ArticleGlycobiology2012
Biosynthesis of the major brain gangliosides GD1a and GT1b.
Article in Glycobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 127 citations in OpenAlex.
- B3GALT4-dependent gangliosides are required for normal late spermatogenesis and male fertility.The Journal of reproduction and development · 2026Article
- Mapping ST3GAL transferase specificities in the glycosylation landscape of N/TERT-1 keratinocytes using Glycogenomics and mass spectrometry.Glycobiology · 2026Article
- Exploration of the structural diversity and distribution pattern of gangliosides and sulfatides in mouse brain tissues and biomarkers for Parkinson's Disease.Lipids in health and disease · 2026Article
- Gangliosides in molecular interactions and cell regulation.The Journal of biological chemistry · 2026Review
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- Role of myeloid cells expressing CD169/Siglec-1 in host-pathogen interactions.FEMS microbiology reviews · 2026Review
- Review
- Spatial lipidomics reveals demyelination and remyelination dynamics in the mouse brain.Journal of lipid research · 2025Article
- When ganglioside pathways go awry: congenital disorders and experimental insights.Journal of human genetics · 2025Review
- Integrated in vivo functional screens and multiomics analyses identify α-2,3-sialylation as essential for melanoma maintenance.Science advances · 2025Article
- DANGO: An MS data annotation tool for glycolipidomics.BBA advances · 2025Article
- Genomic-Inbreeding Landscape and Selection Signatures in the Polo Argentino Horse Breed.International journal of molecular sciences · 2024Article
- MUC1 expression is associated with ST3GAL2 and negatively correlated with the androgen receptor in castration-resistant prostate cancer.Glycoconjugate journal · 2024Article
- Mechanistic and Therapeutic Implications of Protein and Lipid Sialylation in Human Diseases.International journal of molecular sciences · 2024Review
- Deciphering mouse brain spatial diversity via glyco-lipidomic mapping.Nature communications · 2024Article
- Age-Related Effects of Inhalational Anesthetics inCurrent issues in molecular biology · 2024Article
- Atypical Guillain-Barré syndrome with positive anti-sulfatide, anti-GT1b, and anti-GT1a antibodies: A case report.World journal of clinical cases · 2024Article
- Lipid Rafts: The Maestros of Normal Brain Development.Biomolecules · 2024Review
- RREB1 regulates neuronal proteostasis and the microtubule network.Science advances · 2024Article
- Sialyltransferase Mutations Alter the Expression of Calcium-Binding Interneurons in Mice Neocortex, Hippocampus and Striatum.International journal of molecular sciences · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Gangliosides-sialylated glycosphingolipids-are the major glycoconjugates of nerve cells. The same four structures-GM1, GD1a, GD1b and GT1b-comprise the great majority of gangliosides in mammalian brains. They share a common tetrasaccharide core (Galβ1-3GalNAcβ1-4Galβ1-4Glcβ1-1'Cer) with one or two sialic acids on the internal galactose and zero (GM1 and GD1b) or one (GD1a and GT1b) α2-3-linked sialic acid on the terminal galactose. Whereas the genes responsible for the sialylation of the internal galactose are known, those responsible for terminal sialylation have not been established in vivo. We report that St3gal2 and St3gal3 are responsible for nearly all the terminal sialylation of brain gangliosides in the mouse. When brain ganglioside expression was analyzed in adult St3gal1-, St3gal2-, St3gal3- and St3gal4-null mice, only St3gal2-null mice differed significantly from wild type, expressing half the normal amount of GD1a and GT1b. St3gal1/2-double-null mice were no different than St3gal2-single-null mice; however, St3gal2/3-double-null mice were >95% depleted in gangliosides GD1a and GT1b. Total ganglioside expression (lipid-bound sialic acid) in the brains of St3gal2/3-double-null mice was equivalent to that in wild-type mice, whereas total protein sialylation was reduced by half. St3gal2/3-double-null mice were small, weak and short lived. They were half the weight of wild-type mice at weaning and displayed early hindlimb dysreflexia. We conclude that the St3gal2 and St3gal3 gene products (ST3Gal-II and ST3Gal-III sialyltransferases) are largely responsible for ganglioside terminal α2-3 sialylation in the brain, synthesizing the major brain gangliosides GD1a and GT1b.
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