Inhibitors | Comment | Organism | Structure |
---|---|---|---|
L-buthionine-(S,R)-sulfoximine | cotreatment with L-buthionine-(S,R)-sulfoximine, 1-methyl-4-phenylpyridinium and fibroblast growth factor 9 inhibits increased neuron viability compared to the group treated with 1-methyl-4-phenylpyridinium and fibroblast growth factor 9, to levels comparable to those of the 1-methyl-4-phenylpyridinium-treated group | Rattus norvegicus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Rattus norvegicus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
astrocyte | primary astrocyte | Rattus norvegicus | - |
neuron | primary cortical neuron | Rattus norvegicus | - |
Organism | Comment | Expression |
---|---|---|
Rattus norvegicus | fibroblast growth factor 9 treatment alone induces a decrease in hydrogen peroxide level, an increase in glutathione content, and an upregulation of gamma-glutamylcysteine synthetase and heme oxygenase 1 expression in primary cortical neurons but not in astrocytes. Simultaneous treatmentwith fibroblast growth factor 9 and 1-methyl-4-phenylpyridinium prevents 1-methyl-4-phenylpyridinium-induced neuron death and H2O2 overproduction but does not affect the fibroblast growth factor 9-increased gamma-GCS and HO-1 protein expression | up |
General Information | Comment | Organism |
---|---|---|
physiological function | fibroblast growth factor 9 upregulates gamma-GCS and HO-1 expression to protect cortical and dopaminergic neurons from 1-methyl-4-phenylpyridinium-induced oxidative insult. Inhibition of gamma-GCS or HO-1 prevents the inhibitory effect of fibroblast growth factor 9 on 1-methyl-4-phenylpyridinium-induced H2O2 production and death in mesencephalic dopaminergic and cortical neurons. In the absence of 1-methyl-4-phenylpyridinium, the fibroblast growth factor 9-induced H2O2 reduction is blocked by HO-1 inhibitors, but not by gamma-GCS inhibitors | Rattus norvegicus |