학술논문
Growth retardation and early death of β-1, 4-galactosyltransferase knockout mice with augmented proliferation and abnormal differentiation of epithelial cells.
Document Type
Article
Author
Source
Subject
*GALACTOSYLTRANSFERASES
*EPITHELIAL cells
*CELL proliferation
*CELL differentiation
*MICE
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Language
ISSN
0261-4189
Abstract
Carbohydrate chains on a glycoprotein are important not only for protein conformation, transport and stability, but also for cell–cell and cell–matrix interactions. UDP-Gal:N-acetylglucosamine β-1,4-galactosyltransferase (GalT) (EC 2.4.1.38) is the enzyme which transfers galactose (Gal) to the terminal N-acetylglucosamine (GlcNAc) of complex-type N-glycans in the Golgi apparatus. In addition, it has also been suggested that this enzyme is involved directly in cell–cell interactions during fertilization and early embryogenesis through a subpopulation of this enzyme distributed on the cell surface. In this study, GalT-deficient mice were produced by gene targeting in order to examine the pathological effects of the deficiency. GalT-deficient mice were born normally and were fertile, but they exhibited growth retardation and semi-lethality. Epithelial cell proliferation of the skin and small intestine was enhanced, and cell differentiation in intestinal villi was abnormal. These observations suggest that GalT plays critical roles in the regulation of proliferation and differentiation of epithelial cells after birth, although this enzyme is dispensable during embryonic development. [ABSTRACT FROM AUTHOR]