EC Number   |
General Information |
Reference |
|---|
   3.4.21.2 | malfunction |
loss-of-function mutations increase the risk for pancreatitis. Variant p.G214R degrades trypsinogen poorly, is resistant to inhibitors and cleaves their reactive sites. Pathogenic variant p.G214R is a functional paralog of mesotrypsin, an inhibitor-degrading trypsin isoform |
754111 |
| 3.4.21.2 | malfunction |
pancreatitis-associated CTRC mutations can markedly increase the propensity of chymotrypsinogen C to elicit endoplasmic reticulum stress in pancreatic acinar cells. Diminished secretion and intracellular retention/degradation of the p.A73T CTRC mutant. Endoplasmic reticulum stress in AR42J cells is proportional to intracellular levels of the p.A73T CTRC mutant. No activation of the PERK pathway and NFkappaB in acinar cells expressing the p.A73T CTRC mutant. Apoptotic cell death in AR42J cells expressing the p.A73T CTRC mutant |
708628 |
| 3.4.21.2 | malfunction |
the protective effect of chymotrypsin C against pancreatitis can be compromised by loss-of-function mutations in CTRC, which increase risk for sporadic chronic pancreatitis |
754134 |
| 3.4.21.2 | physiological function |
chymotrypsin C protects against pancreatitis by degrading trypsinogen and thereby curtailing harmful intrapancreatic trypsinogen activation |
754111 |
| 3.4.21.2 | physiological function |
intrapancreatic activation of human anionic trypsinogen is prevented through chymotrypsin-mediated degradation. Chymotrypsin C controls activation of human cationic trypsinogen through proteolytic cleavage of regulatory sites. Chymotrypsin C promotes degradation of anionic trypsinogen more effectively than it does with cationic trypsinogen |
754134 |
