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Beta-1,3-glucuronyltransferase 3

The protein encoded by this gene is a member of the glucuronyltransferase gene family, enzymes that exhibit strict acceptor specificity, recognizing nonreducing terminal sugars and their anomeric linkages. This gene product catalyzes the formation of the glycosaminoglycan-protein linkage by way of a glucuronyl transfer reaction in the final step of the biosynthesis of the linkage region of proteoglycans. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: UDP-glucuronosyltransferase, UGT, UGT1A1, ACID, CAN
Papers on Glucuronosyltransferase
Fluoride caused thyroid endocrine disruption in male zebrafish (Danio rerio).
Meiyan et al., China. In Aquat Toxicol, Feb 2016
The transcriptional levels of corticotrophin-releasing hormone (CRH), thyroid-stimulating hormone (TSH), thyroglobulin (TG), sodium iodide symporter (NIS), iodothyronine I (DIO1), and thyroid hormone receptor alpha (TRα) were also elevated in all fluoride-exposed male fish after 90 days of exposure, while the inconsistent expressions were found in the mRNA of iodothyronineⅡ (DIO2), UDP glucuronosyltransferase 1 family a, b (UGT1ab), transthyretin (TTR), and thyroid hormone receptor beta (TRβ).
UGT genotyping in belinostat dosing.
Figg et al., Bethesda, United States. In Pharmacol Res, Feb 2016
UNASSIGNED: Certain genetic polymorphisms of UDP glucuronosyltransferase 1 family, polypeptide A1 (UGT1A1) can reduce gene expression (*28, *60, *93) or activity (*6), thereby altering the pharmacokinetics, pharmacodynamics, and the risk of toxicities of UGT1A1 substrates, of which irinotecan is a widely-described example.
Effects of UGT2B7 genetic polymorphisms on serum concentrations of valproic acid in Chinese epileptic children comedicated with lamotrigine.
Guo et al., Changchun, China. In Ther Drug Monit, Jan 2016
VPA is a substrate of uridine diphosphate glucuronosyltransferase 2B7 (UGT2B7).
UDP-glucuronosyltransferase 1A1*6 and *28 polymorphisms as indicators of initial dose level of irinotecan to reduce risk of neutropenia in patients receiving FOLFIRI for colorectal cancer.
Manabe et al., Saku, Japan. In Int J Clin Oncol, Jan 2016
BACKGROUND: Irinotecan (CPT-11)-induced neutropenia is associated with UDP-glucuronosyltransferase (UGT) 1A1*6 and *28 polymorphisms.
Clinical use of cobicistat as a pharmacoenhancer of human immunodeficiency virus therapy.
von Hentig, Frankfurt am Main, Germany. In Hiv Aids (auckl), Dec 2015
The outstanding property of cobicistat is its cytochrome P450 3A-selective inhibition of hepatic metabolism of antiretroviral drugs, in contrast with ritonavir, which not only inhibits but also induces a number of cytochrome P450 enzymes, UDP-glucuronosyltransferase, P-glycoprotein, and other cellular transporters.
Effects of β-Naphthoflavone on Ugt1a6 and Ugt1a7 Expression in Rat Brain.
Nadai et al., In Biol Pharm Bull, Dec 2015
Uridine 5'-diphosphate-glucuronosyltransferase (UGT) catalyzes a major phase II reaction in a drug-metabolizing enzyme system.
Irinotecan, a key chemotherapeutic drug for metastatic colorectal cancer.
Sasaki et al., Tokyo, Japan. In World J Gastroenterol, Dec 2015
Clinical pharmacological studies have revealed that such severe toxicity is related to exposure to SN-38 and genetic polymorphisms in UDP-glucuronosyltransferase 1A1 gene.
[UGT1A1 Genotyping for Proper Use of Irinotecan].
Ando et al., In Rinsho Byori, Jul 2015
Irinotecan is metabolized to form active SN-38, which is further conjugated and detoxified by the UDP-glucuronosyltransferase (UGT) 1A1 enzyme.
[Progress in quantitative methods based on liquid chromatography-mass spectrometry for drug metabolizing enzymes in human liver microsomes].
Zhang et al., In Se Pu, Jun 2015
Cytochrome P450 (CYP) enzymes and uridine 5-diphospho-glucuronosyltransferase (UGT) enzymes are critical enzymes for drug metabolism.
Identification of Promotor and Exonic Variations, and Functional Characterization of a Splice Site Mutation in Indian Patients with Unconjugated Hyperbilirubinemia.
Aggarwal et al., Lucknow, India. In Plos One, 2014
BACKGROUND: Mild unconjugated hyperbilirubinemia (UH), due to reduced activity of the enzyme uridine diphosphoglucuronate-glucuronosyltransferase family, polypeptide 1 (UGT1A1), is a common clinical condition.
The sonic hedgehog factor GLI1 imparts drug resistance through inducible glucuronidation.
Borden et al., Montréal, Canada. In Nature, 2014
We observe that the sonic hedgehog transcription factor glioma-associated protein 1 (GLI1) and the UDP glucuronosyltransferase (UGT1A) family of enzymes are elevated in resistant cells.
Faulty initiation of proteoglycan synthesis causes cardiac and joint defects.
Hoffmann et al., Berlin, Germany. In Am J Hum Genet, 2011
Reduced GlcAT-I activity impairs skeletal as well as heart development and results in variable combinations of heart malformations.
Impairment of embryonic cell division and glycosaminoglycan biosynthesis in glucuronyltransferase-I-deficient mice.
Kitagawa et al., Kōbe, Japan. In J Biol Chem, 2010
mice with a deletion of GlcAT-I showed remarkable reduction of the synthesis of chondroitin sulfate and heparan sulfate and embryonic lethality before the 8-cell stage because of failed cytokinesis
2-o-phosphorylation of xylose and 6-o-sulfation of galactose in the protein linkage region of glycosaminoglycans influence the glucuronyltransferase-I activity involved in the linkage region synthesis.
Sugahara et al., Kōbe, Japan. In J Biol Chem, 2008
2-o-phosphorylation of xylose and 6-o-sulfation of galactose in the protein linkage region of glycosaminoglycans influence the glucuronyltransferase-I activity involved in the linkage region synthesis
Molecular basis for acceptor substrate specificity of the human beta1,3-glucuronosyltransferases GlcAT-I and GlcAT-P involved in glycosaminoglycan and HNK-1 carbohydrate epitope biosynthesis, respectively.
Fournel-Gigleux et al., Vandœuvre-lès-Nancy, France. In Glycobiology, 2007
A comparison of substrate specificity of beta1,3-glucuronosyltransferases revealed that GlcAT-I was selective toward Galbeta1,3Gal, whereas GlcAT-P presented a broader profile.
Cigarette smoking and irinotecan treatment: pharmacokinetic interaction and effects on neutropenia.
de Jong et al., Rotterdam, Netherlands. In J Clin Oncol, 2007
Although the underlying mechanism is not entirely clear, modulation of CYP3A and uridine diphosphate glucuronosyltransferase isoform 1A1 may be part of the explanation.
UGT1A1 promoter genotype correlates with SN-38 pharmacokinetics, but not severe toxicity in patients receiving low-dose irinotecan.
McGregor et al., Memphis, United States. In J Clin Oncol, 2007
PURPOSE: To study the association between UDP-glucuronosyltransferase 1A1 (UGT1A1) genotypes and severe toxicity as well as irinotecan disposition in pediatric patients with solid tumors receiving low-dose, protracted irinotecan (15 to 75 mg/m2 daily for 5 days for 2 consecutive weeks).
Direct quantitative trait locus mapping of mammalian metabolic phenotypes in diabetic and normoglycemic rat models.
Gauguier et al., London, United Kingdom. In Nat Genet, 2007
Linkage to a gut microbial metabolite (benzoate) can be explained by deletion of a uridine diphosphate glucuronosyltransferase. Mapping metabotypic QTLs provides a practical approach to understanding genome-phenotype relationships in mammals and may uncover deeper biological complexity, as extended genome (microbiome) perturbations that affect disease processes through transgenomic effects may influence QTL detection.
Comprehensive analysis of UGT1A polymorphisms predictive for pharmacokinetics and treatment outcome in patients with non-small-cell lung cancer treated with irinotecan and cisplatin.
Lee et al., South Korea. In J Clin Oncol, 2006
PURPOSE: To determine whether uridine diphosphate-glucuronosyltransferase 1A1, UGT1A7, and UGT1A9 polymorphisms affect the pharmacokinetics (PK) of irinotecan and treatment outcome of Korean patients with advanced non-small-cell lung cancer (NSCLC).
Stimulation of proteoglycan synthesis by glucuronosyltransferase-I gene delivery: a strategy to promote cartilage repair.
Ouzzine et al., Nancy, France. In Proc Natl Acad Sci U S A, 2005
GlcAT-I has a role in controlling and reversing articular cartilage defects
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