The effect of the B subunit of cholera toxin on the action of nerve growth factor on PC12 cells
| Autor: | Gordon Guroff, Akira Tokuda, Norio Fujiki, Tatsuro Mutoh |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Cholera Toxin
Neurite Cytochalasin B G(M1) Ganglioside Biology Protein Serine-Threonine Kinases medicine.disease_cause complex mixtures Biochemistry PC12 Cells Cellular and Molecular Neuroscience chemistry.chemical_compound medicine Neurites Animals Nerve Growth Factors Phosphorylation Oncogene Proteins Ganglioside Ribosomal Protein S6 Kinases Cholera toxin DNA Molecular biology Rats Nerve growth factor nervous system chemistry Cell culture Trk receptor Ribosomal protein s6 embryonic structures Colchicine Signal Transduction |
| Zdroj: | Journal of neurochemistry. 60(4) |
| ISSN: | 0022-3042 |
| Popis: | Exogenous gangliosides, especially ganglioside GM1 (GM1), seem to potentiate the action of nerve growth factor (NGF). We have examined the possible regulation of the NGF signaling pathway in PC12 cells by the B subunit of cholera toxin (CTB), which binds to endogenous GM1 specifically and with a high affinity. CTB treatment (1 micrograms/ml) enhanced NGF-induced neurite outgrowth from PC12 cells, NGF-induced activation of ribosomal protein S6 kinase, and NGF-induced stimulation of trk phosphorylation. CTB plus NGF also caused a greater inhibition of [3H]thymidine incorporation into DNA than did NGF alone. These enhancing effects of CTB were blocked by the presence of cytochalasin B in the culture medium but were not affected by the presence of colchicine or by the depletion of Ca2+ in the medium. 125I-NGF binding experiments revealed that CTB treatment did not affect the specific binding of NGF to the cells. These results strongly suggest that the binding of cell surface GM1 by CTB modulates the pathway of intracellular signaling initiated by NGF and that the association of CTB with a cytoskeletal component is essential for these effects. |
| Databáze: | OpenAIRE |
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