Role of UGT1A1 gene polymorphism in the pathogenesis of Gilbert syndrome / 临床肝胆病杂志
Journal of Clinical Hepatology
;
(12): 609-612, 2016.
Article
in Chinese
| WPRIM
| ID: wpr-778592
ABSTRACT
As a bilirubin metabolic disorder, Gilbert syndrome belongs to the category of congenital non-hemolytic jaundice. Deficiency or decrease in the activity of bilirubin-uridine diphosphate glucuronyltransferase (UGT) is an important reason for the pathogenesis of Gilbert syndrome. UGT1A1, an isoenzyme of UGT, is a key enzyme to direct bilirubin in the liver. Mutations in UGT1A1 gene lead to the structural abnormality of UGT, and thus result in the decrease or loss of the ability of UGT to bind bilirubin. This article summarizes the research advances in the role of UGTA1 and its polymorphism in the pathogenesis and diagnosis of Gilbert syndrome.
Full text:
Available
Index:
WPRIM (Western Pacific)
Type of study:
Etiology study
Language:
Chinese
Journal:
Journal of Clinical Hepatology
Year:
2016
Type:
Article
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