Application | Comment | Organism |
---|---|---|
medicine | the findings emphasize the integration of glucose metabolism, glutamine metabolism, and oncogenic signaling in glioblastoma cells and suggest that exploiting compensatory pathways of glutamine metabolism can improve the efficacy of cancer treatments that impair glucose utilization | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
SF-188 cell | - |
Homo sapiens | - |
Specific Activity Minimum [µmol/min/mg] | Specific Activity Maximum [µmol/min/mg] | Comment | Organism |
---|---|---|---|
additional information | - |
glucose withdrawal stimulates GDH activity | Homo sapiens |
Synonyms | Comment | Organism |
---|---|---|
GDH | - |
Homo sapiens |
glutamate dehydrogenase | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
physiological function | glucose deprivation in SF-188 cells results in an enhanced GDH activity. This results from the loss of glycolysis. Inhibition of Akt signaling, which facilitates glycolysis, increases GDH activity whereas overexpression of Akt suppresses it. Suppression of GDH activity with RNA interference or an inhibitor shows that the enzyme is dispensable in cells able to metabolize glucose but is required for cells to survive impairments of glycolysis brought about by glucose deprivation, 2-deoxyglucose, or Akt inhibition. Inhibition of GDH converts these glutamine-addicted SF-188 cells to glucose-addicted cells | Homo sapiens |