Pharmacogenomics Laboratory, CHUQ Research Center and Faculty of Pharmacy, Laval University, Quebec City, Quebec, Canada.
Drug Metab Rev. 2010 Feb;42(1):24-44. doi: 10.3109/03602530903210682.
The human uridine diphospho (UDP)-glucuronosyltransferase (UGT) superfamily comprises enzymes responsible for a major biotransformation phase II pathway: the glucuronidation process. The UGT enzymes are located in the endoplasmic reticulum of almost all tissues, where they catalyze the inactivation of several endogenous and exogenous molecules, including bilirubin, sex steroids, numerous prescribed drugs, and environmental toxins. This metabolic pathway is particularly variable. The influence of inheritable polymorphisms in human UGT-encoding genes has been extensively documented and was shown to be responsible for a fraction of the observed phenotypic variability. Other key genomic processes are likely underlying this diversity; these include copy-number variations, epigenetic factors, and newly discovered splicing mechanisms. This review will discuss novel molecular aspects that may be determinant to UGT phenotypes.
人尿苷二磷酸（UDP）-葡萄糖醛酸基转移酶（UGT）超家族包括负责主要生物转化 II 期途径的酶：葡萄糖醛酸化过程。UGT 酶位于几乎所有组织的内质网中，在那里它们催化几种内源性和外源性分子的失活，包括胆红素、性激素、许多处方药和环境毒素。该代谢途径具有很大的可变性。人类 UGT 编码基因中遗传多态性的影响已被广泛记录，并被证明是导致观察到的表型变异性的一部分原因。其他关键的基因组过程可能是这种多样性的基础；这些包括拷贝数变异、表观遗传因素和新发现的剪接机制。这篇综述将讨论可能决定 UGT 表型的新的分子方面。
