PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18558634-5 2008 RESULTS: Genetic polymorphisms of the UGT1A1 promoter, specifically the T-3279G phenobarbital responsive enhancer module and the (thymidine-adenine)(7) dinucleotide repeat TATAA box variants, were common. Phenobarbital 80-93 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 38-44 19541828-0 2009 Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver. Phenobarbital 51-64 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 99-105 19541828-0 2009 Genetic polymorphisms in the TATA box and upstream phenobarbital-responsive enhancer module of the UGT1A1 promoter have combined effects on UDP-glucuronosyltransferase 1A1 transcription mediated by constitutive androstane receptor, pregnane X receptor, or glucocorticoid receptor in human liver. Phenobarbital 51-64 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 140-171 19541828-2 2009 The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors. Phenobarbital 133-146 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 188-194 19541828-2 2009 The purpose of this study was to determine whether the genetic polymorphisms in the RNA polymerase II core promoter and the upstream phenobarbital-responsive element module (PBREM) of the UGT1A1 promoter have combined effects on UGT1A1 transcription mediated by the transcription factors. Phenobarbital 133-146 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 229-235 20979879-3 2010 The phenobarbital-responsive enhancer module (PBREM), TATA box and common mutation sites in exons of UGT1A1 gene were amplified by polymerase chain reaction (PCR) and the products screened by direct DNA sequencing. Phenobarbital 4-17 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 101-107 20201778-3 2010 The system was then validated using known ligands of PXR, rifampicin (RIF), clotrimazole (CLOT) sulfinpyrazone (SPZ) and phenobarbital (PB), which produced dose dependent induction of UGT1A1 luciferase activity by 4.4, 5.3, 4.7 and 3.7 fold, respectively, relative to the vehicle control, 0.1 % dimethylsulfoxide (DMSO). Phenobarbital 121-134 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 184-190 18172616-2 2008 A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene. Phenobarbital 33-46 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 77-83 18172616-2 2008 A 290-bp distal enhancer module, phenobarbital-responsive enhancer module of UGT1A1 (gtPBREM), fully accounts for constitutive androstane receptor (CAR)-, pregnane X receptor (PXR)-, glucocorticoid receptor (GR)-, and aryl hydrocarbon receptor (AhR)-mediated activation of the UGT1A1 gene. Phenobarbital 33-46 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 277-283 18328680-6 2008 PB induced CYP3A4, 3A5, 2B6 and 2A6, UGT1A1 and all transporters. Phenobarbital 0-2 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 37-43 17599282-3 2007 In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease. Phenobarbital 126-139 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 15-21 17599282-3 2007 In particular, UGT1A1-dependent bilirubin conjugation plays a critical role in the detoxification of neurotoxic bilirubin and phenobarbital-mediated UGT1A1 induction therapy is commonly used in the treatment of unconjugated hyperbilirubinemic diseases such as Crigler-Najjar type II disease. Phenobarbital 126-139 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 149-155 15771689-3 2005 Recently, it was reported that the -3263T > G mutation in the phenobarbital response enhancer module in UGT1A1 was associated with the majority of cases of Gilbert syndrome. Phenobarbital 65-78 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 107-113 16424820-0 2006 Study of the genetic determinants of UGT1A1 inducibility by phenobarbital in cultured human hepatocytes. Phenobarbital 60-73 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 37-43 16424820-1 2006 UGT1A1 is induced by phenobarbital. Phenobarbital 21-34 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 16424820-6 2006 Significant induction of UGT1A1 catalytic activity was observed in 82% and 100% of the cultures treated with phenobarbital for 2 days (median fold-induction = 1.6, range 1.3-2.8; n = 28) and 6 days (median fold-induction = 2.8, range 1.6-6.4; n = 16), respectively. Phenobarbital 109-122 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 25-31 17259171-8 2007 Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene. Phenobarbital 249-262 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 52-58 17259171-8 2007 Gene mapping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled with functional analysis of Nrf2 expression and binding to anti-oxidant-response elements (ARE) resulted in identification of an ARE in the phenobarbital-response enhancer module region of the UGT1A1 gene. Phenobarbital 249-262 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 302-308 15864124-0 2005 Genetic polymorphism in the phenobarbital-responsive enhancer module of the UDP-glucuronosyltransferase 1A1 gene and irinotecan toxicity. Phenobarbital 28-41 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 76-107 15881424-5 2005 After 2 weeks phenobarbitone was added to promote the enzymatic activity of UDPGT of the transplanted hepatocytes. Phenobarbital 14-28 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 76-81 15557560-2 2005 In a previous article, we described the phenobarbital response activity to a 290-base pair (bp) distal enhancer sequence (-3499/-3210) of the human UGT1A1 gene that is activated by the constitutive androstane receptor (CAR). Phenobarbital 40-53 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 148-154 15849716-3 2005 Concentration-dependent changes in UGT1A1 response were evaluated in hepatocyte cultures after treatment with 3-methylchloranthrene, beta-napthoflavone, rifampicin, or phenobarbital. Phenobarbital 168-181 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 35-41 15849716-7 2005 UGT1A1 was most responsive to the pregnane-X-receptor-agonists rifampicin, ritonavir, and clotrimazole at the mRNA level and, to a lesser extent, the constitutive androstane receptor-activators, phenobarbital and phenytoin. Phenobarbital 195-208 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 15864124-2 2005 The phenobarbital-responsive enhancer module (PBREM) of the UGT1A1 promoter region has been reportedly associated with the transcriptional activity of the gene. Phenobarbital 4-17 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 60-66 12464801-2 2002 UGT1A1 basal transcription is affected by a polymorphic (TA)n repeat, and another important regulatory element is the phenobarbital-responsive enhancer module (PBREM) which might contain variants affecting inducible gene expression. Phenobarbital 118-131 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 14978227-7 2004 In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter. Phenobarbital 42-55 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 108-114 14978227-7 2004 In the reporter gene assays employing the phenobarbital-responsible enhancer module (PBREM) from CYP2B6 and UGT1A1 genes, the splice variants, except for SV1, were inactive, whereas SV1 transactivated the CYP2B6 PBREM but not the UGT1A1 PBREM reporter. Phenobarbital 42-55 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 230-236 15382119-4 2004 We show that IL-1beta decreases CAR expression and decreases phenobarbital- or bilirubin-mediated induction of CYP2B6, CYP2C9, CYP3A4, UGT1A1, GSTA1, GSTA2, and SLC21A6 messenger RNA. Phenobarbital 61-74 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 135-141 11906189-2 2002 We identified a polymorphism that results in a T to G substitution at nucleotide number -3263 of the phenobarbital-responsive enhancer module of the UGT1A1 gene, thereby significantly decreasing transcriptional activity as indicated by the luciferase-reporter assay. Phenobarbital 101-114 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 149-155 11343253-0 2001 The phenobarbital response enhancer module in the human bilirubin UDP-glucuronosyltransferase UGT1A1 gene and regulation by the nuclear receptor CAR. Phenobarbital 4-17 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 94-100 11343253-2 2001 For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver. Phenobarbital 13-26 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 110-116 11343253-2 2001 For decades, phenobarbital (PB) treatment for hyperbilirubinemia has been known to increase expression of the UGT1A1 gene in liver. Phenobarbital 28-30 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 110-116 11343253-3 2001 We have now delineated the PB response activity to a 290-bp distal enhancer sequence (-3483/-3194) of the UGT1A1 gene. Phenobarbital 27-29 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 106-112 8968658-4 1996 Phenobarbital, phenytoin, primidone and carbamazepine are potent inducers of cytochrome P450 (CYP), epoxide hydrolase and uridine diphosphate glucuronosyltransferase (UDPGT) enzyme systems; oxcarbazepine is a weak inducer of CYP enzymes, probably acting on a few specific isoforms only. Phenobarbital 0-13 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 167-172 1900006-0 1991 Induction of alkoxyresorufin O-dealkylases and UDP-glucuronosyl transferase by phenobarbital and 3-methylcholanthrene in primary cultures of porcine ciliary epithelial cells. Phenobarbital 79-92 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 47-75 8869742-3 1996 Treatment of humans or hepatoma cell lines with drugs such as phenobarbital causes the induction of hepatic bilirubin UGT by increased transcription from the UGT1 gene. Phenobarbital 62-75 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 158-162 1900006-7 1991 UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr. Phenobarbital 42-44 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 1900006-7 1991 UDP-GT activity increased about 5-fold in PB-treated PE cells and about 4-fold in PB-treated NPE cells in 48 hr. Phenobarbital 82-84 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 0-6 1900006-9 1991 Induction by PB and MC of ER O-dealkylase, PR O-dealkylase and UDP-GT activities in ciliary NPE and PE cells was inhibited almost completely by 3.5 microM cyclohexamide and 40 nM actinomycin D. Phenobarbital 13-15 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 63-69 26781906-2 2016 The T-3279G mutation in the phenobarbital responsive enhancer module (PBREM), the TA-insertion in the TATA box, creating the A(TA)7TAA motif instead of A(TA)6TAA and the G211A mutation in coding exon 1, particularly in Asian populations, of the human UGT1A1 gene are the three common genotypes found in patients with Gilbert"s syndrome. Phenobarbital 28-41 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 251-257 31142299-2 2019 CNs type II patients usually benefit from phenobarbital treatment that induces residual UGT1A1 activity. Phenobarbital 42-55 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 88-94 27099654-7 2016 Phenobarbitone being an inducer of enzyme UDPGT is used as the first line of treatment and is not teratogenic in the low doses used. Phenobarbital 0-14 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 42-47 33551819-6 2020 As expected, CITCO, the direct activator, and PB, the indirect activator of CAR, induced CYP3A4 (31 and 40-fold), CYP2B6 (24 and 28-fold) and UGT1A1 (2.9 and 4.2-fold), respectively. Phenobarbital 46-48 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 142-148 24865931-4 2014 Genetic polymorphisms of the UGT1A1 promoter, specifically the -3279 T G phenobarbital responsive enhancer module (rs4124874) and (TA)7 dinucleotide repeat (rs8175347) as well as the coding region variants (rs2306283 and rs4149056) of the OATP2 gene were significantly higher among the cases than the controls. Phenobarbital 73-86 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 29-35 25751380-5 2015 RESULTS: Sequencing of the Gilbert syndrome-associated gene, UGT 1A 1, revealed mutations in the upstream promoter phenobarbital-responsive element module (PBREM) (-3279 mutation, 23 cases), in the promoter TATA box (a TA insertion mutation, 21 cases), and in the coding region of exon 1 (a GGA-AGA Gly71Arg mutation, 18 cases); there was no statistical difference found for any of the three mutations among this patient population (x2 =1.640, P more than 0.05). Phenobarbital 115-128 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 61-69