Monosialoganglioside GM1 from bovine brain (C15-1236-392)

Amino Acid Sequence

Cer-Glc-Gal(NeuAc)-GalNAc-Gal

General description

Monosialoganglioside GM1 is a major sialoglycolipid of neuronal membranes.

Gangliosides are major constituents of neuronal cell membranes and endoplasmic reticulum. They contain a sialated polysaccharide chain linked to ceramide through a β-glycosidic linkage. For classification of gangliosides see Svennerholm, L., et al. (eds.), Structure and Function of Gangliosides, New York, Plenum, 1980.

Application

Monosialoganglioside GM1 from bovine brain has been used:

• in GM1 capture enzyme-linked immunosorbent assay (ELISA)
• for the quantification of cholera toxin B subunit (CTB)-p277 protein accumulation
• for Escherichia coli heat-labile enterotoxin (LT-B) detection
• to determine the affinity of the GM1-ganglioside receptor for the plant-derived Escherichia coli heat-labile toxin LTK63 protein

Specific receptors for cholera toxin that accumulate in the brain in late infantile lipidosis.

Biochem/physiol Actions

Monosialoganglioside GM1 maintains calcium homeostasis, neurotrophic factor signaling, membrane integrity, and α-synuclein aggregation. It binds to the cholera toxin B subunit, leading to the activation of adenylate cyclase in a wide variety of cell types. The binding of cholera toxin to membrane-associated monosialoganglioside GM1 causes the translocation of A subunit of cholera toxin to the cell interior for the catalysis of ADP ribosylation. In addition, the binding of cholera toxin to monosialoganglioside GM1 causes translocation of nuclear factor (NF)-kB and activation of dendritic cells. Monosialoganglioside GM1 is effective in treating cerebral ischemia and dementia, stroke, and spinal cord injury in several in vivo and in vitro model systems. Accumulation of GM1, due to defective acid hydrolases, leads to GM1 gangliosidosis, which is a lethal lysosomal disease. It was also found to have a regulatory role in the formation of neurotoxic β-amyloid fibrils associated with Alzheimer′s disease and possible involvement in the pathogenesis of demyelination in relapsing-remitting multiple sclerosis.