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Literature summary for 1.4.1.2 extracted from

  • Yang, C.; Sudderth, J.; Dang, T.; Bachoo, R.G.; McDonald, J.G.; DeBerardinis, R.J.
    Glioblastoma cells require glutamate dehydrogenase to survive impairments of glucose metabolism or Akt signaling (2009), Cancer Res., 69, 7986-7993.
    View publication on PubMedView publication on EuropePMC
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Application

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

Organism UniProt Comment Textmining
Homo sapiens
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-
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Source Tissue

Source Tissue Comment Organism Textmining
SF-188 cell
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 Homo sapiens
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Specific Activity [micromol/min/mg]

Specific Activity Minimum [µmol/min/mg] Specific Activity Maximum [µmol/min/mg] Comment Organism
additional information
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 glucose withdrawal stimulates GDH activity Homo sapiens

Synonyms

Synonyms Comment Organism
GDH
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 Homo sapiens
glutamate dehydrogenase
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 Homo sapiens

General Information

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