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Literature summary extracted from

  • Duan, L.; Ying, G.; Danzer, B.; Perez, R.E.; Shariat-Madar, Z.; Levenson, V.V.; Maki, C.G.
    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.
    View publication on PubMedView publication on EuropePMC

Application

EC Number Application Comment Organism
3.4.16.2 medicine prolyl carboxypeptidase and prolyl endopeptidase regulate insulin receptor substrate IRS-1 stability and PI3K/AKT activation in pancreatic cancer Homo sapiens

Organism

EC Number Organism UniProt Comment Textmining
3.4.16.2 Homo sapiens
-
-
-
3.4.21.26 Homo sapiens
-
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
3.4.16.2 CAPAN-1 cell pancreatic cancer cell line Homo sapiens
-
3.4.16.2 PANC-1 cell pancreatic cancer cell line Homo sapiens
-
3.4.16.2 PK-9 cell pancreatic cancer cell line Homo sapiens
-
3.4.21.26 pancreatic cancer cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3.4.21.26 Z-Gly-Pro-7-amido-4-methylcoumarin + H2O
-
 Homo sapiens ?
-
 ?

Synonyms

EC Number Synonyms Comment Organism
3.4.21.26 PREP
-
 Homo sapiens
3.4.21.26 prolylendopeptidase
-
 Homo sapiens

General Information

EC Number General Information Comment Organism
3.4.16.2 physiological function prolyl carboxypeptidase and the related family member prolyl endopeptidase are essential for proliferation and survival of pancreatic cancer cells. Depletion/inhibition of prolyl carboxypeptidase and prolyl endopeptidase induces serine phosphorylation and degradation of insulin receptor substrate IRS-1, leading to inactivation of the cellular PI3K and AKT. Depletion/inhibition of prolyl carboxypeptidase /prolyl endopeptidase destabilized IRS-1 in the cells treated with rapamycin, blocking the feedback activation PI3K/AKT. Inhibition of prolyl carboxypeptidase /prolyl endopeptidase enhances rapamycin-induced cytotoxicity Homo sapiens
3.4.21.26 malfunction depletion/inhibition of prolylcarboxypeptidase (PRCP)/prolylendopeptidase (PREP) suppresses rapamycin-induced activation of PI3K/AKT with consequent additive/synergistic cytotoxicity Homo sapiens
3.4.21.26 physiological function PRCP and PREP regulate IRS-1 stability and PI3K/AKT activation in pancreatic cancer Homo sapiens