UGT-1A is a uridine diphosphate glucuronosyltransferase (UDP-glucuronosyltransferase, UDPGT), an enzyme of the glucuronidation pathway that transforms small lipophilic (fat-soluble) molecules, such as steroids, bilirubin, hormones, and drugs, into water-soluble, excretable metabolites.[7]
The UGT1A1 gene is part of a complex locus that encodes several UDP-glucuronosyltransferases. The locus includes thirteen unique alternative first exons followed by four common exons. Four of the alternate first exons are considered pseudogenes. Each of the remaining nine 5' exons may be spliced to the four common exons, resulting in nine proteins with different N-termini and identical C-termini. Each first exon encodes the substrate binding site, and is regulated by its own promoter.[7] Over 100 genetic variants within the UGT1A1 gene have been described, some of which confer increased, reduced or inactive enzymatic activity. The has compiled a list of these variants, naming each with a * symbol followed by a number.
Clinical significanceedit
Mutations in this gene cause serious problems for bilirubin metabolism; each syndrome can be caused by one or many mutations, so they are differentiated mostly by symptoms and not particular mutations:[8]
Gilbert syndrome (GS) can be caused by a variety of genetic changes, but in populations of European and African descent, it is most commonly associated with the UGT1A1*28 allele (rs8175347), a homozygous 2-bpinsertion (TA) mutation of the TATA boxpromoter region of the UGT1A1 gene.[8][9][10] This polymorphism impairs proper transcription of UGT1A1 gene, resulting in decreased transcriptional activity of UGT1A1 by about 70%; the resulting reduced enzyme activity leads to the hyperbilirubinemia characteristic of GS.[8][9][11] The *28 polymorphism occurs with a frequency of 26-31% in White and 42-56% of African-Americans.[12] About 10-15% of these populations are homozygous for the *28 allele, but only 5% actually develop UGT1A1-associated hyperbilirubinemia, so it appears that this mutation alone may be a necessary but not sufficient factor in GS, perhaps acting in combination with other UGT1A1 mutation(s) to increase the chances of developing GS.[8][9] In Asian and Pacific Islander populations, UGT1A1*28 is much less common, occurring at a frequency of approximately 9-16% in Asian populations and 4% of Pacific Islanders.[12][13] In these populations, Gilbert's syndrome is more often due to missense mutations in the coding region of the gene, such as UGT1A1*6 (glycine to arginine substitution at position 71 (G71R); rs4148323) [8][9] A special phenobarbital-responsive enhancer module NR3 region (gtPBREM NR3) helps to increase UDPGT enzyme production, which would make it conceptually possible to medically control the bilirubin level, although this is rarely necessary, particularly in adults (usually the level of total serum bilirubin in Gilbert syndrome patients vary from 1 to 6 mg/dL).[8][9]
Crigler–Najjar syndrome, type I is associated with mutation(s) that result in a complete absence of normal UGT1A1 enzyme, which causes a severe hyperbilirubinemia with levels of total serum bilirubin from 20 to 45 mg/dL. Phenobarbital treatment does not help to lower bilirubin level, because it only increases the amount of mutated UGT1A1 enzyme, which is still unable to catalyze the glucuronidation of bilirubin, which on the other hand makes phenobarbital treatment diagnostically relevant.[8][14]
Crigler–Najjar syndrome, type II is associated with other mutation(s) that lead to a reduced activity of the mutated UGT1A1 enzyme, which causes a hyperbilirubinemia with levels of total serum bilirubin from 6 to 20 mg/dL. In this case phenobarbital treatment helps to lower bilirubin lever by more than 30%.[8][15]
Hyperbilirubinemia, familial transient neonatal (also called breastfeedingjaundice) is associated with mutation(s) that alone do not lead to bilirubin level increase in female patients, but their children when breastfed develop from mild to severe hyperbilirubinemia by receiving steroidal substances (with milk) inhibiting glucuronidation of unconjugated bilirubin that may lead to jaundice and even kernicterus.[8][16]
Pharmacogeneticsedit
Genetic variations within the UGT1A1 gene have also been associated with the development of certain drug toxicities. The UGT1A1*28 variant, the same allele behind many cases of Gilbert syndrome. The UGT1A1*28 has been associated with an increased risk for neutropenia and Diarrhea in patients receiving the chemotherapeutic drug irinotecan[17][18] due to the insufficient excrete the active metabolite SN‐38, which primarily undergoes glucuronidation in livers.[19] The U.S. Food and Drug Administration recommends on the irinotecan drug label that patients with the *28/*28 genotype receive a lower starting dose of the drug.[19][20] The *28 allele has also shown associations with an increased risk for developing diarrhea in patients receiving irinotecan.[17][18] The UGT1A1*6 variant, more common in Asian populations than the *28 variant, has also shown associations with the development of irinotecan toxicities. Patients who are heterozygous or homozygous for the *6 allele may have a higher risk for developing neutropenia and diarrhea as compared to those with the UGT1A1*1/*1 genotype.[17][18]
Interactive pathway mapedit
Click on genes, proteins and metabolites below to link to respective articles.[§ 1]
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|alt=Irinotecan Pathway edit]]
Irinotecan Pathway edit
^The interactive pathway map can be edited at WikiPathways: "IrinotecanPathway_WP229".
^ abcGRCh38: Ensembl release 89: ENSG00000241635 – Ensembl, May 2017
^ abcGRCm38: Ensembl release 89: ENSMUSG00000089960 – Ensembl, May 2017
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Mackenzie PI, Owens IS, Burchell B, Bock KW, Bairoch A, Bélanger A, Fournel-Gigleux S, Green M, Hum DW, Iyanagi T, Lancet D, Louisot P, Magdalou J, Chowdhury JR, Ritter JK, Schachter H, Tephly TR, Tipton KF, Nebert DW (August 1997). "The UDP glycosyltransferase gene superfamily: recommended nomenclature update based on evolutionary divergence". Pharmacogenetics. 7 (4): 255–69. doi:10.1097/00008571-199708000-00001. PMID 9295054.
^Strassburg CP, Manns MP, Tukey RH (April 1998). "Expression of the UDP-glucuronosyltransferase 1A locus in human colon. Identification and characterization of the novel extrahepatic UGT1A8". J. Biol. Chem. 273 (15): 8719–26. doi:10.1074/jbc.273.15.8719. PMID 9535849.
^Beutler E, Gelbart T, Demina A (July 1998). "Racial variability in the UDP-glucuronosyltransferase 1 (UGT1A1) promoter: a balanced polymorphism for regulation of bilirubin metabolism?". Proc Natl Acad Sci USA. 95 (14): 8170–4. Bibcode:1998PNAS...95.8170B. doi:10.1073/pnas.95.14.8170. PMC20948. PMID 9653159.
^Tukey RH, Strassburg CP, Mackenzie PI (September 2002). "Pharmacogenomics of human UDP-glucuronosyltransferases and irinotecan toxicity". Mol Pharmacol. 62 (3): 446–50. doi:10.1124/mol.62.3.446. PMID 12181419. S2CID 19666863.
^ abBarbarino JM, Haidar CE, Klein TE, Altman RB (March 2014). "PharmGKB summary: very important pharmacogene information for UGT1A1". Pharmacogenet Genomics. 24 (3): 177–83. doi:10.1097/FPC.0000000000000024. PMC4091838. PMID 24492252.
^AlFadhli S, Al-Jafer H, Hadi M, Al-Mutairi M, Nizam R (October 2013). "The effect of UGT1A1 promoter polymorphism in the development of hyperbilirubinemia and cholelithiasis in hemoglobinopathy patients". PLOS ONE. 8 (10): e77681. Bibcode:2013PLoSO...877681A. doi:10.1371/journal.pone.0077681. PMC3813713. PMID 24204915.
^ abcBarbarino JM, Haidar CE, Klein TE, Altman RB (March 2014). "PharmGKB summary: very important pharmacogene information for UGT1A1". Pharmacogenetics and Genomics. 24 (3): 177–83. doi:10.1097/fpc.0000000000000024. PMC4091838. PMID 24492252.
^ abYau, Tung On (October 2019). "Precision treatment in colorectal cancer: Now and the future". JGH Open. 3 (5): 361–369. doi:10.1002/jgh3.12153. ISSN 2397-9070. PMC6788378. PMID 31633039.
^"CAMPTOSAR (irinotecan hydrochloride injection, solution) drug label". DailyMed. U.S. National Library of Medicine. Retrieved 5 January 2015.
Kadakol A, Ghosh SS, Sappal BS, Sharma G, Chowdhury JR, Chowdhury NR (2000). "Genetic lesions of bilirubin uridine-diphosphoglucuronate glucuronosyltransferase (UGT1A1) causing Crigler-Najjar and Gilbert syndromes: correlation of genotype to phenotype". Hum. Mutat. 16 (4): 297–306. doi:10.1002/1098-1004(200010)16:4<297::AID-HUMU2>3.0.CO;2-Z. PMID 11013440. S2CID 24275067.
King CD, Rios GR, Green MD, Tephly TR (2001). "UDP-glucuronosyltransferases". Curr. Drug Metab. 1 (2): 143–61. doi:10.2174/1389200003339171. PMID 11465080.
Bosma PJ (2003). "Inherited disorders of bilirubin metabolism". J. Hepatol. 38 (1): 107–17. doi:10.1016/S0168-8278(02)00359-8. PMID 12480568.
Innocenti F, Ratain MJ (2003). "Irinotecan treatment in cancer patients with UGT1A1 polymorphisms". Oncology (Williston Park, N.Y.). 17 (5 Suppl 5): 52–5. PMID 12800608.
Lee W, Lockhart AC, Kim RB, Rothenberg ML (2005). "Cancer pharmacogenomics: powerful tools in cancer chemotherapy and drug development". Oncologist. 10 (2): 104–11. doi:10.1634/theoncologist.10-2-104. PMID 15709212.
Navarro SL, Peterson S, Chen C, Makar KW, Schwarz Y, King IB, Li SS, Li L, Kestin M, Lampe JW (2009). "Cruciferous vegetable feeding alters UGT1A1 activity: diet and genotype-dependent changes in serum bilirubin in a controlled trial". Cancer Prev. Res. 2 (4): 345–52. doi:10.1158/1940-6207.CAPR-08-0178. PMC2666928. PMID 19336732.
Barbarino JM, Haidar CE, Klein TE, Altman RB (March 2014). "PharmGKB summary: very important pharmacogene information for UGT1A1". Pharmacogenet Genomics. 24 (3): 177–83. doi:10.1097/FPC.0000000000000024. PMC4091838. PMID 24492252.
glucuronosyltransferase, family, polypeptide, glucuronosyltransferase, also, known, enzyme, that, humans, encoded, ugt1a1, gene, ugt1a1identifiersaliasesugt1a1, biliqtl1, gnt1, udpgt, udpgt, ugt1, ugt1a, glucuronosyltransferase, family, member, a1external, ids. UDP glucuronosyltransferase 1 1 also known as UGT 1A is an enzyme that in humans is encoded by the UGT1A1 gene 5 6 UGT1A1IdentifiersAliasesUGT1A1 BILIQTL1 GNT1 HUG BR1 UDPGT UDPGT 1 1 UGT1 UGT1A UDP glucuronosyltransferase family 1 member A1External IDsOMIM 191740 MGI 98898 HomoloGene 128034 GeneCards UGT1A1Gene location Human Chr Chromosome 2 human 1 Band2q37 1Start233 760 270 bp 1 End233 773 300 bp 1 Gene location Mouse Chr Chromosome 1 mouse 2 Band1 D 1 44 55 cMStart88 139 681 bp 2 End88 146 719 bp 2 RNA expression patternBgeeHumanMouse ortholog Top expressed induodenumright lobe of liverkidneyrectumurinary bladderrenal cortexgallbladderbody of stomachzone of skinskin of abdomenTop expressed induodenumjejunumileumlipcolonhepatobiliary systemliverzone of skinventricular systemchoroid plexusMore reference expression dataBioGPSn aGene ontologyMolecular functiontransferase activity enzyme inhibitor activity retinoic acid binding hexosyltransferase activity protein homodimerization activity glycosyltransferase activity steroid binding protein heterodimerization activity enzyme binding glucuronosyltransferase activity UDP glycosyltransferase activityCellular componentintegral component of membrane endoplasmic reticulum membrane membrane intracellular membrane bounded organelle integral component of plasma membrane cytochrome complex endoplasmic reticulum chaperone complex endoplasmic reticulumBiological processsteroid metabolic process response to organic cyclic compound cellular response to ethanol estrogen metabolic process response to nutrient negative regulation of steroid metabolic process bilirubin conjugation response to steroid hormone response to glucocorticoid retinoic acid metabolic process negative regulation of cellular glucuronidation response to organic substance response to lipopolysaccharide cellular response to hormone stimulus heme catabolic process cellular response to glucocorticoid stimulus acute phase response heterocycle metabolic process animal organ regeneration response to starvation flavone metabolic process liver development metabolism negative regulation of glucuronosyltransferase activity response to ethanol negative regulation of fatty acid metabolic process biphenyl catabolic process cellular response to estradiol stimulus flavonoid glucuronidation cellular glucuronidation xenobiotic glucuronidation cellular response to xenobiotic stimulus negative regulation of catalytic activitySources Amigo QuickGOOrthologsSpeciesHumanMouseEntrez54658394436EnsemblENSG00000241635ENSMUSG00000089960UniProtP22309Q63886RefSeq mRNA NM 000463NM 201645RefSeq protein NP 000454NP 964007Location UCSC Chr 2 233 76 233 77 MbChr 1 88 14 88 15 MbPubMed search 3 4 WikidataView Edit HumanView Edit Mouse UGT 1A is a uridine diphosphate glucuronosyltransferase UDP glucuronosyltransferase UDPGT an enzyme of the glucuronidation pathway that transforms small lipophilic fat soluble molecules such as steroids bilirubin hormones and drugs into water soluble excretable metabolites 7 Contents 1 Gene 2 Clinical significance 3 Pharmacogenetics 4 Interactive pathway map 5 See also 6 References 7 Further reading 8 External linksGene editThe UGT1A1 gene is part of a complex locus that encodes several UDP glucuronosyltransferases The locus includes thirteen unique alternative first exons followed by four common exons Four of the alternate first exons are considered pseudogenes Each of the remaining nine 5 exons may be spliced to the four common exons resulting in nine proteins with different N termini and identical C termini Each first exon encodes the substrate binding site and is regulated by its own promoter 7 Over 100 genetic variants within the UGT1A1 gene have been described some of which confer increased reduced or inactive enzymatic activity The UGT nomenclature committee has compiled a list of these variants naming each with a symbol followed by a number Clinical significance editMutations in this gene cause serious problems for bilirubin metabolism each syndrome can be caused by one or many mutations so they are differentiated mostly by symptoms and not particular mutations 8 Gilbert syndrome GS can be caused by a variety of genetic changes but in populations of European and African descent it is most commonly associated with the UGT1A1 28 allele rs8175347 a homozygous 2 bp insertion T A mutation of the TATA box promoter region of the UGT1A1 gene 8 9 10 This polymorphism impairs proper transcription of UGT1A1 gene resulting in decreased transcriptional activity of UGT1A1 by about 70 the resulting reduced enzyme activity leads to the hyperbilirubinemia characteristic of GS 8 9 11 The 28 polymorphism occurs with a frequency of 26 31 in White and 42 56 of African Americans 12 About 10 15 of these populations are homozygous for the 28 allele but only 5 actually develop UGT1A1 associated hyperbilirubinemia so it appears that this mutation alone may be a necessary but not sufficient factor in GS perhaps acting in combination with other UGT1A1 mutation s to increase the chances of developing GS 8 9 In Asian and Pacific Islander populations UGT1A1 28 is much less common occurring at a frequency of approximately 9 16 in Asian populations and 4 of Pacific Islanders 12 13 In these populations Gilbert s syndrome is more often due to missense mutations in the coding region of the gene such as UGT1A1 6 glycine to arginine substitution at position 71 G71R rs4148323 8 9 A special phenobarbital responsive enhancer module NR3 region gtPBREM NR3 helps to increase UDPGT enzyme production which would make it conceptually possible to medically control the bilirubin level although this is rarely necessary particularly in adults usually the level of total serum bilirubin in Gilbert syndrome patients vary from 1 to 6 mg dL 8 9 Crigler Najjar syndrome type I is associated with mutation s that result in a complete absence of normal UGT1A1 enzyme which causes a severe hyperbilirubinemia with levels of total serum bilirubin from 20 to 45 mg dL Phenobarbital treatment does not help to lower bilirubin level because it only increases the amount of mutated UGT1A1 enzyme which is still unable to catalyze the glucuronidation of bilirubin which on the other hand makes phenobarbital treatment diagnostically relevant 8 14 Crigler Najjar syndrome type II is associated with other mutation s that lead to a reduced activity of the mutated UGT1A1 enzyme which causes a hyperbilirubinemia with levels of total serum bilirubin from 6 to 20 mg dL In this case phenobarbital treatment helps to lower bilirubin lever by more than 30 8 15 Hyperbilirubinemia familial transient neonatal also called breastfeeding jaundice is associated with mutation s that alone do not lead to bilirubin level increase in female patients but their children when breastfed develop from mild to severe hyperbilirubinemia by receiving steroidal substances with milk inhibiting glucuronidation of unconjugated bilirubin that may lead to jaundice and even kernicterus 8 16 Pharmacogenetics editGenetic variations within the UGT1A1 gene have also been associated with the development of certain drug toxicities The UGT1A1 28 variant the same allele behind many cases of Gilbert syndrome The UGT1A1 28 has been associated with an increased risk for neutropenia and Diarrhea in patients receiving the chemotherapeutic drug irinotecan 17 18 due to the insufficient excrete the active metabolite SN 38 which primarily undergoes glucuronidation in livers 19 The U S Food and Drug Administration recommends on the irinotecan drug label that patients with the 28 28 genotype receive a lower starting dose of the drug 19 20 The 28 allele has also shown associations with an increased risk for developing diarrhea in patients receiving irinotecan 17 18 The UGT1A1 6 variant more common in Asian populations than the 28 variant has also shown associations with the development of irinotecan toxicities Patients who are heterozygous or homozygous for the 6 allele may have a higher risk for developing neutropenia and diarrhea as compared to those with the UGT1A1 1 1 genotype 17 18 Interactive pathway map editClick on genes proteins and metabolites below to link to respective articles 1 File nbsp nbsp alt Irinotecan Pathway edit Irinotecan Pathway edit The interactive pathway map can be edited at WikiPathways IrinotecanPathway WP229 See also editGlucuronosyltransferase Lucey Driscoll syndrome Neonatal jaundice Cancer pharmacogenomicsReferences edit a b c GRCh38 Ensembl release 89 ENSG00000241635 Ensembl May 2017 a b c GRCm38 Ensembl release 89 ENSMUSG00000089960 Ensembl May 2017 Human PubMed Reference National Center for Biotechnology Information U S National Library of Medicine Mouse PubMed Reference National Center for Biotechnology Information U S National Library of Medicine Mackenzie PI Owens IS Burchell B Bock KW Bairoch A Belanger A Fournel Gigleux S Green M Hum DW Iyanagi T Lancet D Louisot P Magdalou J Chowdhury JR Ritter JK Schachter H Tephly TR Tipton KF Nebert DW August 1997 The UDP glycosyltransferase gene superfamily recommended nomenclature update based on evolutionary divergence Pharmacogenetics 7 4 255 69 doi 10 1097 00008571 199708000 00001 PMID 9295054 Strassburg CP Manns MP Tukey RH April 1998 Expression of the UDP glucuronosyltransferase 1A locus in human colon Identification and characterization of the novel extrahepatic UGT1A8 J Biol Chem 273 15 8719 26 doi 10 1074 jbc 273 15 8719 PMID 9535849 a b Entrez Gene UGT1A1 UDP glucuronosyltransferase 1 family polypeptide A1 a b c d e f g h i Online Mendelian Inheritance in Man OMIM UDP glycosyltransferase 1 family polypeptide A1 UGT1A1 191740 a b c d e Online Mendelian Inheritance in Man OMIM Gilbert syndrome 143500 Beutler E Gelbart T Demina A July 1998 Racial variability in the UDP glucuronosyltransferase 1 UGT1A1 promoter a balanced polymorphism for regulation of bilirubin metabolism Proc Natl Acad Sci USA 95 14 8170 4 Bibcode 1998PNAS 95 8170B doi 10 1073 pnas 95 14 8170 PMC 20948 PMID 9653159 Tukey RH Strassburg CP Mackenzie PI September 2002 Pharmacogenomics of human UDP glucuronosyltransferases and irinotecan toxicity Mol Pharmacol 62 3 446 50 doi 10 1124 mol 62 3 446 PMID 12181419 S2CID 19666863 a b Barbarino JM Haidar CE Klein TE Altman RB March 2014 PharmGKB summary very important pharmacogene information for UGT1A1 Pharmacogenet Genomics 24 3 177 83 doi 10 1097 FPC 0000000000000024 PMC 4091838 PMID 24492252 AlFadhli S Al Jafer H Hadi M Al Mutairi M Nizam R October 2013 The effect of UGT1A1 promoter polymorphism in the development of hyperbilirubinemia and cholelithiasis in hemoglobinopathy patients PLOS ONE 8 10 e77681 Bibcode 2013PLoSO 877681A doi 10 1371 journal pone 0077681 PMC 3813713 PMID 24204915 Online Mendelian Inheritance in Man OMIM Crigler Najjar syndrome type I 218800 Online Mendelian Inheritance in Man OMIM Crigler Najjar syndrome type II 606785 Online Mendelian Inheritance in Man OMIM Hyperbilirubinemia transient familial neonatal 237900 a b c Marsh S Hoskins JM July 2010 Irinotecan pharmacogenomics Pharmacogenomics 11 7 1003 10 doi 10 2217 pgs 10 95 PMC 2927346 PMID 20602618 a b c Barbarino JM Haidar CE Klein TE Altman RB March 2014 PharmGKB summary very important pharmacogene information for UGT1A1 Pharmacogenetics and Genomics 24 3 177 83 doi 10 1097 fpc 0000000000000024 PMC 4091838 PMID 24492252 a b Yau Tung On October 2019 Precision treatment in colorectal cancer Now and the future JGH Open 3 5 361 369 doi 10 1002 jgh3 12153 ISSN 2397 9070 PMC 6788378 PMID 31633039 CAMPTOSAR irinotecan hydrochloride injection solution drug label DailyMed U S National Library of Medicine Retrieved 5 January 2015 Further reading editTukey RH Strassburg CP 2000 Human UDP glucuronosyltransferases metabolism expression and disease Annu Rev Pharmacol Toxicol 40 581 616 doi 10 1146 annurev pharmtox 40 1 581 PMID 10836148 Kadakol A Ghosh SS Sappal BS Sharma G Chowdhury JR Chowdhury NR 2000 Genetic lesions of bilirubin uridine diphosphoglucuronate glucuronosyltransferase UGT1A1 causing Crigler Najjar and Gilbert syndromes correlation of genotype to phenotype Hum Mutat 16 4 297 306 doi 10 1002 1098 1004 200010 16 4 lt 297 AID HUMU2 gt 3 0 CO 2 Z PMID 11013440 S2CID 24275067 King CD Rios GR Green MD Tephly TR 2001 UDP glucuronosyltransferases Curr Drug Metab 1 2 143 61 doi 10 2174 1389200003339171 PMID 11465080 Bosma PJ 2003 Inherited disorders of bilirubin metabolism J Hepatol 38 1 107 17 doi 10 1016 S0168 8278 02 00359 8 PMID 12480568 Innocenti F Ratain MJ 2003 Irinotecan treatment in cancer patients with UGT1A1 polymorphisms Oncology Williston Park N Y 17 5 Suppl 5 52 5 PMID 12800608 Lee W Lockhart AC Kim RB Rothenberg ML 2005 Cancer pharmacogenomics powerful tools in cancer chemotherapy and drug development Oncologist 10 2 104 11 doi 10 1634 theoncologist 10 2 104 PMID 15709212 Navarro SL Peterson S Chen C Makar KW Schwarz Y King IB Li SS Li L Kestin M Lampe JW 2009 Cruciferous vegetable feeding alters UGT1A1 activity diet and genotype dependent changes in serum bilirubin in a controlled trial Cancer Prev Res 2 4 345 52 doi 10 1158 1940 6207 CAPR 08 0178 PMC 2666928 PMID 19336732 Barbarino JM Haidar CE Klein TE Altman RB March 2014 PharmGKB summary very important pharmacogene information for UGT1A1 Pharmacogenet Genomics 24 3 177 83 doi 10 1097 FPC 0000000000000024 PMC 4091838 PMID 24492252 External links editUGT1A1 protein human at the U S National Library of Medicine Medical Subject Headings MeSH UGT nomenclature homepage PharmGKB page for UGT1A1 Portal nbsp Biology Retrieved from https en wikipedia org w index php title UDP glucuronosyltransferase 1 family polypeptide A1 amp oldid 1185015979, wikipedia, wiki, book, books, library,
