Literature summary for 3.4.16.2 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.

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Application

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

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

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

General Information

General Information	Comment	Organism
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

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Release 2023.1 (January 2023)