CIDeRplusGeneral Information:
| Id: | 6,363 (click here to show other Interactions for entry) |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance Pancreatic cancer - [OMIM] |
| Mammalia | |
| review | |
| Reference: | Cohen R et al.(2015) Targeting cancer cell metabolism in pancreatic adenocarcinoma Oncotarget 19 [PMID: 26164081] |
Interaction Information:
| Comment | Although glutamine is a non-essential AA, most cancer cells exhibit glutamine addiction. The metabolic fate of glutamine is multifaceted; it can be used for lipid biosynthesis, as a nitrogen donor for AA and nucleotide biosynthesis, as a carbonic substrate for the re-feeding of the mitochondrial TCA cycle through a phenomenon called anaplerosis, and even as fuel for cell energy production. PDAC cells metabolize glutamine through a non-canonical pathway in which transaminases play a crucial role. Whereas most cells use glutamate dehydrogenase (GDH-1) to convert glutamine-derived glutamate into alpha-ketoglutarate in the mitochondria to fuel the TCA cycle, PDAC relies on a distinct pathway in which glutamine-derived aspartate is transported into the cytoplasm where it can be converted into oxaloacetate by aspartate transaminase (i.e. glutamic-oxaloacetic transaminase [GOT-1]), then into malate, and finally into pyruvate. |
|
Formal Description Interaction-ID: 59863 |
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| Drugbank entries | Show/Hide entries for GOT1 |