Ganglioside GT1b Specifications
|Product Name||Ganglioside GT1b|
|Chemical Name||GANGLIOSIDE GT1B TRISODIUM SALT; GT1B 3NA; GT1B-GANGLIOSIDE; GT1B (NH4+ SALT); ganglioside,gt1; (ganglioside gt1B) from bovine brain; trisialoganglioside-gt1b from bovine brain; GANGLIOSIDEGT1BTRISODIUMSALT,BOVINEBRAIN; Trisialoganglioside GT1b (NH4+ salt)|
|Molecular Weight||2158.4 g/mol|
|Monoisotopic Mass||2157.119189 g/mol|
What is Ganglioside GT1b?
The name Ganglioside was first used by German scientist Ernst Klenk in 1942 to newly isolated lipids from brain ganglion cells. It is a molecule composed of glycosphingolipids (ceramides and oligosaccharides) and one or more sialic acids linked to a sugar chain. It is a component of the cytoplasmic membrane that regulates cellular signal transduction events. More than 60 types of gangliosides are known, and the main difference between them is the position and number of NANA residues.
Ganglioside GT1b is one of many gangliosides and is a trisialic ganglioside with two sialic acid residues linked to an internal galactose unit. It has an inhibitory effect on the body’s humoral immune response. At 0.1-10 μM, it can inhibit the spontaneous production of IgG, IgM and IgA by human peripheral blood mononuclear cells. Ganglioside GT1b has also been proposed as a host cell receptor for Merkel cell polyoma virus and as a means capable of triggering infections that cause Merkel cell carcinoma.
Ganglioside GT1b has also been implicated in several neuronal cancers and is considered to be a ganglioside associated with brain metastases. Studies have found that GM1, GD1a, and GT1b have inhibitory effects on epidermal growth factor receptor signaling and adhesion and migration of keratinocytes, and their presence may be a useful biomarker for assessing brain metastatic potential.
Ganglioside GT1b also affects the immune system. Ganglioside GT1b has inhibitory effects on human body’s humoral immune response and inhibits immunoglobulins produced by human peripheral blood mononuclear cells. There is evidence that GD1b, GT1b, and GQ1b can enhance the production of Th1 cytokines by inhibiting the activity of adenylate cyclase, while inhibiting the production of Th2.
As a receptor that recognizes various toxins of its oligosaccharide structure, ganglioside GT1b is a receptor through which Clostridium botulinum bacterium botulinum neurotoxin enters nerve cells. Studies have shown that tetanus toxin enters nerve cells by compounding with GT1b and other gangliosides, inhibits the release of neurotransmitters in the central nervous system, and causes spastic paralysis. The botulinum type C neurotoxin entering the nerve has investigated the possible apoptotic effect of cells produced by ganglioside GT1b binding on neuroblastoma.
In addition, ganglioside GT1b negatively regulates cell movement, diffusion, and adhesion to fibronectin (FN) through direct molecular interactions with the α5 subunit of α5β1 integrin, a finding that could be used to develop cancer therapies. The combination of GT1b and MAG on the surface of neurons may thus regulate the interaction of GT1b in the plasma membrane of neurons, resulting in inhibition of neurite growth.
Benefits of Ganglioside GT1b
Ganglioside GT1b is an acidic glycosphingolipid that forms lipid rafts in neuronal cells of the central nervous system and is involved in cell proliferation, differentiation, adhesion, signal transduction, cell-to-cell interaction, tumorigenesis, and metastasis.
Autoimmune responses to gangliosides can lead to Guillain-Barre syndrome. Ganglioside GT1b induces dopaminergic neuron degeneration, which may contribute to the onset or development of Parkinson’s disease.
Ganglioside GT1b is a scavenger of • OH free radicals, which protects the brain from mtDNA damage, seizures and lipid peroxidation caused by active oxygen generators.
Ehrlich tumors express ganglioside GT1b, and anti-GT1b has great therapeutic potential for this cancer. This ganglioside is also associated with Miller Fisher syndrome.
Side effects of Ganglioside GT1b
Gangliosides can bind to lectins, act as immune and cell adhesion receptors, participate in cell signaling, carcinogenesis and cell differentiation, affect placenta formation and nerve growth, participate in myelin stability and nerve regeneration, and act as viruses and Entry point for toxins into cells.
The accumulation of ganglioside GT1b has been linked to several diseases including Thai-Sachs disease and Sandhof disease.
Ganglioside GT1b inhibits antigen or mitogen-induced T cell proliferation response and has been identified as a botulinum toxin receptor, a rare toxin with severe physiological consequences.
Ganglioside GT1b is present almost exclusively in nerve cells and is expressed on the adventitia. GT1b promotes neuronal differentiation and dendritic formation, which produces noxious behavior and enhances hyperalgesia and allodynia.
Ganglioside GT1b can affect the immune system. It has an inhibitory effect on the human body’s humoral immune response and inhibits the immunoglobulin produced by human peripheral blood mononuclear cells.
In addtion, Ganglioside GT1b is relative with the following diseases: influenza, guillain–garré syndrome, cholera, tetanus, botulism, leprosy and obesity.
- Erickson, K.D., Garcea, R.L., and Tsai, B. Ganglioside GT1b is a putative host cell receptor for the Merkel cell polyomavirus. Journal of Virology 83(19), 10275-10279 (2009).
- Kanda, N., and Tamaki, K. Ganglioside GT1b suppresses immunoglobulin production by human peripheral blood mononuclear cells. Immunology 96(4), 628-633 (1999).
- Schengrund, C.-L., DasGupta, B.R., and Ringler, N.J. Binding of botulinum and tetanus neurotoxins to ganglioside GT1b and derivatives thereof. J. Neurochem. 57(3), 1024-1032 (1991).
- Gangliosides, structure, occurrence, biology and analysis”. Lipid Library. The American Oil Chemists’ Society. Archived from the original on 2009-12-17.
- Nicole Gaude, Journal of Biological Chemistry, Vol. 279:33 pp. 34624-34630, 2004.
- Elizabeth R Sturgill, Kazuhiro Aoki, Pablo HH Lopez, etc. Biosynthesis of the major brain gangliosides GD1a and GT1b. Glycobiology, Volume 22, Issue 10, October 2012, Pages 1289–
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