Abstract
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.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Amidohydrolases / metabolism
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Amino Acid Sequence
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Amino Sugars / biosynthesis
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Animals
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Brain / metabolism
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Carbohydrate Sequence
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Galactosyltransferases / genetics
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Galactosyltransferases / metabolism*
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Glycoproteins / biosynthesis
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Humans
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Mice
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Mice, Knockout
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Molecular Sequence Data
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Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase
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Sequence Alignment
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Sialic Acids / metabolism
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Substrate Specificity
Substances
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Amino Sugars
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Glycoproteins
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Sialic Acids
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polysialic acid
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N-acetyllactosamine
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Galactosyltransferases
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beta-1,4-galactosyltransferase I
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beta-1,4-galactosyltransferase IV
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glucosylceramide beta-1-4-galactosyltransferase
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Amidohydrolases
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Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase