Furukawa K, Sato T
Department of Biosignal Research, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo, Japan.
Biochim Biophys Acta. 1999 Dec 6;1473(1):54-66. doi: 10.1016/s0304-4165(99)00169-5.
Most beta-1,4-galactosyltransferase (beta-1,4-GalT)-knockout mice die after birth. Although several defects were found transiently in these animals, the primary cause of death is obscure. Not only beta-1,4-linked galactose residues on N-glycans, but also beta-1, 4-GalT activities were found in some of the tissues. Recently, five human genes which encode beta-1,4-GalTs have been cloned, and the possible presence of such novel beta-1,4-GalTs in mice is considered to bring about survival of the mutant animal beyond birth. In order to understand the semi-lethal nature of this animal, it is inevitable to clarify how individual novel beta-1,4-GalTs are involved in the biosynthesis of glycoconjugates based on their acceptor-substrate specificities.