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Literature summary for 3.4.21.26 extracted from
- The prolyl peptidases PRCP/PREP regulate IRS-1 stability critical for rapamycin-induced feedback activation of PI3K and AKT (2014), J. Biol. Chem., 289, 21694-21705.
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | - |
- |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| pancreatic cancer cell | - |
Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| Z-Gly-Pro-7-amido-4-methylcoumarin + H2O | - |
Homo sapiens | ? | - |
? |  |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| PREP | - |
Homo sapiens |
| prolylendopeptidase | - |
Homo sapiens |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | depletion/inhibition of prolylcarboxypeptidase (PRCP)/prolylendopeptidase (PREP) suppresses rapamycin-induced activation of PI3K/AKT with consequent additive/synergistic cytotoxicity | Homo sapiens |
| physiological function | PRCP and PREP regulate IRS-1 stability and PI3K/AKT activation in pancreatic cancer | Homo sapiens |
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Release 2023.1 (January 2023)
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