St3gal2/3-double-null mice are half the weight of wild-type mice at weaning and display early hindlimb dysreflexia. Brain GD1a and GT1b in St3gal2-null mice is about half the level in wild-type mice, while GD1a and GT1b level in St3gal2/3-double-null mice is less than 5% of the level in wild-type mice. The St3gal2 and St3gal3 gene products (ST3Gal-II and ST3Gal-III sialyltransferase, respectively) are largely responsible for ganglioside terminal α2-3 sialylation of GM1a and GD1b to produce GD1a and GT1b in the brain. GM1a and GD1b contain one or two sialic acids on the internal galactose, respectively, and no sialic acid on the terminal galactose. These four gangliosides share the same neutral tetrasaccharide core (Galβ1-3GalNAcβ1-4Galβ1-4Glcβ1-1′Cer), but differ from each other by their sialic acid residue(s). Among the hundreds of ganglioside structures, GM1a, GD1a, GD1b and GT1b comprise up to 97% of gangliosides in the human brain. Glycolipids constitute >80% of mammalian brain glycans, with gangliosides being the major glycans in nerve cells. Gangliosides are grouped based on the number of sialic acid residues per molecule, GM gangliosides contain one sialic acid residue, GD gangliosides contain two, GT contain three, GQ contain four sialic acid residues. The German scientist Ernst Klenk used the term ganglioside in 1942 to refer to lipids isolated from ganglions. Gangliosides are sialic acid-containing oligoglycosylceramides. kláve Species ReactivityĪnti-GD1a Ganglioside Antibody, clone GD1a-1 (Azide Free) 100% Performance Guaranteed Tabulka spec.
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