Abstract
This article is an updated report of a symposium held at the June 2000 annual meeting of the American Society for Pharmacology and Experimental Therapeutics in Boston. The symposium was sponsored by the ASPET Divisions for Drug Metabolism and Molecular Pharmacology. The report covers research from the authors' laboratories on the structure and regulation of UDP-glucuronosyltransferase (UGT) genes, glucuronidation of xenobiotics and endobiotics, the toxicological relevance of UGTs, the role of UGT polymorphisms in cancer susceptibility, and gene therapy for UGT deficiencies.
Footnotes
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↵2 Abbreviations used are: UGT, UDP-glucuronosyltransferase; B[a]P, benzo-[a]pyrene; CN-1, Crigler-Najjar syndrome type 1; HCA, heterocyclic amine; HNF1, hepatocyte nuclear factor 1; OR, odds ratio; SN-38, 7-ethyl-10-hydroxycamptothecin; NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone; P450, cytochrome P450; rAAV, recombinant adenoassociated virus.
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This work was supported in part by grants from the Canadian Institutes of Health Research (P.G.W., C.G.), the National Health and Medical Research Council of Australia and the Anti-Cancer Foundation of South Australia (P.I.M., P.A.G., A.J.H., Y.I.), the Canada Research Chair Program and the Fonds de la Recherche en Sante du Quebec (C.G.), and United States Public Health Service Grants R01-DK46057, R01-DK34357 and P30DK41296 (J.R.C., N.R.C.), and R01ES07762 (J.K.R.).
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↵1 These authors contributed equally as symposium speakers.
- Received October 10, 2003.
- Accepted December 11, 2003.
- The American Society for Pharmacology and Experimental Therapeutics
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