	134-142	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	33-39
26957994-6	2015	Furthermore, concentration-dependent behaviour was determined for the inhibition of oleanolic acid and betulinic acid towards UGT1A6 and UGT1A8.	Oleanolic Acid	84-98	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	137-143
26957994-6	2015	Furthermore, concentration-dependent behaviour was determined for the inhibition of oleanolic acid and betulinic acid towards UGT1A6 and UGT1A8.	betulinic acid	103-117	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	137-143
26957994-7	2015	At various concentrations of oleanolic acid and betulinic acid, the inhibition of oleanolic acid towards UGT1A6 and UGT1A8 was higher than betulinic acid.	Oleanolic Acid	29-43	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	116-122
26957994-7	2015	At various concentrations of oleanolic acid and betulinic acid, the inhibition of oleanolic acid towards UGT1A6 and UGT1A8 was higher than betulinic acid.	betulinic acid	48-62	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	116-122
26957994-7	2015	At various concentrations of oleanolic acid and betulinic acid, the inhibition of oleanolic acid towards UGT1A6 and UGT1A8 was higher than betulinic acid.	Oleanolic Acid	82-96	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	116-122
26957994-8	2015	CONSLUSION: Given that UGT1A6 and UGT1A8 play key role in the the inhibition of oleanolic acid towards UGT1A6 and UGT1A8 will induce drug-drug interaction and the risk of diseases.	Oleanolic Acid	80-94	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	34-40
26957994-8	2015	CONSLUSION: Given that UGT1A6 and UGT1A8 play key role in the the inhibition of oleanolic acid towards UGT1A6 and UGT1A8 will induce drug-drug interaction and the risk of diseases.	Oleanolic Acid	80-94	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	114-120
26247833-0	2016	Raloxifene glucuronidation in liver and intestinal microsomes of humans and monkeys: contribution of UGT1A1, UGT1A8 and UGT1A9.	Raloxifene Hydrochloride	0-10	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	109-115
26320626-0	2015	Glucuronidation of bavachinin by human tissues and expressed UGT enzymes: Identification of UGT1A1 and UGT1A8 as the major contributing enzymes.	bavachinin	19-29	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	103-109
26320626-4	2015	Reaction phenotyping assay showed that UGT1A1, UGT1A3 and UGT1A8 were involved in BCI-4"-O-glucuronidation, while UGT1A1 and UGT1A8 displayed the higher catalytic ability among all tested UGT isoforms.	bci-4"-o	82-90	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	58-64
26320626-4	2015	Reaction phenotyping assay showed that UGT1A1, UGT1A3 and UGT1A8 were involved in BCI-4"-O-glucuronidation, while UGT1A1 and UGT1A8 displayed the higher catalytic ability among all tested UGT isoforms.	bci-4"-o	82-90	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	125-131
26320626-9	2015	These findings suggested that UGT1A1 and UGT1A8 were the primary isoforms involved in BCI-4"-O-glucuronidation in HLM, and HIM, respectively.	bci-4"-o	86-94	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	41-47
26957994-4	2015	RESULTS: The inhibition of capability of oleanolic acid towards UGT1A6 and UGT1A8 were higher than betulinic acid.	Oleanolic Acid	41-55	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	75-81
26163112-8	2015	Glucuronidation of homoegonol to M5 was mediated by UGT1A1, UGT1A3, UGT1A4, and UGT2B7 enzymes, whereas M4 was formed from 4-O-demethylhomoegonol by UGT1A1, UGT1A8, UGT1A10, and UGT2B15 enzymes.	homoegonol	19-29	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	157-163
25870101-0	2015	Glucuronidation of OTS167 in Humans Is Catalyzed by UDP-Glucuronosyltransferases UGT1A1, UGT1A3, UGT1A8, and UGT1A10.	OTS167	19-25	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	97-103
25903196-4	2015	The inhibition difference capability was observed for the inhibition of (R)-zaltoprofen and (S)-zaltoprofen towards UGT1A8 and UGT2B7, but not for other tested UGT isoforms.	(R)-Zaltoprofen	72-87	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	116-122
25903196-4	2015	The inhibition difference capability was observed for the inhibition of (R)-zaltoprofen and (S)-zaltoprofen towards UGT1A8 and UGT2B7, but not for other tested UGT isoforms.	pyranoprofen	92-107	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	116-122
25903196-8	2015	Based on the reported maximum plasma concentration of (R)-zaltoprofen in vivo, a high drug-drug interaction between (R)-zaltoprofen and the drugs mainly undergoing UGT1A7, UGT1A8, and UGT2B7-catalyzed glucuronidation was indicated.	(R)-Zaltoprofen	116-131	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	172-178
25760534-4	2015	While other UGT members such as UGT1A8, UGT2B7, and UGT2B15 showed glucuronidation activity toward trovafloxacin, the metabolic velocity was extremely low.	trovafloxacin	99-112	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	32-38
25586184-2	2015	Using recombinant human UGT isoforms, we show that glucuronic acid conjugation of the model substrate, (-)-epicatechin, is catalyzed mainly by UGT1A8 and UGT1A9.	Glucuronic Acid	51-66	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	143-149
25586184-2	2015	Using recombinant human UGT isoforms, we show that glucuronic acid conjugation of the model substrate, (-)-epicatechin, is catalyzed mainly by UGT1A8 and UGT1A9.	Catechin	103-118	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	143-149
25496264-7	2015	UGT1A8 (an intestinal enzyme), UGT1A9 and UGT2B7 were the enzymes showing the highest activity towards gingerols.	gingerol	103-112	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
24635759-4	2014	Among 12 recombinant human UDP-glucuronosyltransferases (UGTs), UGT1A1, UGT1A8, UGT1A9, and UGT1A10 showed catalyzing activity toward leonurine glucuronidation.	leonurine	134-143	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	72-78
25364403-3	2014	The current study demonstrates that rapamycin may enhance the chemopreventive effects of SFN on Caco-2 cells; this may be partially attributed to nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2)- and human pregnane X receptor (hPXR)-mediated UGT1A1, UGT1A8 and UGT1A10 induction.	Sirolimus	36-45	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	277-283
23842475-4	2014	In extra-hepatic cells, Caco2, the activity of UGT1A9 proximal promoter increased to 73.4 +- 8.5% of that of the UGT1A8 proximal promoter with only 4 base changes: -160C, -152A, -62T, and -59G.	caco2	24-29	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	113-119
23527766-9	2013	Among the 16 human UGTs tested, UGT1A8 and UGT1A9 were able to form both (S) and (R)bicalutamide-G from pure or racemic substrates.	bicalutamide	84-96	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	32-38
23721685-0	2013	Genetic polymorphisms of UGT1A8, UGT1A9 and HNF-1alpha and gastrointestinal symptoms in renal transplant recipients taking mycophenolic acid.	Mycophenolic Acid	123-140	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
24349450-7	2013	We also found that BPAF glucuronidation could be mediated through several human recombinant UDP-glucuronosyltransferases (UGTs) including UGT1A1, UGT1A3, UGT1A8, UGT1A9, UGT2B4, UGT2B7, UGT2B15 and UGT2B17, among which UGT2B7 showed the highest efficiency of glucuronidation.	4,4'-hexafluorisopropylidene diphenol	19-23	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	154-160
23527766-11	2013	Kinetic parameters of the recombinant UGT2B7, UGT1A8 and UGT1A9 enzymes support a predominant role of the UGT1A9 isoform in bicalutamide metabolism.	bicalutamide	124-136	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	46-52
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	108-111	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
23682072-0	2013	Characterization of raloxifene glucuronidation: potential role of UGT1A8 genotype on raloxifene metabolism in vivo.	Raloxifene Hydrochloride	20-30	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	66-72
23682072-8	2013	These data suggest that raloxifene metabolism may be dependent on UGT1A8 genotype and that UGT1A8 genotype may play an important role in overall response to raloxifene.	Raloxifene Hydrochloride	24-34	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	66-72
23682072-8	2013	These data suggest that raloxifene metabolism may be dependent on UGT1A8 genotype and that UGT1A8 genotype may play an important role in overall response to raloxifene.	Raloxifene Hydrochloride	157-167	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	91-97
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	Glucuronides	116-127	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	129-132	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	Sulfates	143-150	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
23670235-5	2013	RESULTS: UGT1A1, UGT1A4, UGT1A8, UGT2B7, and SULT1A1 were found to be involved in the formation of inactive ABT-751 glucuronide (ABT-751G) and sulfate (ABT-751S).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	129-132	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	25-31
23670235-7	2013	UGT1A8 rs6431558 was associated with a 28% increase in glucuronidation metabolic ratios (P=0.022), and UGT1A4*2 was associated with a 65% decrease in ABT-751 C trough (P=0.009).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	150-153	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	0-6
23299247-6	2013	Demethylation was inhibited significantly by furafylline and predominantly catalysed by recombinant CYP1A2, whereas glucuronidation was inhibited by silibinin, quercetin, as well as 1-naphthol and catalysed by recombinant UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9 and UGT1A10.	1-naphthol	182-192	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	246-252
23713759-5	2013	In contrast, although UGT1A8 reacted with 3,2"-dihydroxychalcone and 4,2"-dihydroxychalcone to yield 2"-O-glucuronide products, the presence of a B-ring hydroxy group at the 4" position on cardamonin and 2",4"-dihydroxychalcone quenched the reaction at the OH-2" position.	3,2'-DIHYDROXYCHALCONE	42-64	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
23713759-5	2013	In contrast, although UGT1A8 reacted with 3,2"-dihydroxychalcone and 4,2"-dihydroxychalcone to yield 2"-O-glucuronide products, the presence of a B-ring hydroxy group at the 4" position on cardamonin and 2",4"-dihydroxychalcone quenched the reaction at the OH-2" position.	4,2'-DIHYDROXYCHALCONE	69-91	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
23713759-5	2013	In contrast, although UGT1A8 reacted with 3,2"-dihydroxychalcone and 4,2"-dihydroxychalcone to yield 2"-O-glucuronide products, the presence of a B-ring hydroxy group at the 4" position on cardamonin and 2",4"-dihydroxychalcone quenched the reaction at the OH-2" position.	2"-o-glucuronide	101-117	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
23713759-5	2013	In contrast, although UGT1A8 reacted with 3,2"-dihydroxychalcone and 4,2"-dihydroxychalcone to yield 2"-O-glucuronide products, the presence of a B-ring hydroxy group at the 4" position on cardamonin and 2",4"-dihydroxychalcone quenched the reaction at the OH-2" position.	2',4'-dihydroxychalcone	204-227	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	22-28
23237733-4	2013	The results showed that 100muM of isoliquiritigenin inhibited the activity of UGT1A1, UGT1A3, UGT1A6, UGT1A7, UGT1A8, UGT1A9, and UGT1A10 by 95.2%, 76.1%, 78.9%, 87.2%, 67.2%, 94.8%, and 91.7%, respectively.	isoliquiritigenin	34-51	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	110-116
23277092-4	2013	RESULTS: Two haplotypes in UGT1A1/UGT1A8 were weak predictors of reduced M6G/morphine and M3G/morphine serum ratios after oral administration (false discovery rate-corrected P-values<0.1).	Morphine	77-85	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	34-40
23277092-4	2013	RESULTS: Two haplotypes in UGT1A1/UGT1A8 were weak predictors of reduced M6G/morphine and M3G/morphine serum ratios after oral administration (false discovery rate-corrected P-values<0.1).	Morphine	94-102	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	34-40