ライフサイエンスコーパス: UGT1A1

1 UGT1A1 catalyzes the conjugation of bilirubin with glucu

2 UGT1A1 genotype and total bilirubin levels are strongly

3 UGT1A1 genotype did not influence clearance of TAS-103.

4 UGT1A1 genotype was not associated with weight gain.

5 UGT1A1 genotypes were determined using reverse-transcrip

6 UGT1A1 protein level correlated strongly with both liver

7 UGT1A1 status was wildtype (*1|*1) in 40%, heterozygous

8 UGT1A1 variants (-3279G>T, -3156G>A, promoter TA indel,

9 UGT1A1 was also induced in the human intestinal Caco-2 c

10 UGT1A1*28 genotype was not associated with grade 3 and 4

11 UGT1A1, the sole enzyme responsible for the metabolism o

12 omoter of the UDP-glucuronosyltransferase 1 (UGT1A1) gene has been shown to cause Gilbert syndrome, a

13 hosphoglucuronate glucuronosyltransferase-1 (UGT1A1) completely or partially abolish hepatic bilirubi

14 e uridine diphosphate glycosyltransferase 1 (UGT1A1) gene.

15 pression of UDP-glucuronosyltransferase 1A1 (UGT1A1) and the inability to metabolize bilirubin.

16 UDP-glucuronosyltransferase 1A1 (UGT1A1) catalyzes the glucuronidation of the active meta

17 reatment on UDP-glucuronosyltransferase 1A1 (UGT1A1) expression and bilirubin metabolism in humanized

18 onal TCS on UDP-glucuronosyltransferase 1A1 (UGT1A1) expression and bilirubin metabolism in humanized

19 ine diphosphate glucuronosyltransferase 1A1 (UGT1A1) gene are associated with increased adverse event

20 ion between UDP-glucuronosyltransferase 1A1 (UGT1A1) genotypes and severe toxicity as well as irinote

21 UDP-glucuronosyltransferase 1A1 (UGT1A1) is a vital metabolic enzyme responsible for the

22 In mammals, UDP-glucuronosyltransferase 1A1 (UGT1A1) is the sole enzyme responsible for bilirubin glu

23 UDP-glucuronosyltransferase 1A1 (UGT1A1) plays an important physiological role by contrib

24 sphoglucuronate glucuronosyltransferase 1A1 (UGT1A1), the absence of which leads to severe unconjugat

25 ily through UDP-glucuronosyltransferase 1A1 (UGT1A1)-catalyzed glucuronidation.

26 osphate glucuronosyltransferase isoform 1A1 (UGT1A1).

27 f Crigler-Najjar type 1 syndrome (CN1) in 28 UGT1A1 c.222C>A homozygotes followed for 520 aggregate p

28 236G>A for fluoropyrimidines, and UGT1A1*28, UGT1A1*6, and UGT1A1*27 for irinotecan) received drug or

29 glucuronosyltransferase family 1 member A1 (UGT1A1), was protective against malaria in mice.

30 A C127Y substitution abolished UGT1A1 activity, but not its dimerization.

31 AE incidence varied across UGT1A1 subgroups; however, discontinuation rates remaine

32 ically significant DDIs when co-administered UGT1A1 or 2B17 substrates.

33 which exhibited a NIR signal at 720 nm after UGT1A1 metabolism.

34 ibited potent competitive inhibition against UGT1A1 activity with a Ki of 0.5 muM.

35 oropyrimidines, and UGT1A1*28, UGT1A1*6, and UGT1A1*27 for irinotecan) received drug or dose adjustme

36 estionnaire (CLDQ)], vitamins assessment and UGT1A1 polymorphisms.

37 ociations were characterized with CYP2B6 and UGT1A1 genotypes that affect efavirenz and INSTI metabol

38 rate for P-glycoprotein, CYP3A4, CYP3A5, and UGT1A1.

39 EPARE, pretreatment application of DPYD- and UGT1A1-guided treatment appeared to increase safety and

40 nd DPYD c.1236G>A for fluoropyrimidines, and UGT1A1*28, UGT1A1*6, and UGT1A1*27 for irinotecan) recei

41 ned by ABCC1 1684T>C, ABCB1 IVS9 -44A>G, and UGT1A1*93 (P = .004).

42 limited to specific tissues, both GSTM1 and UGT1A1 are involved in the conjugation (and thus transpo

43 gnificantly toward intestinal maturation and UGT1A1 induction.

44 SWI/SNF target promoter templates (c-myc and UGT1A1), we observed hSWI/SNF-driven depletion of normal

45 genes in liver, including CYP3A, Oatp2, and UGT1A1.

46 ity, pharmacokinetics, pharmacodynamics, and UGT1A1 genotype.

47 Pharmacokinetic studies and UGT1A1 genotyping were performed.

48 etween the prevalence of severe toxicity and UGT1A1 genetic variation.

49 and UGT1A10 > UGT1A9 > UGT2B7 approximately UGT1A1 > UGT1A7 for (+)-BPD.

50 in protein and catalytic activity as well as UGT1A1 mRNA.

51 Because UGT1A1 in humans is responsible for 100% of the conjugat

52 No association between UGT1A1 genotype (n = 61) and toxicity or pharmacokinetic

53 To date, no significant association between UGT1A1*28 and cardiovascular disease (CVD) events has be

54 There was no association between UGT1A1*28 genotype and toxicity or pharmacokinetic param

55 ncrease in AUC of drugs primarily cleared by UGT1A1 or 2B17.

56 ll therapy phases and were largely driven by UGT1A1 and PNPLA3 variants.

57 f the variation in ANC nadir is explained by UGT1A1*93, ABCC1 IVS11 -48C>T, SLCO1B1*1b, ANC baseline

58 dated bilirubin at 1/10 the level of that by UGT1A1 with a Km (bilirubin) of 25 microM compared to th

59 droquinone and beta-naphthoflavone, cellular UGT1A1 glucuronidation activities were increased.

60 mine the molecular interactions that control UGT1A1 expression, the gene was characterized and induct

61 ple genes, including CYP1A1, CYP1A2, CYP1B1, UGT1A1, UGT1A6, IL6, and SAA1.

62 n the regulation of CYP4F12, CYP3A4, CYP2B6, UGT1A1 and P-glycoprotein.

63 he results suggest that Nrf2-Keap1-dependent UGT1A1 induction by prooxidants might represent a key ad

64 TATAA box of the gene, an allele designated UGT1A1*28, decreases gene transcription.

65 rt) was associated with IP-related diarrhea; UGT1A1 (G-3156A)A/A (drug metabolism) was associated wit

66 l benefit and utility of implementing a DPYD/UGT1A1 pharmacogenetic-informed therapy with fluoropyrim

67 -associated virus serotype 8 vector encoding UGT1A1 in patients with the Crigler-Najjar syndrome that

68 used for the real-time imaging of endogenous UGT1A1 in living cells and animals and to monitor the bi

69 The liver enzymes UGT1A1 and UGT2B7 formed BPD-7S-Gluc as the major diaste

70 kinetic profiles of a panel of UGT enzymes (UGT1A1, 1A3, 1A4, 1A6, 1A7, 1A8, 1A9, 1A10, 2B4, 2B7, 2B

71 Hepatocellular and biliary tissue expressed UGT1A1 and UGT1A4 but hepatocellular tissue uniquely exp

72 P (n = 495, median age 61 years, 68% female; UGT1A1*28 homozygous, n = 46; 9.3%), 41 (8.3%) permanent

73 rtium, we suggest twelve new loci (PKN, FN1, UGT1A1, PPARG, DMDGH, PPARD, CDK6, VPS13B, GAD2, GAB2, A

74 6 atazanavir/r recipients were evaluable for UGT1A1.

75 Genomic DNA was genotyped for UGT1A1*28, and patients were designated as 6/6, 6/7, or

76 r-infrared (NIR) fluorescent probe, HHC, for UGT1A1, which exhibited a NIR signal at 720 nm after UGT

77 Individuals homozygous for UGT1A1*28 (genotype 7/7) have increased serum bilirubin

78 cal and disease processes, and the roles for UGT1A1 and SLCO1B1 in drug metabolism, these genetic fin

79 bilirubin) of 25 microM compared to that for UGT1A1 of 5.0 microM.

80 To date, four UGT1A1 variant alleles characterized by a variation in t

81 B (n = 124), as well as the known functional UGT1A1*28 and UGT2B17 CNV (copy number variation) polymo

82 ery of clinically predictive genotypes (e.g. UGT1A1*28, TYMS TSER), haplotypes (e.g. VKORC1 Haplotype

83 ations in one of the five exons of the gene (UGT1A1) encoding the uridinediphosphoglucuronate glucuro

84 patients based on their germline genotypes [UGT1A1: 124 probe sets, false discovery rate (FDR)=13%,

85 y used in cancer therapy, such as genotyping UGT1A1 to reduce the incidence of severe toxicity of iri

86 uridine diphosphate-glucuronosyltransferase (UGT1A1).

87 animal lacking UDP-glucuronosyltransferase (UGT1A1), was used as recipient.

88 The UDP-glucuronosyltransferase, UGT1A1, is the critical enzyme responsible for detoxific

89 in elimination, UDP-glucuronosyltransferase, UGT1A1.

90 y progression, as in Gilbert's Syndrome (GS; UGT1A1*28 polymorphism), aggravated health effects have

91 olymorphisms in CYP3A4, CYP3A5, MDR1, GSTP1, UGT1A1, and VDR.

92 ined by K(m) analysis was UGT1A10 > UGT1A9 > UGT1A1 > UGT1A7 for (-)-BPD and UGT1A10 > UGT1A9 > UGT2B

93 However, hepatic UGT1A1 was not induced upon iAs exposure.

94 en considered as a means of inducing hepatic UGT1A1 expression.

95 UGT1 mice show delayed expression of hepatic UGT1A1 and are severely hyperbilirubinemic.

96 e reduced with a robust induction of hepatic UGT1A1, leaving us to conclude that CAR is not tied to U

97 r TSB levels along with induction of hepatic UGT1A1.

98 h TCS, we observed superinduction of hepatic UGT1A1.

99 greatly reduced due to induction of hepatic UGT1A1.

100 aralpha(-/-)) were treated with TCS, hepatic UGT1A1 was not induced.

101 In hUGT1 mice, expression of the hepatic UGT1A1 gene is developmentally delayed resulting in elev

102 eonatal mice was not associated with hepatic UGT1A1 expression.

103 As a series of hereditary UGT1A1 mutations have been identified that are associate

104 Homozygote UGT1A1*28 allele carriers with higher serum bilirubin co

105 Homozygous UGT1A1*28 GS individuals were simultaneously homozygous

106 The homozygous UGT1A1*28 allele observed in 9% of patients was associat

107 Human UGT1A1 was markedly increased in small and large intesti

108 al that the Ah receptor is involved in human UGT1A1 induction.

109 ons indicate that some mutant forms of human UGT1A1 (hUGT1A1) may be dominant-negative, suggesting th

110 iven the lack of in vivo regulation of human UGT1A1 by chrysin in a transgenic animal model.

111 n of oxidants toward the regulation of human UGT1A1 in vivo, transgenic mice bearing the human UGT1 l

112 ecipient rats against the F-protein or human UGT1A1.

113 cted against the amino terminal of the human UGT1A1 isoform showed that 5 hepatocyte donors exhibited

114 l hUGT1/Pxr(-/-) mice were treated with iAs, UGT1A1 was superinduced in both tissues, confirming PXR

115 -exposed donors exhibited marked declines in UGT1A1 mRNA levels during culturing.

116 te donors exhibited a >50-fold difference in UGT1A1 level.

117 all grades) was numerically more frequent in UGT1A1*28 homozygotes (28/46; 60.9%) than heterozygotes

118 review the role of genetic polymorphisms in UGT1A1 and TPMT, as well as mutations in DPD, in influen

119 computer program, this hydrophobic region in UGT1A1 is located between residues 159-177 and defines a

120 disease or gallstones, top bilirubin SNPs in UGT1A1 and SLCO1B1 were not associated.

121 in the marked interindividual variability in UGT1A1 expression.

122 The top variants in UGT1A1 and SLCO1B1 explain approximately 18.0 and approx

123 DP-glucuronosyltransferase family, including UGT1A1, an enzyme known to metabolise bilirubin.

124 locus, encoding all 9-UGT1A genes including UGT1A1, was expressed in Ugt1(-/-) mice.

125 inase signaling pathways to maximally induce UGT1A1.

126 ess the human UGT1 locus is unable to induce UGT1A1 expression in either the small intestine or liver

127 In the hUGT1 mice, glucose induced UGT1A1 in the small intestine, while it did not affect t

128 s an important dietary substance and induces UGT1A1 protein expression in cell culture.

129 Rifampicin (RIF) induces UGT1A1, an enzyme involved in raltegravir (RAL) eliminat

130 this inhibitor's known potential to inhibit UGT1A1, but did not appear to have significant clinical

131 Liver and intestinal UGT1A1 were induced, along with murine CYP2B10, a consen

132 d to repression of both liver and intestinal UGT1A1.

133 lirubinemia leads to induction of intestinal UGT1A1 and a reduction in total serum bilirubin values.

134 emia in hUGT1 neonates because of intestinal UGT1A1 gene derepression.

135 Breast milk reduces expression of intestinal UGT1A1, which leads to hyperbilirubinemia and BIND; supp

136 mice because of ROS induction of intestinal UGT1A1.

137 pSB-hUGT1A1 (4-8 microg/day, 1-4 doses) into UGT1A1-deficient hyperbilirubinemic Gunn rats (model of

138 yped for those polymorphisms that are known (UGT1A1*28) or likely (HMOX-1 microsatellites) to impact

139 nst several UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by axitinib; and

140 microsomal bilirubin UGT activity and liver UGT1A1 mRNA level (r(2) =.82 and.72, respectively).

141 mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10 by PEITC was prevented.

142 hat the nuclear receptor PXR represses liver UGT1A1 in neonatal hUGT1 mice.

143 al 14-day post-conception Tg-UGT1mice, liver UGT1A1, UGT1A4, and UGT1A6 were induced, with the levels

144 In liver, UGT1A1, UGT1A3, UGT1A4, and UGT1A9 are expressed, and ar

145 rinotecan, suggesting that patients with low UGT1A1 activity, such as those with Gilbert's syndrome,

146 Of the 4 patients with the lowest UGT1A1 levels, 3 were homozygotes for the UGT1A1 promote

147 cent probe has been developed for monitoring UGT1A1 activity in living systems, high-throughput scree

148 Tg(UGT1(A1*28))Ugt1(-/-) mice] or the normal UGT1A1*1 allele [Tg(UGT1(A1*1))Ugt1(-/-) mice].

149 systems, high-throughput screening of novel UGT1A1 inhibitors and visual evaluation of bile excretio

150 A1 promoter repeat polymorphism [A(TA)nTAA] (UGT1A1*28) and GSTM1 deletion were significant predictor

151 s, we emphasize here the impaired ability of UGT1A1 to eliminate bilirubin that contributes to hyperb

152 in Ah receptor recognition and activation of UGT1A1 by chrysin exist when compared with classical mec

153 ed with mRNA expression and/or activities of UGT1A1, UGT1A3 and UGT2B17.

154 ar result was observed following analysis of UGT1A1 expression in liver.

155 analyses suggested a stronger association of UGT1A1 genotype with estrogen receptor (ER)-negative bre

156 hUGT1 mice (hUGT1/Pxr(-/-)), derepression of UGT1A1 was evident in both liver and intestinal tissue i

157 idization, we determined the distribution of UGT1A1 and UGT1A7 through UGT1A10 mRNAs and found them f

158 We identified putative causal effects of UGT1A1/UGT1A4 expression on gallbladder disorders throug

159 However, polymorphic expression of UGT1A1 (29%), UGT1A3 (21%), and UGT1A6 (36%) was detecte

160 he events that control delayed expression of UGT1A1 during development remain a mystery.

161 ence has verified that delayed expression of UGT1A1 during the early stages of neonatal development i

162 2 and provided evidence of the expression of UGT1A1 in breast cancer tissue, where a positive signal

163 ion-PCR analysis confirmed the expression of UGT1A1 in human liver in the hepatocarcinoma cell line H

164 e, while it did not affect the expression of UGT1A1 in the liver.

165 e would lead to the sufficient expression of UGT1A1 in the small intestine to reduce serum bilirubin

166 lear factor-kappaB and loss of expression of UGT1A1, leading to hyperbilirubinemia.

167 se chain reaction revealed the expression of UGT1A1, UGT1A3, UGT1A4, UGT1A6, and UGT1A9 in the colon,

168 UGT) 1A1, it is now known that immaturity of UGT1A1, in combination with the overproduction of biliru

169 rubinemic effects of UDCA are independent of UGT1A1.

170 estigated the expression and inducibility of UGT1A1 in human donor livers and their corresponding pri

171 Induction of UGT1A1 by PCN and TCDD is believed to be highly dependen

172 e actively promote PCN and TCDD induction of UGT1A1 in Tg-UGT1 primary hepatocytes.

173 bilirubin, which resulted from induction of UGT1A1 in the gastrointestinal tract.

174 ent (XRE) in support of chrysin induction of UGT1A1 in the human hepatoma cell line HepG2.

175 -4050) were responsible for the induction of UGT1A1 in the intestinal cells.

176 The induction of UGT1A1 proceeded following the overexpression of Nrf2 an

177 nti-oxidative response leads to induction of UGT1A1 through the Nrf2-Keap1 pathway.

178 l interfering RNA revealed that induction of UGT1A1 was not seen in Nrf2 knock-out cells.

179 In addition, we evaluated the influence of UGT1A1 genotype on the pharmacokinetics and toxicity of

180 confirm the substantial genetic influence of UGT1A1 variants, consistent with past linkage and associ

181 Comparative expression levels of UGT1A1 in intestinal tumors and normal surrounding tissu

182 t when compared with classical mechanisms of UGT1A1 induction by TCDD.

183 rious mutations in this microregion (MRA) of UGT1A1 in CN-I patients are evidence of a critical and d

184 he -3156G>A variant is a better predictor of UGT1A1 status than the previously reported TA indel requ

185 Methods for absolute quantification of UGT1A1 and UGT1A6 were previously established utilizing

186 ly, and were managed similarly regardless of UGT1A1 status.

187 2 bp duplication within the coding region of UGT1A1 can be a founder mutation in the Sudanese populat

188 to a TA insertion at the promoter region of UGT1A1.

189 e association may be driven by regulation of UGT1A1 in the intestines, but not in the liver.

190 servation of differential down-regulation of UGT1A1, UGT1A3, UGT1A6, and UGT1A10 and up-regulation of

191 nts that control developmental repression of UGT1A1 and hyperbilirubinemia.

192 ay a role in the developmental repression of UGT1A1.

193 tions are warranted to elucidate the role of UGT1A1 in breast cancer risk.

194 ess may be associated with superinduction of UGT1A1.

195 rs such as Nrf2 leading to superinduction of UGT1A1.

196 hyperbilirubinemia because of suppression of UGT1A1 in the gastrointestinal tract.

197 pping experiments including transfections of UGT1A1 reporter gene constructs into HepG2 cells coupled

198 ew discusses the role of genetic variants of UGT1A1, TS and EGFR to exemplify the potential impact of

199 The dependence of the XRE on UGT1A1-luciferase activity was demonstrated by a loss of

200 60.9%) than heterozygotes (69/180; 38.3%) or UGT1A1*1 wild type (59/177; 33.3%).

201 the UGT1A1 (TA) 7/7 genotype from the other UGT1A1 genotypes included HDAC1, RELA and SLC2A1; those

202 Three hundred GS patients (UGT1A1*28 homozygous) and 249 healthy blood donors (HBD)

203 tion test results in the general population, UGT1A1 variant rs887829 and PNPLA3 variant rs738409 were

204 With the recombinant UGT1A1 enzyme and its mutants, P167G, F170del, F170L, F1

205 Thus, PXR serves to repress UGT1A1 gene expression during development.

206 methylcholanthrene (2.5 micromol/L) revealed UGT1A1-inducing effects of phenobarbital, oltipraz, and,

207 GT1 mice that expressed either the Gilbert's UGT1A1*28 allele [Tg(UGT1(A1*28))Ugt1(-/-) mice] or the

208 finding that is independent of the Gilbert's UGT1A1*28 promoter polymorphism.

209 In this study, UGT1A1 expression levels were determined in the liver an

210 ction of FDA approved pharmacogenetic tests (UGT1A1*28) and the initiation of a genotype-guided clini

211 her glucuronidation of 17beta-estradiol than UGT1A1.

212 unoprecipitation results also confirmed that UGT1A1 was capable of forming heterodimer complexes with

213 These results demonstrate that UGT1A1 is the isoform responsible for SN-38 glucuronidat

214 This technique demonstrated that UGT1A1, UGT1A3, UGT1A4, UGT1A6, UGT1A7, UGT1A8, UGT1A9,

215 re also explored, and it was determined that UGT1A1 was capable of binding with UGT1A3, UGT1A4, UGT1A

216 Our findings suggest that UGT1A1 may be a major gene controlling serum bilirubin l

217 The UGT1A1 6/6 genotype predicted lower catechol AUC.

218 The UGT1A1 6/6, VDR intron 8 GG, and VDR Fok 1 CC genotypes

219 The UGT1A1 enzyme is a major UGT involved in estradiol glucu

220 The UGT1A1 gene has been shown to be inducible by nuclear re

221 The UGT1A1*28 genotype can be used to individualize dosing o

222 The UGT1A1*28 variant has been associated with hyperbilirubi

223 xpress the entire UGT1 locus (hUGT1) and the UGT1A1 gene, develop neonatal hyperbilirubinemia, with 8

224 e found significant associations between the UGT1A1*28 allele and decreased risk of CVD.

225 show that in human hepatoma HepG2 cells the UGT1A1 gene is also inducible with aryl hydrocarbon rece

226 Genes whose expression distinguished the UGT1A1 (TA) 7/7 genotype from the other UGT1A1 genotypes

227 st UGT1A1 levels, 3 were homozygotes for the UGT1A1 promoter variant sequence associated with Gilbert

228 In GS the UGT1A1*28 variant reduces bilirubin conjugation by 70% a

229 consequence of a deleterious mutation in the UGT1A1 (HUG-Br1) isozyme of a Crigler-Najjar (CN) Type I

230 r type I disease results from lesions in the UGT1A1 gene and is often fatal.

231 ence of UDPGT enzyme due to mutations in the UGT1A1 gene.

232 depending on the number of TA repeats in the UGT1A1 promoter region.

233 racterized by an allelic polymorphism in the UGT1A1 promoter, hyperbilirubinemia was monitored in hum

234 has been known to increase expression of the UGT1A1 gene in liver.

235 be prevented by enhancing regulation of the UGT1A1 gene in neonatal mice.

236 Steroid induction of the UGT1A1 gene indicates that xenobiotic sensors, such as t

237 ification of SN-38, whereas induction of the UGT1A1 gene may serve to limit toxicity and improve the

238 Transcriptional silencing of the UGT1A1 gene was relieved in neonatal hUGT1 hepatocytes t

239 f a developmental delay in expression of the UGT1A1 gene, were treated with PEITC, TSB levels were re

240 that Keap1 suppresses Nrf2 activation of the UGT1A1 gene.

241 istal enhancer sequence (-3483/-3194) of the UGT1A1 gene.

242 ions in the noncoding intronic region of the UGT1A1 gene.

243 ion (c.55_76dup) in the coding exon 1 of the UGT1A1 gene.

244 oth a positive and negative regulator of the UGT1A1 gene.

245 bital-response enhancer module region of the UGT1A1 gene.

246 Here, we show permanent correction of the UGT1A1 genetic defect in Gunn rat liver with site-specif

247 Our results indicate that correction of the UGT1A1 genetic lesion in the Gunn rat restores enzyme ex

248 c influence on serum bilirubin levels of the UGT1A1 locus (P < 5 x 10(-324)) and a 12p12.2 locus.

249 t only the proximal region (-1300/-7) of the UGT1A1 promoter, but also distal region (-6500/-4050) we

250 the examination of the responsiveness of the UGT1A1 to PB in the human population, particularly indiv

251 Of the 16 loci, only the UGT1A1 promoter repeat polymorphism [A(TA)nTAA] (UGT1A1*

252 entify genetic variation, in addition to the UGT1A1*28 polymorphism, that can explain the variability

253 f nuclear proteins specifically bound to the UGT1A1-XRE, and competition experiments with Ah receptor

254 ved only in HK293 cells transfected with the UGT1A1 isozyme.

255 he promoter polymorphism associated with the UGT1A1*28 allele contributes to hyperbilirubinemia in mi

256 ingle guanosine (G) base deletion within the UGT1A1 gene.

257 Therefore, UGT1A1 genotyping is not a useful prognostic indicator o

258 Nucleotide sequence analysis of this UGT1A1 enhancer region revealed a xenobiotic response el

259 atment with irinotecan is related in part to UGT1A1*28, a variant that reduces the elimination of SN-

260 aving us to conclude that CAR is not tied to UGT1A1 induction.

261 djusted for individual genotypes for the top UGT1A1 variant, the top SLCO1B1 variant remained highly

262 ical tests for toxicity avoidance (eg, TPMT, UGT1A1) and efficacy prediction (eg, epidermal growth fa

263 variants in four genes (DPYD, NUDT15, TPMT, UGT1A1) associated with toxicity induced by five drugs u

264 blood donors (HBD) were genotyped for UGT1A (UGT1A1*28, UGT1A3-66 T>C, UGT1A6*3a, UGT1A7*3) and trans

265 cription levels of five major hepatic UGT1A (UGT1A1, UGT1A3, UGT1A4, UGT1A6 and UGT1A9) and five UGT2

266 corresponding immunoblot showed that UGT1A6, UGT1A1, and CYP3A4 were immunoprecipitated.

267 Western blots showed that UGT2B7, UGT1A6, UGT1A1, and CYP3A4 were successfully immunoprecipitated

268 with specific antibodies to UGT2B7, UGT1A6, UGT1A1, and CYP3A4, and the immunoprecipitates were run

269 We suggest that the unstable UGT1A1 polymorphism may serve to "fine-tune" the plasma

270 models: a pathological jaundice model using UGT1A1(-/-) neonatal mice and an adult bilirubin exposur

271 kinetics, the lowest P value with AUCVAR was UGT1A1 rs887829 (P = 1.8 x 10-4), which was also associa

272 y that differed between the two clusters was UGT1A1 (P=0.002; Fisher's exact test).

273 77.1 mul.min(-1).mg of protein(-1)), whereas UGT1A1 was most efficient at forming AalphaC-HON(2)-Gl (

274 zed estrogens and their derivatives, whereas UGT1A1, -1A3, -1A7, and -1A8 differentially exhibited re

275 Whether UGT1A1 status could impact SG toxicity and efficacy rema

276 eart Study population to investigate whether UGT1A1*28 is associated with the risk of CVD events.

277 ave been identified that are associated with UGT1A1 deficiency, new evidence has verified that delaye

278 n, an event that is directly associated with UGT1A1 induction.

279 erall glucuronidation of BPD in humans, with UGT1A1, UGT1A7, UGT1A9, UGT1A10 and potentially UGT1A8 p